Wetenschappelijk onderzoek over cardiomyopathie en hartfalen

Het protocol voor de behandeling cardiomyopathie (hartfalen) is op basis van wetenschappelijke publicaties ontwikkeld. Hierbij is gebruik gemaakt van de National Library of Medicine (PubMed). Daar waar mogelijk werden studies die opgezet zijn volgens het “placebo controlled cross-over” principe gebruikt. Andere vormen die vaak werden gebruik zijn reviews en epidemiologisch onderzoek. Publicaties uit bladen als The Lancet, American Journal of Cardiology, The New England Journal of Medicine hadden de voorkeur

Oorzaken van cardiomyopathie en hartfalen

Hartfalen als complicatie bij een hartinfarct

    National Library of Medicine (PubMed)
  1. Weir RA, McMurray JJ Curr Heart Fail Rep. 2006 Dec;3(4):175-80. Epidemiology of heart failure and left ventricular dysfunction after acute myocardial infarction
    The development of heart failure and/or left ventricular systolic dysfunction has long been regarded as an ominous complication, significantly increasing the morbidity and short- and long-term mortality of survivors of acute myocardial infarction.Although the incidence of heart failure after myocardial infarction has fallen over the last few decades, it remains common, complicating up to 45% of infarcts. Moreover, up to 60% of myocardial infarcts will result in left ventricular systolic dysfunction, depending on the exact definition used.Those at greatest risk of developing heart failure are the elderly, females, and those with prior myocardial infarction. Advances in the management of acute myocardial infarction have led to reduced in-hospital mortality (even when complicated by heart failure), but longer-term mortality remains high in these patients.[Abstract]
  2. Thomas KL, Velazquez EJ Curr Heart Fail Rep. 2005 Dec;2(4):174-82. Therapies to prevent heart failure post-myocardial infarction
    Heart failure (HF) is a common complication of myocardial infarction (MI) that carries a poor prognosis when present. HF and/or left ventricular systolic dysfunction (LVSD) occur in approximately 40% of patients who suffer acute MI. The estimated mortality of patients developing HF or LVSD post-MI is 20% to 30%, with that risk varying based on the presence of HF upon initial assessment versus occurring later during the MI hospitalization. Clinical factors and comorbidities associated with post-MI HF include age, diabetes, hypertension, female gender, infarct size, and tachycardia. Factors associated with decreased survival in patients with post-MI HF include Killip class, age, low blood pressure, tachycardia, male gender, and anterior location of MI. Despite extensive data identifying this patient population as high risk, patients with post-MI HF or LVSD are significantly less likely to receive evidence-based medications or revascularization procedures than those without HF. Despite the high prevalence of HF after MI, few studies have examined therapies to prevent it. This review summarizes studies that reported the incidence, risk factors, and outcomes of patients with post-MI HF or LVSD. Additionally, we discuss therapies to prevent post-MI HF and treatment of patients with post-MI HF and/or LVSD.[Abstract]
  3. Aronow WS. Clin Geriatr Med. 2007 Feb;23(1):123-39. Heart-failure-complicating acute myocardial infarction
    Findings have shown that acute MI complicated by congestive heart failure (CHF) is associated with a high mortality, and that women with acute MI are more likely to be older and to develop CHF than men with acute MI.[Abstract]
  4. Weir RA, McMurray JJ, Velazquez EJ. Am J Cardiol. 2006 May 22;97(10A):13F-25F Epidemiology of heart failure and left ventricular systolic dysfunction after acute myocardial infarction: prevalence, clinical characteristics, and prognostic importance
    The development of heart failure and/or left ventricular systolic dysfunction (LVSD) in the setting of acute myocardial infarction (AMI) results in significant risk far above that of AMI independently. In patients admitted to the hospital for AMI, concomitant heart failure and/or LVSD on hospital admission or development of either or both of these conditions during admission are among the strongest predictors of inhospital death and are associated with significant increases in inhospital, 30-day, and long-term mortality and rehospitalization rates. Given the high risks in this population, aggressive treatment, comprising early initiation and sustained use of evidence-based treatments, is essential for improving prognosis.[Abstract]
  5. Diabetische cardiomyopathie

  6. Giles TD. Am J Med. 2003 Dec 8;115 Suppl 8A:107S-110S. The patient with diabetes mellitus and heart failure: at-risk issues
    The risk for cardiovascular disease, particularly congestive heart failure, is significantly higher in patients with type 2 diabetes mellitus than in individuals without diabetes. The presence of hyperglycemia has been associated with changes in the myocardium that are characteristic of diabetic cardiomyopathy and heart failure. Furthermore, insulin resistance may be associated with cardiomyopathy, even in the absence of hyperglycemia, and has been linked with cardiovascular remodeling. The association between heart failure and insulin resistance suggests that agents that improve insulin sensitivity, such as the thiazolidinediones (TZDs), are likely to be of cardiovascular benefit in patients with diabetes and heart failure. Although TZDs have beneficial cardiovascular effects in patients with type 2 diabetes, such as reducing blood pressure, improving endothelial function, and exerting potential antiatherosclerotic effects, one must be aware of the potential of these agents to cause edema or weight gain as a result of fluid retention and fat accumulation. These issues are of particular concern in patients with diabetes who have heart failure. However, the glycemic and cardiovascular benefits of TZDs may outweigh the potential problems of weight gain and fluid retention noted in some patients. Thus the risk-benefit ratio of using TZDs in patients who have diabetes and heart failure must be carefully considered in this patient population with comorbid disorders.[Abstract]
  7. Boudina S, Abel ED. Circulation. 2007 Jun 26;115(25):3213-23 Diabetic cardiomyopathy revisited
    Diabetes mellitus increases the risk of heart failure independently of underlying coronary artery disease, and many believe that diabetes leads to cardiomyopathy. The underlying pathogenesis is partially understood. Several factors may contribute to the development of cardiac dysfunction in the absence of coronary artery disease in diabetes mellitus. This review discusses the latest findings in diabetic humans and in animal models and reviews emerging new mechanisms that may be involved in the development and progression of cardiac dysfunction in diabetes.[Article]
  8. Codinach Huix P, Freixa Pamias R. An Med Interna. 2002 Jun;19(6):313-20. Diabetic cardiomyopathy: concept, heart function, and pathogenesis
    The diabetic cardiomyopathy is a disease caused by diabetes and is characterised by the presence of diastolic and/or systolic left ventricular dysfunction. Diabetes may produce metabolic alterations, interstitial fibrosis, myocellular hypertrophy, microvascular disease and autonomic dysfunction. It is thought that all of them may cause cardiomyopathy. Other abnormalities that are usually associated with diabetes such as hypertension, coronary artery disease and nephropathy should be excluded before diagnosing diabetic cardiomyopathy. There is no evidence that diabetic cardiomyopathy alone can produce heart failure. However, subclinical ventricular dysfunction has been described in young asymptomatic diabetic patients without other diseases that could affect the cardiac muscle. In these cases we should consider that diabetes is the only cause of the myocardial disease. More studies are needed to know the natural history of diabetic cardiomyopathy.[Abstract]
  9. Cosson S, Kevorkian JP. Diabetes Metab. 2003 Nov;29(5):455-66. Left ventricular diastolic dysfunction: an early sign of diabetic cardiomyopathy?
    The existence of a diabetic cardiomyopathy has been proposed as evidence has accumulated for the presence of myocardial dysfunction in diabetic patients in the absence of ischemic, valvular or hypertensive heart disease.Diastolic dysfunction has been described as an early sign of this diabetic heart muscle disease preceding the systolic damage. Abnormalities in diastolic performance have been first demonstrated by cardiac catheterisation and subsequently by mainly using echocardiography. The pathogenesis of this left ventricular dysfunction is not clearly understood. Microangiopathy, increased extracellular collagen deposition, or abnormalities in calcium transport alone or in combination are considered to be associated with this dysfunction. The relationship between diastolic dysfunction and glycemic control is still a matter of debate. Some epidemiological and clinical arguments suggest that diastolic abnormalities may contribute to the high morbidity and mortality among diabetic patients. However, the prognostic importance of subclinical diastolic dysfunction and the possibilities for intervention are not fully known. Eventually, despite numerous studies, evidence of an intrinsic diastolic dysfunction in diabetes mellitus remains questionable. Indeed, quite contradictory results have been reported. They have been obtained in small, inhomogeneous populations, with sometimes confounding factors, using various echocardiographic indices with known limitations. Also, further studies using more refined techniques for the evaluation of diastolic function are needed, as a prerequisite, to unequivocally relate diabetes mellitus to a specific cardiomyopathy.[Article]
  10. Karnik AA, Fields AV, Shannon RP. Curr Hypertens Rep. 2007 Dec;9(6):467-73. Diabetic cardiomyopathy
    Diabetes mellitus is well recognized as a potent and prevalent risk factor for accelerated atherosclerosis and ischemic heart disease. However, there is also evidence of cardiac dysfunction in diabetes in the absence of coronary atherosclerosis, termed diabetic cardiomyopathy. Changes in ventricular structure and left ventricular systolic and diastolic dysfunction have all been noted even in patients with well-controlled diabetes and without overt macrovascular complications. Insulin resistance, hyperglycemia, and increased free fatty acid metabolism promote coronary microvascular disease, sympathetic nervous system dysfunction, and ventricular remodeling, and may contribute to the altered cardiac phenotype seen in diabetes. In addition to standard therapy (angiotensin-converting enzyme inhibitors and beta-blockers), diabetic patients with left ventricular dysfunction are likely to benefit from targeted therapies to reduce insulin resistance and modulate substrate use.[Abstract]
  11. An D, Rodrigues B Am J Physiol Heart Circ Physiol. 2006 Oct;291(4):H1489-506 Role of changes in cardiac metabolism in development of diabetic cardiomyopathy
    In patients with diabetes, an increased risk of symptomatic heart failure usually develops in the presence of hypertension or ischemic heart disease. However, a predisposition to heart failure might also reflect the effects of underlying abnormalities in diastolic function that can occur in asymptomatic patients with diabetes alone (termed diabetic cardiomyopathy). Evidence of cardiomyopathy has also been demonstrated in animal models of both Type 1 (streptozotocin-induced diabetes) and Type 2 diabetes (Zucker diabetic fatty rats and ob/ob or db/db mice). During insulin resistance or diabetes, the heart rapidly modifies its energy metabolism, resulting in augmented fatty acid and decreased glucose consumption. Accumulating evidence suggests that this alteration of cardiac metabolism plays an important role in the development of cardiomyopathy. Hence, a better understanding of this dysregulation in cardiac substrate utilization during insulin resistance and diabetes could provide information as to potential targets for the treatment of cardiomyopathy. This review is focused on evaluating the acute and chronic regulation and dysregulation of cardiac metabolism in normal and insulin-resistant/diabetic hearts and how these changes could contribute toward the development of cardiomyopathy.[Article]
  12. Khavandi K, Khavandi A, Asghar O, Greenstein A, Withers S, Heagerty AM, Malik RA Best Pract Res Clin Endocrinol Metab. 2009 Jun;23(3):347-60. Diabetic cardiomyopathy–a distinct disease?
    Diabetic individuals have a significantly increased likelihood of developing cardiovascular disease. Whilst part of this association is explained by the presence of concomitant risk factors, large epidemiological studies have consistently reported diabetes as a strong risk factor for the development of heart failure after adjusting for such covariates. This has resulted in the notion that there is a distinct cardiomyopathy specific to diabetes, termed ‘diabetic cardiomyopathy’. The natural history is characterized by a latent subclinical period, during which there is evidence of diastolic dysfunction and left ventricular hypertrophy, before overt clinical deterioration and systolic failure ensue. These clinical findings have been supported by a growing body of experimental data which support the notion that diabetes inflicts a direct insult to the myocardium, with cellular, structural and functional changes manifest as the diabetic myocardial phenotype. Several of these mechanisms appear to work in unison, forming complicated reciprocal pathways of disease. Reactive oxygen species and alterations in intracellular calcium homeostasis appear to play significant roles in many of these mechanisms. Determining the hierarchy of this cascade of disease will allow identification of the pathological trigger most responsible for disease. Translational research in this field is currently hindered by a lack of clinical studies and intervention trials specifically in patients with diabetic cardiomyopathy. Future clinical and experimental studies of accurate models of diabetic cardiomyopathy should help to define the true aetiology and lead to the development of specific pharmacotherapies for this condition, ultimately reducing the increased cardiovascular morbidity and mortality in diabetic patients.[Abstract]
  13. Zwangerschapscardiomyopathie

  14. Palmer DG J Perinat Neonatal Nurs. 2006 Oct-Dec;20(4):324-32. Peripartum cardiomyopathy
    Peripartum cardiomyopathy is a rare and potentially lethal cardiac complication of pregnancy occurring in the final month of pregnancy through the first 5 months after birth. It is characterized by the development of congestive heart failure and left ventricular systolic dysfunction, in previously healthy women with no other identifiable cause for heart failure. The etiology of peripartum cardiomyopathy is not well understood. Potential causal mechanisms include infection, autoimmune disease, and abnormal response to the hemodynamic stresses of pregnancy. There is significant risk of reoccurrence in subsequent pregnancies. The purpose of this article is to review the pathophysiology, diagnosis, management, prognosis, and nursing implications of peripartum cardiomyopathy.[Abstract]
  15. Al-Shamiri MQ, Al-Nozha MM Saudi Med J. 2003 Oct;24(10):1048-51 Peripartum cardiomyopathy searching for a better understanding
    Congestive heart failure is an uncommon complication of pregnancy with potentially life-threatening consequences. Peripartum cardiomyopathy (PPCM) is a disease of unknown cause in which severe left ventricular dysfunction occurs during late pregnancy or the early puerperium. In the past, the diagnosis of this entity was made on clinical grounds; however, modern echocardiographic techniques have allowed more accurate diagnoses by excluding cases of diseases that mimic the clinical symptoms and signs of heart failure. Risk factors for peripartum cardiomyopathy include advanced maternal age, multiparity, African descent, twinning, and long-term tocolysis. An extensive search for the causes of peripartum cardiomyopathy has been unrevealing. Treatment does not differ from treatment of idiopathic cardiomyopathy. The prognosis of peripartum cardiomyopathy is related to the recovery of ventricular function. Caution is advised in recommending subsequent pregnancy, especially if left ventricular dysfunction is persistent. In this review, we will discuss different aspects of PPCM as the initial patient contact, obstetricians and family practitioners must recognize this malady early and rapidly institute the proper medical therapy directed towards the congestive state.[Abstract]
  16. Abboud J, Murad Y, Chen-Scarabelli C, Saravolatz L, Scarabelli TM. Int J Cardiol. 2007 Jun 12;118(3):295-303 Peripartum cardiomyopathy: a comprehensive review
    Peripartum cardiomyopathy (PPCM) is a rare disorder in which left ventricular dysfunction and symptoms of heart failure occur in the peripartum period in previously healthy women. Incidence of PPCM ranges from 1 in 1300 to 1 in 15,000 pregnancies. The etiology of PPCM is unknown, but viral, autoimmune, and idiopathic causes may contribute. The diagnostic criteria are onset of heart failure in the last month of pregnancy or in first 5 months postpartum, absence of determinable cause for cardiac failure, and absence of a demonstrable heart disease before the last month of pregnancy. Risk factors for PPCM include advanced maternal age, multiparity, African race, twinning, gestational hypertension, and long-term tocolysis. The clinical presentation of patients with PPCM is similar to that of patients with dilated cardiomyopathy. Early diagnosis and initiation of treatment are essential to optimize pregnancy outcome. Treatment is similar to medical therapy for other forms of dilated cardiomyopathy. About half the patients of PPCM recover without complications. The prognosis is poor in patients with persistent cardiomyopathy. Persistence of disease after 6 months indicates irreversible cardiomyopathy and portends worse survival.[Abstract]
  17. Bahloul M, Ben Ahmed MN, Laaroussi L, Chtara K, Kallel H, Dammak H, Ksibi H, Samet M, Chelly H, Ben Hamida C, Chaari A, Amouri H, Rekik N, Bouaziz M. Ann Fr Anesth Reanim. 2009 Jan;28(1):44-60. Epub 2008 Dec 25. Peripartum cardiomyopathy: incidence, pathogenesis, diagnosis, treatment and prognosis
    Prognosis is highly related to reversal of ventricular dysfunction. Compared to historically higher mortality rates, recent reports describe better outcome, probably because of advances in medical care. Based on current information, future pregnancy is usually not recommended in patients who fail to recover normal heart function.[Abstract]
  18. Tako-tsubocardiomyopathie

  19. Koulouris S, Pastromas S, Sakellariou D, Kratimenos T, Piperopoulos P, Manolis AS. Hellenic J Cardiol. 2010 Sep-Oct;51(5):451-7. Takotsubo cardiomyopathy: the “broken heart” syndrome
    Takotsubo cardiomyopathy (TTC), a seemingly rare but in fact underrecognized transient left ventricular dysfunction, is a clinical entity mimicking an acute coronary syndrome. Its main characteristics are chest pain, ischemic electrocardiographic changes, mildly elevated cardiac enzymes and wall motion abnormalities.[ Article]
  20. Wikipedia Takotsubo cardiomyopathy
    Takotsubo cardiomyopathy, also known as transient apical ballooning syndrome, apical ballooning cardiomyopathy, stress-induced cardiomyopathy, broken-heart-syndrome, Gebrochenes-Herz-Syndrom, and simply stress cardiomyopathy, is a type of non-ischemic cardiomyopathy in which there is a sudden temporary weakening of the myocardium (the muscle of the heart). Because this weakening can be triggered by emotional stress, such as the death of a loved one, a break-up, or constant rejection, the condition is also known as broken heart syndrome. Stress cardiomyopathy is a well-recognized cause of acute heart failure, lethal ventricular arrhythmias, and ventricular rupture.[Article]
  21. Sinning Ch, Keller T, Abegunewardene N, Kreitner KF, Münzel T, Blankenberg S Clin Res Cardiol. 2010 Dec;99(12):771-80. Tako-Tsubo syndrome: dying of a broken heart?
    The aim of the article is to review the etiology, pathology and epidemiology of a disease entity named Tako-Tsubo syndrome, receiving this name according to the picture obtained during ventriculography resembling a Japanese octopus trap. The Tako-Tsubo syndrome is a diagnosis encountered in patients with acute coronary syndrome and, therefore, is important to consider.METHODS: The literature search was performed in the MEDLINE database to identify the relevant topics. The references reported were used to complete the literature search.RESULTS: The Tako-Tsubo syndrome is rising in incidence and makes up a relevant part of patients with acute coronary syndrome. The prevalence is described to be 0.6-2.5%. Especially, older women in the postmenopause with emotional stress are affected. The clinical changes and ECG alterations resemble the same characteristics like in acute coronary syndrome; however, the coronary arteries often show no impaired blood flow or only marginal changes. The reason for this syndrome is allocated to stress reactions with increased levels of stress hormones. As well, some patients develop contraction abnormalities like in Tako-Tsubo syndrome during intracranial bleeding, pheochromocytoma, seizures, infectious causes and sepsis, showing that not only emotional stress is responsible for the manifestation of this disease.CONCLUSION: The prevalence of Tako-Tsubo syndrome is about 2%, therefore this syndrome has to be considered in patients with acute coronary syndrome. Despite the life-threatening complications during the acute phase, a complete regression of the contraction abnormality is often reported.[Abstract]
  22. Roggenbach J, Roggenbach R, Ehlermann P. Anaesthesist. 2010 Jul;59(7):636-42. Tako-Tsubo cardiomyopathy
    Tako-Tsubo cardiomyopathy (TK) is an acutely appearing myocardial disease leading to impaired cardiac function, which can barely be distinguished clinically from an acute myocardial infarction. It occurs mainly in postmenopausal women and usually has a good prognosis. The pathophysiology of TK still remains to be elucidated but the favoured hypothesis is myocardial damage induced by catecholamine excess. Various acute diseases, emotional stress, surgical procedures and anaesthesia have been described as possible causes for TK. Little is known about the optimal therapy, however, there might be potential differences in the therapy of TK compared to contemporary therapy algorithms for heart failure. Knowledge of TK as a differential diagnosis for acute myocardial infarction is necessary to avoid incorrect treatment.[Abstract]
  23. Slivnjak V, Lakusi? N, Cerovec D, Richter D Lijec Vjesn. 2009 Jan-Feb;131(1-2):14-7. Tako-Tsubo cardiomyopathy; reversible left ventricular dysfunction mimicking acute myocardial infarction with ST-elevation
    Tako-Tsubo cardiomyopathy is still en entity of unknown etiology and pathophysiology which clinically manifests with sudden, severe chest pain and/or dyspnea. It is generally triggered by emotional or physical stress and most cases are reported in postmenopausal women. Electrocardiographic changes are similar to acute myocardial infarction with ST-elevation, laboratory markers of myocardial lesion are usually mild to moderately high, and coronary angiography shows no significant pathomorphological changes of epicardial coronary arteries. Ventriculography and echocardiography show reversible akinesis and ballooning of the left ventricular apex with reduced ejection fraction which is usually normalized within 2-4 weeks. Generally, Tako-Tsubo cardiomyopathy has a good prognosis, in-hospital mortality rate is about 1%. In this article, we present a review about todays knowledge on Tako-Tsubo cardiomyopathy.[Abstract]
  24. Aronov DM.`Kardiologiia. 2008;48(10):51-5 Takotsubo cardiomyopathy: origin and variants
    This literature review is devoted to the ” tako-tsubo ” cardiomyopathy – rare type of cardiomyopathy characterized by transient myocardial stunning. In acute phase the disease resembles myocardial infarction. However no involvement of coronary arteries is found at angiography. Echocardiography and ventriculography reveal a- or – hypokinesia of various parts of the left ventricle. Classic (initial) variant of the disease is associated with concomitant apical akinesia and hyperkinesis of basal segments. The heart acquires a distinctive configuration with ballooning apex which resembles device used to trap octopus. The author refers to described by him 11 cases of myocardial damage with infarct-like clinic without changes of coronary arteries in healthy men younger than 35 years (D.M.Aronow, 1968, 1974). These cases occurred during severe physical stress and had in their basis hypercatecholaminemia which led to reversible myocardial damage of the myocardium which corresponded to modern concept of myocardial stunning. During exercise tests these patients had 3 times greater increase of urinal epinephrine excretion compared with 61 patients of the same age with atherosclerotic heart disease.[Abstract]
  25. Hoge bloeddruk als oorzaak van hartfalen

  26. Vasan RS, Levy D. Arch Intern Med. 1996 Sep 9;156(16):1789-96. The role of hypertension in the pathogenesis of heart failure. A clinical mechanistic overview
    Hypertension plays a key role in the evolution of the syndrome of heart failure. Hypertension has been identified as the chief precursor of left ventricular hypertrophy.Hypertensive left ventricular hypertrophy can lead to ventricular diastolic dysfunction; it is also a risk factor for myocardial infarction, which is a principal cause of left ventricular systolic dysfunction. Asymptomatic left ventricular dysfunction, whether systolic or diastolic, culminates in clinically overt heart failure when a threshold is exceeded or when other precipitating factors are superimposed. The onset of overt heart failure heralds a bleak outcome. These structural and functional changes associated with hypertension evolve over decades and are preventable with effective antihypertensive treatment. These observations emphasize the importance of early diagnosis and effective treatment of hypertension to prevent cardiac complications.[Article]
  27. Kazzam E, Ghurbana BA, Obineche EN, Nicholls MG. J Hum Hypertens. 2005 Apr;19(4):267-75. Hypertension–still an important cause of heart failure?
    Hypertension has been the single most important risk factor for heart failure until the last few decades. Now, it is frequently claimed that atherosclerotic coronary artery disease dominates as the major underlying cause, and hypertension is of lesser importance. We here review evidence regarding the contribution of hypertension to heart failure in the recent decades. It is not possible, in our view, to be confident of the relative importance of hypertension and coronary artery disease since there are significant limitations in the available data. The often-questionable diagnostic criteria used in defining heart failure is one such limitation. The absence or inadequacy of blood pressure recordings over the years prior to a diagnosis of heart failure seriously hinders the reaching of firm conclusions in many reports. Extrapolations from aetiological observations in one racial group to those in other racial groups, and from highly selected study groups in tertiary referral centres to patients with heart failure in primary and secondary care, may not be justified. Finally, the situation of heart failure primarily due to impaired left ventricular diastolic function, where hypertension is a frequent precursor, is often ignored in discussions of aetiology. Our view is that hypertension remains and probably is the single most, important modifiable risk factor for cardiac failure in some races and countries, where the dominant cardiac abnormality is left ventricular diastolic dysfunction. The situation is less clear for patients with heart failure primarily due to left ventricular systolic dysfunction.[Article]
  28. Meredith PA, Ostergren J. J Renin Angiotensin Aldosterone Syst. 2006 Jun;7(2):64-73. From hypertension to heart failure — are there better primary prevention strategies?
    Although in the developed world the incidence of and mortality from coronary heart disease (CHD) and stroke have been declining over the last 15 years, heart failure is increasing in incidence, prevalence and overall mortality, despite advances in the diagnosis and management of the condition.Hypertension, alone or in combination with CHD, precedes the development of heart failure in the majority of both men and women. Whilst there have been improvements in the overall management of hypertension, as reflected in rates of diagnosis, awareness, treatment and control of blood pressure (BP), there are still many patients with hypertension who remain undiagnosed or untreated and of those who do receive treatment many fail to achieve current targets for BP control. Placebo-controlled trials in hypertension, largely based on diuretic and beta-blocker-based regimens, have unequivocally demonstrated that the treatment of hypertension can significantly reduce the incidence of heart failure. Newer treatment strategies offer theoretical and proven practical advantages over established antihypertensive therapy. In particular, AT1-receptor blockers appear to provide benefits beyond BP control and are effective in the treatment of both hypertension and heart failure. Thus, the primary prevention of heart failure in hypertensive patients should be based upon strategies that provide tight and sustained BP control necessitating the use of multiple drugs. However, there is now compelling evidence to suggest that this therapy should include an antihypertensive agent that inhibits the reninangiotensin- aldosterone system (RAAS).[Article]
  29. Himmelmann A. Blood Press. 1999;8(5-6):253-60 Hypertension: an important precursor of heart failure
    Hypertension is an important risk factor for cardiovascular morbidity and mortality. Hypertension is associated with the development of congestive heart failure by way of left ventricular hypertrophy, with left ventricular dilatation and through myocardial ischemia and left ventricular damage.Reports on the natural history of untreated hypertension indicate that at least 50% of affected subjects develop congestive heart failure. Hypertension is an important precursor of heart failure, and still the most common risk factor for congestive heart failure in the population. In clinical trials, particularly in elderly patients, a reduction in the incidence of congestive heart failure has been observed. Despite increments in the use of antihypertensive drugs, mortality from congestive heart failure among the elderly is increasing. Moreover, several patients with hypertension are unaware, untreated and uncontrolled for the most important risk factor for congestive heart failure. For the primary prevention of heart failure, improvements in blood pressure control are of vast importance.[Abstract]
  30. Cardiomyopathie als complicatie na een virale infectie

  31. Sano T. Nippon Rinsho. 2006 Oct;64(10):1916-20. Influenza myocarditis and pericarditis
    The true incidence of influenza myocarditis in the general population is unknown, because of the variable clinical presentation and the absence of a established noninvasive diagnostic test that can confirm the diagnosis. Influenza is, however, one of the frequently implicated viruses caused myocarditis as well as Coxsackie B, adenovirus, echovirus and cytomegalovirus.The clinical manifestations of viral myocarditis vary greatly from asymptomatic electrocardiographic changes to fulminant heart failure with fatal arrhythmias. We should recognize that subtle cardiac symptoms and signs in many subclinical cases may be overshadowed by systemic manifestations of the underlying influenza infection. Although specific therapy consisted of anti-viral agents, intravenous gamma-globulin treatment or mechanical ventricular supports may be available for influenza myocarditis, it has not been established that the myocarditic process itself will be favorably affected.[Abstract]
  32. Maisch B, Ristic AD, Portig I, Pankuweit S Front Biosci. 2003 Jan 1;8:s39-67 Human viral cardiomyopathy
    Viral infection of the heart is relatively common, usually asymptomatic and has a spontaneous and complete resolution.It can, however, in rare cases, lead to substantial cardiac damage, development of viral cardiomyopathy and congestive heart failure.Viral cardiomyopathy is defined as viral persistence in a dilated heart. It may be accompanied by myocardial inflammation and then termed inflammatory viral cardiomyopathy (or viral myocarditis with cardiomegaly). If no inflammation is observed in the biopsy of a dilated heart (<14 lymphocytes and macrophages/mm ) the term viral cardiomyopathy or viral persistence in dilated cardiomyopathy should be applied. The diagnosis of myocarditis and viral cardiomyopathy can be made only by endomyocardial biopsy, implementing the WHO/WHF criteria, and PCR techniques for identification of viral genome.The most frequent cardiotropic viruses detected by endomyocardial biopsy are Parvo B19, enteroviruses, adenoviruses, cytomegalovirus, and less frequently Epstein-Barr virus, and influenza virus.[Abstract]
  33. Fett JD. Expert Opin Ther Targets. 2008 Sep;12(9):1073-5. Diagnosis of viral cardiomyopathy by analysis of peripheral blood?
    Polymerase chain reaction testing has become an important tool in assessing the role of virus in inflammatory cardiomyopathies, including fulminant myocarditis, lymphocytic myocarditis, peripartum cardiomyopathy, unknown cause or idiopathic dilated cardiomyopathy, and acute myocarditis of suspected viral etiology. While this tool has been traditionally reserved for application to endomyocardial biopsy tissue, there is increasing evidence that it may also be helpful in the study of peripheral blood samples, particularly during the viremic phase when there may also be IgM antibodies present against one or more of the cardiotropic viruses.[Abstract]
  34. Knowlton KU. Curr Top Microbiol Immunol. 2008;323:315-35. CVB infection and mechanisms of viral cardiomyopathy
    Coxsackievirus infection has been demonstrated to be a cause of acute and fulminant viral myocarditis and has been associated with dilated cardiomyopathy. While considerable attention has focused on the role of the cellular and humoral, antigen-specific immune system in viral myocarditis, the interaction between the virus and the infected host myocyte is also important. Coxsackievirus has a relative tropism for the heart that is in part mediated by relatively high levels of the coxsackievirus and adenovirus receptor (CAR) on the cardiac myocyte. Once within the myocyte, coxsackievirus produces proteases, such as protease 2A, that have an important role in viral replication, but can also affect host cell proteins such as dystrophin. Cleavage of dystrophin may have a role in release of the virus from the myocyte since viral infection is increased in the absence of dystrophin. In addition to the direct effect of viral proteins on cardiac myocytes, there is now evidence that the cardiac myocyte has a potent innate immune defense against coxsackieviral infection. Suppressors of cytokine signaling (SOCS) can inhibit an interferon-independent mechanism within the cardiac myocyte. In summary, the interaction between coxsackievirus and the infected myocyte has a significant role in the pathogenesis of viral myocarditis and the susceptibility to viral infection.[Abstract]
  35. Donal E, Piriou N, Nanadoumgar H, Mignot A, Bressolette C, Toquet C, Trochu JN. Arch Mal Coeur Vaiss. 2005 Oct;98(10):984-91 Viral cardiomyopathy
    In too many cases, the cause of dilated cardiomyopathy (DCM) remains undetermined. Coronary or valvular heart diseases, connective tissue disorders, toxic causes and signs of infection are systematically investigated. With the exceptions of coronary and sometimes valvular heart disease, the treatment of cardiac failure remains symptomatic treating the consequences but not the cause of DCM, which is therefore diagnosed as “idiopathic”. This artericle reports the clinical history of 4 patients followed up for apparently “idiopathic” DCM in whom the presence of chronic Parvovirus B-19 infection was demonstrated. Based on these 4 cases, the hypothesis of an infectious cause of DCM and the role of myocardial biopsy, given the progress in molecular biology, are reconsidered. Parvovirus B-19 infection has recently been recognised not only as a cause of myocarditis but also of chronic viral cardiomyopathy, as in adeno and enteroviral infection. The authors conclude that the progress in molecular biology, the recognition of a viral aetiology and the efficacy of immuno-modulator therapy such as beta-interferon, may lead to a new management strategy of patients with DCM in cardiological referral centres.[Abstract]
  36. Kühl U, Schultheiss HP. Heart Fail Clin. 2010 Oct;6(4):483-96, viii-ix. Myocarditis in children
    Myocarditis is an inflammatory disease of the cardiac muscle caused by myocardial infiltration of immunocompetent cells following any kind of cardiac injury.Acute myocarditis in childhood is often a result of a viral infection that produces myocardial necrosis and triggers an immune response to eliminate the infectious agent. Chronic myocardial injury may develop by postinfectious immune or autoimmune processes or be associated with systemic autoimmune diseases, which, in the long run, are responsible for persistent or progressive ventricular dysfunction, arrhythmias, and cardiac complaints. The disease often presents as an acute form of dilated cardiomyopathy, but because of its broad spectrum of presentation the clinical diagnosis is frequently misleading. If the underlying infectious or immune-mediated causes of the disease are carefully defined by clinical and biopsy-based tools, specific immunosuppressive and antiviral treatment options in addition to basic symptomatic therapy may avoid unnecessary interventions and improve prognosis in many patients with acute and chronic disease.[Abstract]
  37. Lymecarditis

  38. Lamaison D. Med Mal Infect. 2007 Jul-Aug;37(7-8):511-7. Cardiac involvement in Lyme disease
    Cardiac manifestations of Lyme Borreliosis are relatively infrequent, occurring within weeks after the infectious tick bite (median of 21 days), and resulting at this stage from a direct borrelial infection of the myocardium, as indicated by reports of spirochete isolation from pericardium and myocardium. They may persist or appear in the late, tertiary phase of the illness, being then more likely due to infection-triggered autoimmunity. Lyme carditis typically presents with a fluctuating degree of atrioventricular block that spontaneously resolves in several days. Rarely, myocarditis may occur with or without pericardial involvement, in patients presenting with chest pain, ST depression or T wave inversion, mimicking an acute myocardial infarction, and various arrhythmias are reported, as well as pericardial effusion or heart failure. A complete recovery is usually observed, spontaneous or after antibiotherapy. Severe myocarditis or Pericarditis leading to death is exceptional. The diagnosis of Lyme carditis is based on the same association of clinical and laboratory features as in Lyme disease without cardiac involvement. But the occurrence of conduction disturbances in healthy young people suggests screening for other criteria of Lyme disease. The management of Lyme carditis does not differ from the treatment of Lyme disease without carditis and is mainly based upon the use of doxycycline or ceftriaxone.[Abstract]
  39. Pinto DS Med Clin North Am. 2002 Mar;86(2):285-96. Cardiac manifestations of Lyme disease
    Lyme disease is a vector-borne illness that can affect numerous organ systems during the early disseminated phase, including the heart. The clinical course of Lyme carditis is usually benign with most patients recovering completely. In rare instances, death from Lyme carditis has been reported. The cardinal manifestation of Lyme carditis is conduction system disease, which generally is self-limited. Heart block occurs usually at the level of the atrioventricular node but often is unresponsive to atropine sulfate. Temporary pacing may be necessary in more than 30% of patients, but permanent heart block rarely develops. Myocardial and pericardial involvement can occur but generally is mild and self-limited. Diagnosis is made by associating the clinical and historical features of borreliosis, such as previous tick bite, EM, or neurologic involvement, with electrocardiographic abnormalities and symptoms such as chest pain, palpitations, syncope, and dyspnea. Serologic studies and endomyocardial biopsy can support the diagnosis in the correct clinical setting, and MR imaging, echocardiography, and gallium scanning have utility in selected circumstances. No treatment has been shown clearly to attenuate or prevent the development of Lyme carditis, but mild carditis generally is treated with oral antibiotics and severe carditis with intravenous antibiotics in an effort to eradicate the infection and prevent late complications of Lyme disease. There is conflicting evidence regarding the role that B. burgdorferi plays in the development and progression of chronic congestive heart failure. Because of the significant false-positive ELISA rate in this population and the unclear benefit of antibiotic therapy, confirmatory Western blot analysis is recommended. Routine therapy and screening of patients with idiopathic dilated cardiomyopathy is of limited utility and should be reserved for patients with clear history of antecedent Lyme disease or tick bite.[Abstract]
  40. McAlister HF, Klementowicz PT, Andrews C, Fisher JD, Feld M, Furman S. Ann Intern Med. 1989 Mar 1;110(5):339-45. Lyme carditis: an important cause of reversible heart block
    Lyme disease is a tick-borne spirochetal infection, characterized by erythema chronicum migrans and an acute systemic illness. The disease is endemic in many parts of the north-eastern United States. Without treatment, late rheumatic, neurologic, and cardiac complications frequently occur. We report four serologically confirmed cases of Lyme carditis in previously healthy young men (mean age, 45 years) from endemic areas. Each presented with severe symptomatic atrioventricular block, three with episodes of prolonged ventricular asystole. Two had permanent pacemakers implanted (one was later removed), and another, very nearly did, before diagnosis. All four patients were treated with antibiotics, and in each case their rhythm returned to sinus, though one patient has Wenckebach second degree block with atrial pacing at 120 beats/min 16 months later. Carditis occurs in 4% to 10% of cases of Lyme disease and usually begins 3 to 6 weeks after the initial illness. It manifests as a transient myocarditis with varying degrees of atrioventricular block. The diagnosis is made primarily on clinical grounds and confirmed by serologic testing. Temporary cardiac pacing is frequently needed by patients who have severe heart block with hemodynamic instability. The evidence suggests that, in most cases, the block is at the level of the atrioventricular node. The block generally resolves completely with antibiotic treatment. Complete heart block rarely persists more than 1 week and the long-term prognosis appears to be excellent. Consideration and prompt recognition of this potentially lethal, but reversible, cause of heart block is crucial in order to avoid inappropriate permanent pacemaker implantation.[Abstract]
  41. Chemokuur bij de behandeling van kanker

  42. Guglin M, Cutro R, Mishkin JD. J Card Fail. 2008 Jun;14(5):437-44. Trastuzumab-induced cardiomyopathy
    Trastuzumab is a recombinant humanized monoclonal antibody used for the treatment of advanced breast cancer. It improves survival and increases response to chemotherapy.The major side effect of trastuzumab is cardiotoxicity manifesting as a reduction in left ventricular systolic function, either asymptomatic or with signs and symptoms of heart failure. Although reversible in most cases, cardiotoxicity frequently results in the discontinuation of trastuzumab. The objective of this review is to summarize facts about trastuzumab-induced cardiotoxicity and to highlight the areas of future investigations. We searched PubMed for trials involving trastuzumab used as an adjuvant therapy for breast cancer, including the metastatic breast cancer setting, and focused on cardiotoxicity.[Abstract]
  43. Singal PK, Iliskovic N, Li T, Kumar D. FASEB J. 1997 Oct;11(12):931-6. Adriamycin cardiomyopathy: pathophysiology and prevention
    Current knowledge about adriamycin cardiomyopathy indicates that the major cause of this condition is increased oxidative stress although the drug’s antitumor action in patients may involve other mechanisms.Controversies about the different antioxidants in preventing cardiomyopathy likely stem from the fact that antioxidants must be effective in both the lipid and water phases, and the dose must be optimal, in order to be protective. Probucol, an antioxidant and promoter of endogenous antioxidants, is one such agent. Conducting clinical trials with an optimal dose of probucol is the next step and should make this great anticancer drug safer and more efficient in the fight against the cancer.[Abstract]
  44. Chen T, Xu T, Li Y, Liang C, Chen J, Lu Y, Wu Z, Wu S. Cancer Treat Rev. 2011 Jun;37(4):312-20 Risk of cardiac dysfunction with trastuzumab in breast cancer patients: a meta-analysis
    Trastuzumab is used widely for the treatment of early and advanced breast cancer. However, concerns have arisen regarding its cardiac toxicity. We did a systematic review and meta-analysis of published randomized controlled trials (RCTs) to assess the overall risk of cardiac dysfunction associated with trastuzumab treatment.METHODS: We searched PubMed and Web of Science (January 1966-July 2009) and American Society of Clinical Oncology conferences held (January 2000-July 2009) for relevant articles and abstracts. Summary incidence rates, relative risks (RRs), and 95% confident intervals (CIs) were calculated using a fixed-effects or random-effects model.RESULTS: 11,882 patients from 10 RCTs were included for analysis. The incidences of LVEF decrease and congestive heart failure (CHF) were 7.5% (95% CI 4.2-13.1) and 1.9% (95% CI 1.0-3.8) among patients receiving trastuzumab. Trastuzumab significantly increased the risk of LVEF decrease (RR = 2.13, 95% CI, 1.31-3.49; p = 0.003). In addition, it significantly increased the risk of CHF (RR = 4.19, 95% CI 2.73-6.42; p < 0.00001). The increased risk of CHF was observed in patients with early stage (RR = 4.05, 95% CI 2.49-6.58; p < 0.00001) as well as metastatic disease (RR = 4.75, 95% CI 1.93-11.71; p = 0.0007). Furthermore, trastuzumab significantly increased the risk of CHF (RR = 4.27, 95% CI 2.75-6.61, p < 0.00001) in patients receiving anthracycline-based chemotherapy, but not in patients receiving non-anthracycline chemotherapy (RR = 2.42, 95% CI 0.36-16.19, p = 0.36).CONCLUSION: The addition of trastuzumab to anthracycline-based chemotherapy significantly increase the risk of cardiac dysfunction in breast cancer patients. Further studies are recommended for non-anthracycline chemotherapy.[Abstract]
  45. Senkus E, Jassem J. Cancer Treat Rev. 2011 Jun;37(4):300-11. Cardiovascular effects of systemic cancer treatment
    Many methods of systemic anticancer treatment have detrimental effects on the cardiovascular system, thus limiting the possibility of further therapy, worsening patients’ quality of life and increasing mortality.The best recognized and most clinically relevant is the cardiotoxicity of anthracyclines.Other cytotoxic drugs associated with significant risk of cardiovascular complications include alkylating agents, 5-fluorouracil and paclitaxel. Cardiovascular adverse effects are also associated with the use of targeted therapies, such as trastuzumab, bevacizumab and tyrosine kinase inhibitors, and some of the drugs used in the treatment of hematological malignancies, such as all-trans-retinoic acid and arsenic trioxide. The most serious cardiac complication of anticancer therapy is congestive heart failure, associated predominantly with the use of anthracyclines, trastuzumab and high-dose cyclophosphamide. Myocardial ischemia is mainly caused by antimetabolite and interferon alpha treatment. Other adverse effects may include hypotension, hypertension, arrhythmias and conduction disorders, edema, pericarditis and thrombo-embolic complications. The aim of this review is to summarize and critically analyze the available evidence on the cardiovascular toxicity of systemic anticancer therapies, with particular attention to the recently recognized adverse effects of targeted therapies.[Abstract]
  46. Geiger S, Lange V, Suhl P, Heinemann V, Stemmler HJ. Anticancer Drugs. 2010 Jul;21(6):578-90 Anticancer therapy induced cardiotoxicity: review of the literature
    Innovative anticancer strategies have contributed to an improved survival of patients suffering from malignancies, and in some cases, have turned cancer into a chronic disease. Therefore, the early and particularly late onsets of adverse cardiovascular effects of systemic anticancer treatments are of increasing interest. Among a rapidly increasing variety of anticancer drugs, the anthracyclines and the monoclonal antibody, trastuzumab, are the agents with a well-known cardiotoxicity. The diagnostic work-up, the cardiotoxic risk of anthracyclines and trastuzumab, and additionally, cardiotoxicity as a risk factor of a multimodal therapeutic approach in breast cancer patients is discussed in this study.[Abstract]
  47. Telli ML, Hunt SA, Carlson RW, Guardino AE. J Clin Oncol. 2007 Aug 10;25(23):3525-33. Trastuzumab-related cardiotoxicity: calling into question the concept of reversibility
    To assess the spectrum and reversibility of the cardiotoxicity observed in the adjuvant trastuzumab trials.DESIGN: The design and efficacy of the major adjuvant trastuzumab trials was assessed, including the National Surgical Adjuvant Breast and Bowel Project (NSABP) B-31, North Central Cancer Treatment Group N9831, Herceptin Adjuvant, Breast Cancer International Research Group 006, and Finland Herceptin trials. The cardiotoxicity data were evaluated with a focus on the follow-up cardiac evaluations of women who were diagnosed with cardiotoxicity. Proposed mechanisms of trastuzumab-related cardiotoxicity were considered. The natural history of congestive heart failure (CHF) was reviewed with the goal of placing the trastuzumab experience in context.RESULTS: Up to 4% of patients enrolled onto the adjuvant trastuzumab trials experienced severe CHF during treatment. In these trials, early stopping rules that identified an unacceptable level of cardiotoxicity were never reached. Despite this, a large number of patients on these trials experienced some form of cardiotoxicity that ultimately required discontinuation of trastuzumab. Approximately 14% of patients in the NSABP B-31 trial discontinued trastuzumab because of asymptomatic decreases in left ventricular ejection fraction (LVEF). Results of follow-up cardiac evaluations of patients diagnosed with any degree of cardiotoxicity in the NSABP B-31 trial document that a clinically significant proportion of patients have sustained decrements in their LVEF to less than 50%.CONCLUSION: Adjuvant trastuzumab provides substantial benefits to patients with human epidermal growth factor receptor 2-positive breast cancer, however, competing immediate and long-term cardiovascular risks are a great concern. Continued cardiac follow-up of these women is of critical importance.[Abstract]
  48. Genetisch

  49. Caforio AL, Vinci A, Iliceto S Autoimmunity. 2008 Sep;41(6):462-9 Anti-heart autoantibodies in familial dilated cardiomyopathy
    Familial aggregation is a feature of myocarditis and dilated cardiomyopathy (DCM). Myocarditis, a clinically polymorphic inflammatory disease of the myocardium, is diagnosed by endomyocardial biopsy (EMB) and may lead to DCM. Mutations in several genes encoding myocyte structural proteins are known monogenic DCM causes, but because of high etiologic and genetic heterogeneity, the gene defects identified so far account for a minority of cases. In the last decade, it has been discovered that autoimmunity plays a pivotal role in myocarditis and DCM that are thought to represent different stages of an organ-specific autoimmune disease in genetically predisposed individuals. None of the available genetic studies in familial DCM has taken into account the autoimmune phenotype markers in the characterization of index patients and relatives, thus it is not known whether or not the described gene defects are involved in the autoimmune form of the disease. In animal models autoimmune myocarditis/DCM can be induced by viral infection, immunization with heart-specific autoantigens, or develop spontaneously in genetically predisposed strains. It may be cell or antibody-mediated; susceptibility is based upon multiple MHC and non-MHC genes. In patients, the diagnosis of autoimmune myocarditis/DCM requires exclusion of viral genome on EMB and detection of serum heart-reactive autoantibodies. They are found in index patients and relatives from about 60% of both familial and non-familial pedigrees and predict DCM development among healthy relatives. Some antibodies have functional effects on cardiac myocytes in vitro, in animal models and possibly in a DCM subset without inflammation, responsive to extracorporeal immunoadsorption. Cardiac-specific autoantibodies, which are shown to be disease-specific for myocarditis/DCM, can be used as biomarkers for identifying patients in whom, in the absence of active infection of the myocardium, immunosuppression and/or immunomodulation may be beneficial and their relatives at risk. Future studies should clarify genetic basis of human autoimmune myocarditis/DCM as well as genotype/immune phenotype correlations.[Abstract]
  50. Schmaltz AA. Z Kardiol. 2001 Apr;90(4):263-8. Dilated cardiomyopathy in childhood
    In childhood, dilative cardiomyopathy (DCM) has a prevalence of 2.6 patients in 100,000 inhabitants. Manifestation age is, in 75%, the first two years of life. There are no specific symptoms. Diagnosis is often made, when congestive heart failure occurs. Despite intensive therapy with digitalis, diuretics and ACE inhibitors, DCM is the main indication for heart transplantation. The prognosis is critical: 11 studies with approximately 450 children showed a mean 1-year survival rate of 75% and a 5-year survival rate of 60%. In most cases etiology of DCM remains unclear (“idiopathic”). In the second position (approximately 40%) is inflammatory pathogenesis. While familiar DCM is manifested mainly during the 3rd and 4th decade, specific cardiomyopathy is often found during infancy: inborn errors of metabolism, neuromuscular diseases or malformation syndromes are the causes of a cardiomyopathy, which can appear as dilative or hypertrophic cardiomyopathy. A causal therapy exists only in a few cases.[Abstract]

  51. .[Abstract]
  52. Alcohol misbruik

  53. Laonigro I, Correale M, Di Biase M, Altomare E. Eur J Heart Fail. 2009 May;11(5):453-62 Alcohol abuse and heart failure
    Alcoholic patients who consume >90 g of alcohol a day for >5 years are at risk of developing asymptomatic alcoholic cardiomyopathy (ACM). Those patients who continue to drink may become symptomatic and develop signs and symptoms of heart failure (HF). This distinct form of congestive HF is responsible for 21-36% of all cases of non-ischaemic dilated cardiomyopathy in Western Society. Without complete abstinence, the 4 year mortality for ACM is close to 50%. This short review summarizes the experimental and clinical evidence regarding the role of alcohol in the pathophysiology of ACM and HF.[Article]
  54. Skotzko CE, Vrinceanu A, Krueger L, Freudenberger R Heart Fail Rev. 2009 Mar;14(1):51-5. Alcohol use and congestive heart failure: incidence, importance, and approaches to improved history taking
    Alcohol use, abuse, and dependence have the potential to result in alcoholic cardiomyopathy (ACM). This distinct form of congestive heart failure (CHF) is responsible for 21-36% of all cases of nonischemic dilated cardiomyopathy in Western society. Without complete abstinence, the 4-year mortality for ACM approaches 50%. Therefore, accurate and detailed assessment of alcohol use in congestive heart failure is essential. The prevalence of problematic alcohol use is unrecognized by many clinicians. Clinical assessment of alcohol intake is often reduced to a simple question such as, “Do you drink?” Denial and minimization are hallmarks of alcohol abuse, with many individuals underreporting their use of alcohol. Clinicians can overcome these hurdles by implementing practical history taking measures to improve the accuracy of self-reported alcohol use. The data regarding the dangers of ongoing alcohol use in individuals with ACM make attempts to engage individuals in treatment to support abstinence essential. Suggestions for detailed and accurate assessment are discussed.[Abstract]
  55. Carnitine deficiëntie


  56. .[Abstract]

  57. .[Abstract]
  58. Veroudering

  59. Shih H, Lee B, Lee RJ, Boyle AJ. J Am Coll Cardiol. 2011 Jan 4;57(1):9-17. The aging heart and post-infarction left ventricular remodeling
    Aging is a risk factor for heart failure, which is a leading cause of death world-wide. Elderly patients are more likely than young patients to experience a myocardial infarction (MI) and are more likely to develop heart failure following MI. The poor clinical outcome of aging in cardiovascular disease is recapitulated on the cellular level. Increase in stress exposure and shifts in signaling pathways with age change the biology of cardiomyocytes. The progressive accumulation of metabolic waste and damaged organelles in cardiomyocytes blocks the intracellular recycling process of autophagy and increases the cell’s propensity toward apoptosis. Additionally, the decreased cardiomyocyte renewal capacity in the elderly, due to reduction in cellular division and impaired stem cell function, leads to further cardiac dysfunction and maladaptive responses to disease or stress. We review the cellular and molecular aspects of post-infarction remodeling in the aged heart, and relate them to the clinical problem of post-infarction remodeling in elderly patients.[Article]
  60. Yamasaki N, Kitaoka H, Matsumura Y, Furuno T, Nishinaga M, Doi Y. Intern Med. 2003 May;42(5):383-8. Heart failure in the elderly
    Heart failure is common in the elderly population. Approximately 6 to 10 percent of the population 65 years or older have heart failure. Heart failure is the most common reason for hospitalization in elderly patients. Etiology of heart failure is often multifactorial in the elderly. The common causes of heart failure include ischemic heart disease, valvular heart disease, hypertensive heart disease, and cardiomyopathy. Exacerbation of heart failure in the elderly is often accompanied by precipitating factors which include arrhythmia, renal failure, anemia, infection, adverse effect of drugs and non-compliance with medication and/or diet. Diagnosis of heart failure may be difficult in the elderly because symptoms of heart failure are often atypical or even absent. Heart failure with preserved systolic function is common in the elderly because aging has a greater impact on diastolic function. It is important to recognize that very old patients with heart failure are underrepresented in clinical trials.[Article]
  61. Georgiopoulou VV, Kalogeropoulos AP, Psaty BM, Rodondi N, Bauer DC, Butler AB, Koster A, Smith AL, Harris TB, Newman AB, Kritchevsky SB, Butler J. Am J Med. 2011 Apr;124(4):334-41. Lung function and risk for heart failure among older adults: the Health ABC Study
    The impact of abnormal spirometric findings on risk for incident heart failure among older adults without clinically apparent lung disease is not well elucidated.METHODS: We evaluated the association of baseline lung function with incident heart failure, defined as first hospitalization for heart failure, in 2125 participants of the community-based Health, Aging, and Body Composition (Health ABC) Study (age, 73.6 ± 2.9 years; 50.5% men; 62.3% white; 37.7% black) without prevalent lung disease or heart failure. Abnormal lung function was defined either as forced vital capacity (FVC) or forced expiratory volume in 1(st) second (FEV(1)) to FVC ratio below lower limit of normal. Percent predicted FVC and FEV(1) also were assessed as continuous variables.RESULTS: During follow-up (median, 9.4 years), heart failure developed in 68 of 350 (19.4%) participants with abnormal baseline lung function, as compared with 172 of 1775 (9.7%) participants with normal lung function (hazard ratio [HR] 2.31; 95% confidence interval [CI], 1.74-3.07; P <.001). This increased risk persisted after adjusting for previously identified heart failure risk factors in the Health ABC Study, body mass index, incident coronary heart disease, and inflammatory markers (HR 1.83; 95% CI, 1.33-2.50; P <.001). Percent predicted (%) FVC and FEV(1) had a linear association with heart failure risk (HR 1.21; 95% CI, 1.11-1.32 and 1.18; 95% CI, 1.10-1.26, per 10% lower %FVC and %FEV(1), respectively; both P <.001 in fully adjusted models). Findings were consistent in sex and race subgroups and for heart failure with preserved or reduced ejection fraction.CONCLUSIONS: Abnormal spirometric findings in older adults without clinical lung disease are associated with increased heart failure risk.[Abstract]
  62. Rich MW. J Am Geriatr Soc. 1997 Aug;45(8):968-74. Epidemiology, pathophysiology, and etiology of congestive heart failure in older adults
    To review the epidemiology, pathophysiology, and etiology of congestive heart failure (CHF) in older adults.METHODS: Published reports relevant to the epidemiology, pathophysiology, and etiology of CHF were systematically reviewed. Studies involving older adults and more recent studies were emphasized.RESULTS: More than 75% of patients with CHF in the United States are older than 65 years of age, and CHF is the leading cause of hospitalization in older adults. CHF is also a major cause of chronic disability, and annual expenditures for CHF currently exceed $10 billion. In addition, both the incidence and prevalence of CHF are increasing, largely as a result of the aging of the population. Older adults are predisposed to developing CHF as a result of age-related changes in the cardiovascular system and the high prevalence of hypertension, coronary artery disease, and valvular heart disease in this age group. Although the fundamental pathophysiology of CHF is similar in younger and older patients, older individuals are more prone to develop CHF in the setting of preserved left ventricular systolic function. This syndrome, referred to as diastolic heart failure, accounts for up to 50% of all cases of CHF in adults more than 65 years of age. Coronary heart disease and hypertension are the most common etiologies of CHF in older adults, and they often coexist. Valvular heart disease, especially aortic stenosis and mitral regurgitation, are also common in older adults, whereas nonischemic dilated cardiomyopathy, hypertrophic cardiomyopathy, and restrictive cardiomyopathy occur less frequently.CONCLUSIONS: Congestive heart failure is a major public health problem in the United States today as a result of its high and increasing prevalence in the older population as well as its substantial impact on healthcare costs and quality of life. There is an urgent need to develop more effective strategies for the prevention and treatment of CHF in older individuals.[Abstract]

  63. .[Abstract]

Orthomoleculaire behandeling van cardiomyopathie en hartfalen

CoQ10

Coenzyme Q10 (CoQ10) or ubiquinone is essentially a vitamin or vitamin-like substance. Disagreements on nomenclature notwithstanding, vitamins are defined as organic compounds essential in minute amounts for normal body function acting as coenzymes or precursors to coenzymes. They are present naturally in foods and sometimes are also synthesised in the body. CoQ10 likewise is found in small amounts in a wide variety of foods and is synthesised in all tissues. The biosynthesis of CoQ10 from the amino acid tyrosine is a multistage process requiring at least eight vitamins and several trace elements. Coenzymes are cofactors upon which the comparatively large and complex enzymes absolutely depend for their function.

Coenzyme Q10 is the coenzyme for at least three mitochondrial enzymes (complexes I, II and III) as well as enzymes in other parts of the cell. Mitochondrial enzymes of the oxidative phosphorylation pathway are essential for the production of the high-energy phosphate, adenosine triphosphate (ATP), upon which all cellular functions depend.

The electron and proton transfer functions of the quinone ring are of fundamental importance to all life forms; ubiquinone in the mitochondria of animals, plastoquinone in the chloroplast of plants, and menaquinone in bacteria. The term “bioenergetics” has been used to describe the field of biochemistry looking specifically at cellular energy production. In the related field of free radical chemistry, CoQ10 has been studied in its reduced form as a potent antioxidant.

    Tekorten aan Q10 bij cardiomyopathie en hartfalen

  1. Mortensen SA. Biofactors. 2003;18(1-4):79-89. Overview on coenzyme Q10 as adjunctive therapy in chronic heart failure. Rationale, design and end-points of “Q-symbio”–a multinational trial
    Energy starvation of the myocardium is probably a dominant feature of heart failure and attention has been directed towards agents which may stabilize myocardial metabolism and maintain adequate energy stores. A reduced myocardial tissue content of the essential redox-component and natural antioxidant Coenzyme Q10 (CoQ10) has been detected in patients with heart failure and the observed level of CoQ10 deficiency was correlated to the severity of heart failure. [Abstract]
  2. Singh RB, Niaz MA, Rastogi V, Rastogi SS. J Assoc Physicians India. 1998 Mar;46(3):299-306. Coenzyme Q in cardiovascular disease
    Coenzyme Q10 or ubiquinone normally present in many plant and animal cells is an antioxidant. Coenzyme Q10 deficiency has been observed in patients with congestive heart failure, angina pectoris, coronary artery disease, cardiomyopathy, hypertension, mitral valve prolapse and after coronary revascularization. Coenzyme Q10 is involved in the synthesis of ATP and hence is useful in preventing cellular damage during ischaemia-reperfusion injury.[Abstract]
  3. Allard ML, Jeejeebhoy KN, Sole MJ. Heart Fail Rev. 2006 Mar;11(1):75-82. The management of conditioned nutritional requirements in heart failure
    Patients suffering from congestive heart failure exhibit impaired myocardial energy production, myocyte calcium overload and increased oxidative stress. Nutritional factors known to be important for myocardial energy production, calcium homeostasis and the reduction of oxidative stress, such as thiamine, riboflavin, pyridoxine, L-carnitine, coenzyme Q10, creatine and taurine are reduced in this patient population. [Abstract]
  4. Sole MJ, Jeejeebhoy KN. Curr Opin Clin Nutr Metab Care. 2000 Nov;3(6):417-24. Conditioned nutritional requirements and the pathogenesis and treatment of myocardial failure
    Several specific deficiencies have been found in the failing myocardium: a reduction in the content of L-carnitine, coenzyme Q10, creatine and thiamine, nutrient cofactors that are important for myocardial energy production; a relative deficiency of taurine, an amino acid that is integral to the modulation of intracellular calcium levels; and an increase in myocardial oxidative stress, and a reduction of both endogenous and exogenous antioxidant defences. [Abstract]
  5. Sole MJ, Jeejeebhoy KN. Herz. 2002 Mar;27(2):174-8. Conditioned nutritional requirements: therapeutic relevance to heart failure
    The advent of disease, genetic predisposition or certain drug therapies may significantly alter the nutritional demands of specific organs. Several specific metabolic deficiencies have been found in the failing myocardium: (1) a reduction in L-carnitine, coenzyme Q10, creatine, and thiamine–nutrient cofactors important for myocardial energy production; (2) a relative deficiency of taurine, an amino acid integral to intracellular calcium homeostasis; (3) increased myocardial oxidative stress and a reduction of antioxidant defenses. Deficiencies of carnitine or taurine alone are well documented to result in dilated cardiomyopathy in animals and humans.[Abstract]
  6. Kumar A, Kaur H, Devi P, Mohan V. Pharmacol Ther. 2009 Dec;124(3):259-68. Role of coenzyme Q10 (CoQ10) in cardiac disease, hypertension and Meniere-like syndrome
    Coenzyme Q10 (ubiquinone) is a mitochondrial coenzyme which is essential for the production of ATP. Being at the core of cellular energy processes it assumes importance in cells with high energy requirements like the cardiac cells which are extremely sensitive to CoQ10 deficiency produced by cardiac diseases. CoQ10 has thus a potential role for prevention and treatment of heart ailments by improving cellular bioenergetics. s. Recently it has been found to be an independent predictor of mortality in congestive heart failure. [Abstract]
  7. Mortensen SA, Vadhanavikit S, Muratsu K, Folkers K Int J Tissue React. 1990;12(3):155-62. Coenzyme Q10: clinical benefits with biochemical correlates suggesting a scientific breakthrough in the management of chronic heart failur
    There are obviously several causes of myocardial dysfunction but energy deficiency of the myocytes may play a significant role and probably is a common mechanism during the progression of myocardial failure. Theoretically, a poor utilization efficiency of oxygen may be due to exhaustion of the myocardial stores of bioenergetics. In this report the authors review their biochemical results from measurements of coenzyme Q10 (CoQ10) levels in blood and human endomyocardial biopsies using an HPLC method from patients with suspected myocardial disease (n = 45). The levels of CoQ10, which has a key role in the respiratory chain and the synthesis of ATP, was found to be significantly decreased in various groups of patients with myocardial failure (dilated and restrictive cardiomyopathy and alcoholic heart disease) as compared to “normal” myocardium (0.42 +/- 0.04 micrograms/mg dry weight). The deficiency of CoQ10 was more pronounced with increasing symptoms; e.g. patients with dilated cardiomyopathy in NYHA Classes III and IV had lower tissue CoQ10 content than those of Classes I and II (0.28 +/- 0.04 vs. 0.37 +/- 0.06 micrograms/mg, p less than 0.001).[Abstract]
  8. Cholesterolverlagers van de statine klasse verlagen Q10

  9. Nawarskas JJ. Cardiol Rev. 2005 Mar-Apr;13(2):76-9 HMG-CoA reductase inhibitors and coenzyme Q10
    The most concerning adverse reaction with HMG-CoA reductase inhibitors (statins) is myotoxicity. Statins inhibit the production of mevalonate, a precursor of both cholesterol and coenzyme Q10, a compound believed to be crucial for mitochondrial function and the provision of energy for cellular processes. There is speculation that a reduction in coenzyme Q10 concentrations may promote the myopathies that have been associated with statin treatment as a result of mitochondrial damage.[Abstract]
  10. Caso G, Kelly P, McNurlan MA, Lawson WE. Am J Cardiol. 2007 May 15;99(10):1409-12. Effect of coenzyme q10 on myopathic symptoms in patients treated with statins
    Myopathy may be related in part to statin inhibition of the endogenous synthesis of coenzyme Q10, an essential cofactor for mitochondrial energy production. In conclusion, results suggest that coenzyme Q10 supplementation may decrease muscle pain associated with statin treatment. Thus, coenzyme Q10 supplementation may offer an alternative to stopping treatment with these vital drugs.[Abstract]
  11. Langsjoen PH, Langsjoen AM. Biofactors. 2003;18(1-4):101-11. The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications
    Statin-induced CoQ10 depletion is well documented in animal and human studies with detrimental cardiac consequences in both animal models and human trials. This drug-induced nutrient deficiency is dose related and more notable in settings of pre-existing CoQ10 deficiency such as in the elderly and in heart failure.[Abstract]
  12. Rundek T, Naini A, Sacco R, Coates K, DiMauro S. Arch Neurol. 2004 Jun;61(6):889-92. Atorvastatin decreases the coenzyme Q10 level in the blood of patients at risk for cardiovascular disease and stroke
    Even brief exposure to atorvastatin causes a marked decrease in blood CoQ(10) concentration. Widespread inhibition of CoQ(10) synthesis could explain the most commonly reported adverse effects of statins, especially exercise intolerance, myalgia, and myoglobinuria.[Article]
  13. Mabuchi H, Higashikata T, Kawashiri M, Katsuda S, Mizuno M, Nohara A, Inazu A, Koizumi J, Kobayashi J. J Atheroscler Thromb. 2005;12(2):111-9. Reduction of serum ubiquinol-10 and ubiquinone-10 levels by atorvastatin in hypercholesterolemic patients
    As atorvastatin reduces serum ubiquinol-10 as well as serum cholesterol levels in all patients, it is imperative that physicians are forewarned about the risks associated with ubiquinol-10 depletion.[Article]
  14. Behandeling van cardiomyopathie en hartfalen met Q10

  15. Mortensen SA. Clin Investig. 1993;71(8 Suppl):S116-23. perspectives on therapy of cardiovascular diseases with coenzyme Q10 (ubiquinone)
    A defective myocardial energy supply–due to lack of substrates and/or essential cofactors and a poor utilization efficiency of oxygen–may be a common final pathway in the progression of myocardial diseases of various etiologies. The vitamin-like essential substance coenzyme Q10, or ubiquinone, is a natural antioxidant and has a key role in oxidative phosphorylation. In the author’s open clinical protocol study with coenzyme Q10 therapy (100 mg daily) nearly two-thirds of patients revealed clinical improvement, most pronounced in those with dilated cardiomyopathy. Double-blind placebo-controlled trials have definitely confirmed that coenzyme Q10 has a place as adjunctive treatment in heart failure with beneficial effects on the clinical outcome, the patients’ physical activity, and their quality of life. The positive results have been above and beyond the clinical status obtained from treatment with traditional principles–including angiotensin-converting enzyme inhibitors.[Abstract]
  16. Crane FL. J Am Coll Nutr. 2001 Dec;20(6):591-8. Biochemical functions of coenzyme Q10
    Coenzyme Q is well defined as a crucial component of the oxidative phosphorylation process in mitochondria which converts the energy in carbohydrates and fatty acids into ATP to drive cellular machinery and synthesis. New roles for coenzyme Q in other cellular functions are only becoming recognized. The new aspects have developed from the recognition that coenzyme Q can undergo oxidation/reduction reactions in other cell membranes such as lysosomes. Golgi or plasma membranes. In mitochondria and lysosomes, coenzyme Q undergoes reduction/oxidation cycles during which it transfers protons across the membrane to form a proton gradient. The presence of high concentrations of quinol in all membranes provides a basis for antioxidant action either by direct reaction with radicals or by regeneration of tocopherol and ascorbate. Evidence for a function in redox control of cell signaling and gene expression is developing from studies on coenzyme Q stimulation of cell growth, inhibition of apoptosis, control of thiol groups, formation of hydrogen peroxide and control of membrane channels. Deficiency of coenzyme Q has been described based on failure of biosynthesis caused by gene mutation, inhibition of biosynthesis by HMG coA reductase inhibitors (statins) or for unknown reasons in ageing and cancer. Correction of deficiency requires supplementation with higher levels of coenzyme Q than are available in the diet.[Article]
  17. Belardinelli R, Muçaj A, Lacalaprice F, Solenghi M, Principi F, Tiano L, Littarru GP Biofactors. 2005;25(1-4):137-45. Coenzyme Q10 improves contractility of dysfunctional myocardium in chronic heart failure
    Oral CoQ(10) improves LV contractility in CHF without any side effects. This improvement is associated with an enhanced functional capacity.[Abstract]
  18. Soja AM, Mortensen SA. Mol Aspects Med. 1997;18 Suppl:S159-68 Treatment of congestive heart failure with coenzyme Q10 illuminated by meta-analyses of clinical trials
    In conclusion, supplemental treatment of CHF with CoQ10 is consistent with an improvement of SV, EF, CO, CI and EDVI. [Abstract]
  19. P H Langsjoen, S Vadhanavikit, and K Folkers Proc Natl Acad Sci U S A. 1985 June; 82(12): 4240–4244. Response of patients in classes III and IV of cardiomyopathy to therapy in a blind and crossover trial with coenzyme Q10
    These patients, steadily worsening and expected to die within 2 years under conventional therapy, generally showed an extraordinary clinical improvement, indicating that CoQ10 therapy might extend the lives of such patients. This improvement could be due to correction of a myocardial deficiency of CoQ10 and to enhanced synthesis of CoQ10-requiring enzymes.[Article]
  20. Langsjoen PH, Langsjoen PH, Folkers K. Int J Tissue React. 1990;12(3):169-71. A six-year clinical study of therapy of cardiomyopathy with coenzyme Q10
    One hundred and forty-three cases of chronic, stable, non-secondary, non-hypertrophic cardiomyopathy, 98% of whom were in NYHA Classes III and IV, were given 100 mg of coenzyme Q10 orally in addition to their conventional medical programme in an open-label long-term study. Mean ejection fraction of 44% measured by systolic time interval analysis rose to 60% within 6 months and stabilized at that level with 84% of patients showing statistically significant improvement. Eighty-five percent of patients improved by one or two NYHA Classes. [Abstract]
  21. Berman M, Erman A, Ben-Gal T, Dvir D, Georghiou GP, Stamler A, Vered Y, Vidne BA, Aravot D. Clin Cardiol. 2004 May;27(5):295-9. Coenzyme Q10 in patients with end-stage heart failure awaiting cardiac transplantation: a randomized, placebo-controlled study
    The administration of CoQ10 to heart transplant candidates led to a significant improvement in functional status, clinical symptoms, and quality of life. However, there were no objective changes in echo measurements or ANF and TNF blood levels. Coenzyme Q10 may serve as an optional addition to the pharmacologic armamentarium of patients with end-stage heart failure. The apparent discrepancy between significant clinical improvement and unchanged cardiac status requires further investigation.[Abstract]
  22. Folkers K, Langsjoen P, Langsjoen PH. Biochem Biophys Res Commun. 1992 Jan 15;182(1):247-53. Therapy with coenzyme Q10 of patients in heart failure who are eligible or ineligible for a transplant
    We treated eleven exemplary transplant candidates with CoQ10; all improved; three improved from Class IV to Class I; four improved from Classes III-IV to Class II; and two improved from Class III to Class I or II. After CoQ10, some patients required no conventional drugs and had no limitation in lifestyle. [Abstract]
  23. Mortensen SA, Vadhanavikit S, Baandrup U, Folkers K. Drugs Exp Clin Res. 1985;11(8):581-93. Long-term coenzyme Q10 therapy: a major advance in the management of resistant myocardial failure
    Coenzyme Q10 (CoQ10) treatment, orally administered as 100 mg daily dose, was initiated in a series of patients with advanced heart failure in an open, controlled design. They were all showing an insufficient response to classical therapy with diuretics and digitalis. With a mean latency period of 30 days, eight out of 12 patients (67%) showed definite clinical improvement. Subjectively, the patients felt less tired, their general activity tolerance increased and dyspnoea at rest disappeared. There were obvious signs of decreased right-sided stasis (hepatic congestion). The heart rate fell significantly, and the heart volume (chest X-ray) decreased in the eight responders (although n.s.). A significant reduction in the left atrial size (ECHO) was registered, suggesting a reduced preload of the left ventricle, Furthermore, a significant decline in the PEP/LVET ratio (STI) was indicative of an improved myocardial performance. [Abstract]
  24. Belardinelli R, Muçaj A, Lacalaprice F, Solenghi M, Seddaiu G, Principi F, Tiano L, Littarru GP.Eur Heart J. 2006 Nov;27(22):2675-81. Coenzyme Q10 and exercise training in chronic heart failure
    Oral CoQ(10) improves functional capacity, endothelial function, and LV contractility in CHF without any side effects. The combination of CoQ(10) and ET resulted in higher plasma CoQ(10) levels and more pronounced effects on all the abovementioned parameters. However, significant synergistic effect of CoQ(10) with ET was observed only for peak SWTI suggesting that ET amplifies the already described effect of CoQ(10) on contractility of dysfunctional myocardium.[Article]
  25. Langsjoen H, Langsjoen P, Langsjoen P, Willis R, Folkers K.Mol Aspects Med. 1994;15 Suppl:s165-75. Usefulness of coenzyme Q10 in clinical cardiology: a long-term study.
    In conclusion, CoQ10 is a safe and effective adjunctive treatment for a broad range of cardiovascular diseases, producing gratifying clinical responses while easing the medical and financial burden of multidrug therapy.[Abstract]
  26. Keogh A, Fenton S, Leslie C, Aboyoun C, Macdonald P, Zhao YC, Bailey M, Rosenfeldt F. Heart Lung Circ. 2003;12(3):135-41 Randomised double-blind, placebo-controlled trial of coenzyme Q, therapy in class II and III systolic heart failure
    This pilot study accords with published data suggesting that CoQ10 therapy improves cardiac functional status in patients with moderately severe dilated cardiomyopathy receiving maximal non beta-blocker therapy. [Abstract]
  27. Witte KK, Nikitin NP, Parker AC, von Haehling S, Volk HD, Anker SD, Clark AL, Cleland JG. Eur Heart J. 2005 Nov;26(21):2238-44. The effect of micronutrient supplementation on quality-of-life and left ventricular function in elderly patients with chronic heart failure
    Long-term multiple micronutrient supplementation can improve LV volumes and LVEF and QoL scores in elderly patients with heart failure due to LV systolic dysfunction.[Article]
  28. Morisco C, Trimarco B, Condorelli M. Clin Investig. 1993;71(8 Suppl):S134-6. Effect of coenzyme Q10 therapy in patients with congestive heart failure: a long-term multicenter randomized study
    Our results demonstrate that the addition of coenzyme Q10 to conventional therapy significantly reduces hospitalization for worsening of heart failure and the incidence of serious complications in patients with chronic congestive heart failure.[Abstract]
  29. Langsjoen PH, Vadhanavikit S, Folkers K. Proc Natl Acad Sci U S A. 1985 Jun;82(12):4240-4. Response of patients in classes III and IV of cardiomyopathy to therapy in a blind and crossover trial with coenzyme Q10
    Coenzyme Q10 (CoQ10), a biochemically established redox component of respiration including the coupled mechanisms of electron transfer and oxidative phosphorylation, is naturally present in the human myocardium. These patients, steadily worsening and expected to die within 2 years under conventional therapy, generally showed an extraordinary clinical improvement, indicating that CoQ10 therapy might extend the lives of such patients. This improvement could be due to correction of a myocardial deficiency of CoQ10 and to enhanced synthesis of CoQ10-requiring enzymes.[Article]
  30. Baggio E, Gandini R, Plancher AC, Passeri M, Carmosino G. Mol Aspects Med. 1994;15 Suppl:s287-94. Italian multicenter study on the safety and efficacy of coenzyme Q10 as adjunctive therapy in heart failure. CoQ10 Drug Surveillance Investigators
    Apart from the clinical seriousness, heart failure is always characterized by an energy depletion status, as indicated by low intramyocardial ATP and coenzyme Q10 levels. After three months of test treatment the proportions of patients with improvement in clinical signs and symptoms were as follows: cyanosis 78.1%, oedema 78.6%, pulmonary rales 77.8%, enlargement of liver area 49.3%, jugular reflux 71.81%, dyspnoea 52.7%, palpitations 75.4%, sweating 79.8%, subjective arrhytmia 63.4%, insomnia 662.8%, vertigo 73.1% and nocturia 53.6%. Moreover we observed a contemporary improvement of at least three symptoms in 54% of patients; this could be interpreted as an index of improved quality of life.[Abstract]
  31. Langsjoen PH, Folkers K, Lyson K, Muratsu K, Lyson T, Langsjoen P. Klin Wochenschr. 1988 Jul 1;66(13):583-90 Effective and safe therapy with coenzyme Q10 for cardiomyopathy
    Coenzyme Q10 (CoQ10) is indispensable in mitochondrial bioenergetics and for human life to exist. Of the 88 patients 75%-85% showed statistically significant increases in two monitored cardiac parameters. Patients with the lowest ejection fractions (approx. 10%-30%) showed the highest increases (115 delta %-210 delta %) and those with higher ejection fractions (50%-80%) showed increases of approx. 10 delta %-25 delta % on therapy.[Abstract]
  32. Mortensen SA. Clin Investig. 1993;71(8 Suppl):S116-23. Perspectives on therapy of cardiovascular diseases with coenzyme Q10 (ubiquinone)
    A defective myocardial energy supply–due to lack of substrates and/or essential cofactors and a poor utilization efficiency of oxygen–may be a common final pathway in the progression of myocardial diseases of various etiologies. Double-blind placebo-controlled trials have definitely confirmed that coenzyme Q10 has a place as adjunctive treatment in heart failure with beneficial effects on the clinical outcome, the patients’ physical activity, and their quality of life. The positive results have been above and beyond the clinical status obtained from treatment with traditional principles–including angiotensin-converting enzyme inhibitors.[Abstract]
  33. Greenberg S, Frishman WH. J Clin Pharmacol. 1990 Jul;30(7):596-60 Co-enzyme Q10: a new drug for cardiovascular disease
    Co-enzyme Q10 (ubiquinone) is a naturally occurring substance which has properties potentially beneficial for preventing cellular damage during myocardial ischemia and reperfusion. It plays a role in oxidative phosphorylation and has membrane stabilizing activity. The substance has been used in oral form to treat various cardiovascular disorders including angina pectoris, hypertension, and congestive heart failure. Its clinical importance is now being established in clinical trails worldwide.[Abstract]
  34. Behandeling van kinderen met cardiomyopathie en hartfalen met Q10

  35. Coenzyme Q10 improves diastolic function in children with idiopathic dilated cardiomyopathy
    Our results, therefore, indicate that administration of coenzyme Q10 is useful in ameliorating cardiac failure in patients with idiopathic dilated cardiomyopathy through its significant effect on improving diastolic function.[Abstrat]
  36. Soongswang J, Sangtawesin C, Durongpisitkul K, Laohaprasitiporn D, Nana A, Punlee K, Kangkagate C. The effect of coenzyme Q10 on idiopathic chronic dilated cardiomyopathy in children
    In addition to the conventional antifailure drugs, CoQ10 may improve NYHA class and CT ratio and shorten ventricular depolarization in children with chronic idiopathic DCM.[Abstract]
  37. Bhagavan HN, Chopra RK. Clin Nutr. 2005 Jun;24(3):331-8. Potential role of ubiquinone (coenzyme Q10) in pediatric cardiomyopathy
    Based upon the biochemical rationale and a large body of data on patients with adult cardiomyopathy, heart failure, and mitochondrial diseases with heart involvement, a role for coenzyme Q10 therapy in PCM patients is indicated, and preliminary results are promising. Additional studies on the potential usefulness of coenzyme Q10 supplementation as an adjunct to conventional therapy in PCM, particularly in children with dilated cardiomyopathy, are therefore warranted.[Abstract]
  38. Molyneux SL, Florkowski CM, George PM, Pilbrow AP, Frampton CM, Lever M, Richards AM. J Am Coll Cardiol. 2008 Oct 28;52(18):1435-41. Coenzyme Q10: an independent predictor of mortality in chronic heart failure
    Plasma CoQ(10) concentration was an independent predictor of mortality in this cohort. The CoQ(10) deficiency might be detrimental to the long-term prognosis of CHF, and there is a rationale for controlled intervention studies with CoQ(10).[Abstract]
  39. Veiligheid Q10

  40. Molyneux SL, Florkowski CM, George PM, Pilbrow AP, Frampton CM, Lever M, Richards AM. J Am Coll Cardiol. 2008 Oct 28;52(18):1435-41. Coenzyme Q10: an independent predictor of mortality in chronic heart failure
    The acceptable daily intake (ADI) is 12mg/kg/day, calculated from the no-observed-adverse-effect level (NOAEL) of 1200 mg/kg/day derived from a 52-week chronic toxicity study in rats, i.e., 720 mg/day for a person weighing 60 kg. Risk assessment for CoQ10 based on various clinical trial data indicates that the observed safety level (OSL) for CoQ10 is 1200 mg/day/person. Additionally, analysis of CoQ10 bioavailability or its pharmacokinetics provides the pertinent safety evaluation for CoQ10.[Abstract]
  41. Hathcock JN, Shao A. Regul Toxicol Pharmacol. 2006 Aug;45(3):282-8. Risk assessment for coenzyme Q10 (Ubiquinone)
    The OSL risk assessment method indicates that the evidence of safety is strong at intakes up to 1200 mg/day, and this level is identified as the OSL. Much higher levels have been tested without adverse effects and may be safe, but the data for intakes above 1200 mg/day are not sufficient for a confident conclusion of safety.[Abstract]
  42. EXTRA
  43. Langsjoen PH, Vadhanavikit S, Folkers K. Proc Natl Acad Sci U S A. 1985 Jun;82(12):4240-4. Response of patients in classes III and IV of cardiomyopathy to therapy in a blind and crossover trial with coenzyme Q10
    A double-blind and double-crossover trial has been conducted by administering CoQ10 and a matching placebo orally to two groups of patients having class III or IV cardiomyopathy (classification according to criteria of the New York Heart Association). For group A, significant increases in CoQ10 blood levels and cardiac function occurred during CoQ10 treatment and then decreased during crossover to placebo. For group B, there was no change in CoQ10 blood levels and cardiac function during placebo treatment, but increases in both parameters occurred in crossover to CoQ10. These patients, steadily worsening and expected to die within 2 years under conventional therapy, generally showed an extraordinary clinical improvement, indicating that CoQ10 therapy might extend the lives of such patients. This improvement could be due to correction of a myocardial deficiency of CoQ10 and to enhanced synthesis of CoQ10-requiring enzymes.[Article]

  44. .[Abstract]

Carnitine

L-carnitine and its derivative, propionyl-L-carnitine, are organic amines produced and metabolized endogenously. These compounds are essential in the process of fatty acid oxidation and have also been shown to reduce intracellular accumulation of toxic metabolites during ischemia. Currently, exogenous administration of carnitine is indicated only as therapy for primary and secondary carnitine deficiency. However, it has been hypothesized that because of its ability to enhance energy production and remove toxic metabolites during ischemia, carnitine therapy may be useful in the treatment of various cardiac diseases. In fact, there is increasing evidence that endogenous carnitine has beneficial effects in the treatment of dilated Cardiomyopathy, arrhythmia, peripheral vascular disease, and acute ischemia.

    Carnitine tekort bij cardiomyopathie en hartfalen

  1. Rubio-Gozalbo ME, Bakker JA, Waterham HR, Wanders RJ Mol Aspects Med. 2004 Oct-Dec;25(5-6):521-32 Carnitine-acylcarnitine translocase deficiency, clinical, biochemical and genetic aspects
    The carnitine-acylcarnitine translocase (CACT) is one of the components of the carnitine cycle. The carnitine cycle is necessary to shuttle long-chain fatty acids from the cytosol into the intramitochondrial space where mitochondrial beta-oxidation of fatty acids takes place. The oxidation of fatty acids yields acetyl-coenzyme A (CoA) units, which may either be degraded to CO(2) and H(2)O in the citric acid cycle to produce ATP or converted into ketone bodies which occurs in liver and kidneys.[Abstract]
  2. Brady PS, Ramsay RR, Brady LJ. FASEB J. 1993 Aug;7(11):1039-44 Regulation of the long-chain carnitine acyltransferases
    Long-chain carnitine acyltransferases are a family of enzymes found in mitochondria, peroxisomes, and endoplasmic reticulum that catalyze the exchange of carnitine for coenzyme A in the fatty acyl-CoA. Conversion of the fatty acyl-CoA to fatty acylcarnitine renders the fatty acid more permeable to the various cellular membranes. The mitochondrial carnitine palmitoyltransferases are considered important in the regulation of mitochondrial beta-oxidation of long-chain fatty acids.[Article]
  3. Bremer J. Physiol Rev. 1983 Oct;63(4):1420-80. Carnitine–metabolism and functions
    The only firmly established function of carnitine is its function as a carrier of activated fatty acids and activated acetate across the inner mitochondrial membrane. [Abstract]
  4. Professor Gary D. Lopaschuk Cardiovascular Research Group, University of Alberta, Edmonton, Canada Metabolic agents: a new approach in treating ischemic heart disease
    Normally a balance between these two pathways exists, with fatty acid oxidation providing 60–70% of overall cardiac ATP supply, and glucose and lactate providing the remainder.[Article]
  5. Gong Xin Liu, Peter J. Hanley, John Ray, ürgen Daut; (Circulation Research. 2001;88:918.) © 2001 American Heart Association, Inc Long-Chain Acyl–Coenzyme A Esters and Fatty Acids Directly Link Metabolism to KATP Channels in the Heart
    Long-chain (LC) acyl–coenzyme A (CoA) esters are synthesized from fatty acids and serve as the principal metabolic substrates of the heart. [Article]
  6. Scholte HR, Rodrigues Pereira R, de Jonge PC, Luyt-Houwen IE, Hedwig M, Verduin M, Ross JD J Clin Chem Clin Biochem. 1990 May;28(5):351-7. Primary carnitine deficiency
    Carnitine deficiency can be defined as a decrease of intracellular carnitine, leading to an accumulation of acyl-CoA esters and an inhibition of acyl-transport via the mitochondrial inner membrane. This may cause disease by the following processes. A. Inhibition of the mitochondrial oxidation of long-chain fatty acids during fasting causes heart or liver failure. In a patient with cardiomyopathy and without myopathy, we found that carnitine transport at the level of the small intestinal epithelial brush border was also inhibited. The patient was cured by carnitine supplementation. [Abstract]
  7. Vikre-Jørgensen J. Ugeskr Laeger. 1993 Oct 18;155(42):3390-2. Cardiomyopathy caused by carnitine deficiency
    Primary carnitine deficiency often presents as progressive cardiomyopathy. Primary carnitine deficiency is a treatable disorder and therefore skeletal muscle biopsy and blood chemistry should be performed in all children with undiagnosed cardiomyopathy. Treatment with oral carnitine must be initiated quickly to avoid sudden death.[Abstract]
  8. Soukoulis V, Dihu JB, Sole M, Anker SD, Cleland J, Fonarow GC, Metra M, Pasini E, Strzelczyk T, Taegtmeyer H, Gheorghiade M J Am Coll Cardiol. 2009 Oct 27;54(18):1660-73. Micronutrient deficiencies an unmet need in heart failure
    HF is often accompanied by a deficiency in key micronutrients required for unimpeded energy transfer. Correcting these deficits has been proposed as a method to limit or even reverse the progressive myocyte dysfunction and/or necrosis in HF. This review summarizes the existing HF literature with respect to supplementation trials of key micronutrients involved in cardiac metabolism: coenzyme Q10, l-carnitine, thiamine, and amino acids, including taurine.[Abstract]
  9. Sole MJ, Jeejeebhoy KN. Herz. 2002 Mar;27(2):174-8. Conditioned nutritional requirements: therapeutic relevance to heart failure
    The advent of disease, genetic predisposition or certain drug therapies may significantly alter the nutritional demands of specific organs. Several specific metabolic deficiencies have been found in the failing myocardium: (1) a reduction in L-carnitine, coenzyme Q10, creatine, and thiamine–nutrient cofactors important for myocardial energy production; (2) a relative deficiency of taurine, an amino acid integral to intracellular calcium homeostasis; (3) increased myocardial oxidative stress and a reduction of antioxidant defenses. These experiments suggest that a comprehensive restoration of adequate myocyte nutrition may be important to any therapeutic strategy designed to benefit patients suffering from congestie heart failure. Future studies in this area are of clinical importance.[Abstract]
  10. Evangeliou A, Vlassopoulos D. Curr Pharm Biotechnol. 2003 Jun;4(3):211-9. Carnitine metabolism and deficit–when supplementation is necessary?
    Carnitine is an ammo acid derivative found in high energy demanding tissues (skeletal muscles, myocardium, the liver and the suprarenal glands). It is essential for the intermediary metabolism of fatty acids. Carnitine is indispensable for beta-oxidation of long-chain fatty acids in the mitochondria but also regulates CoA concentration and removal of the produced acyl groups. Although primary deficiency is unusual, depletion due to secondary causes, such as a disease or a medication side effect, can occur. Other chronic conditions like diabetes mellitus, heart failure, Alzheimer disease may cause carnitine deficiency also observed in conditions with increased catabolism as in critical illness.[Abstract]
  11. Scholte HR, Luyt-Houwen IE, Vaandrager-Verduin MH. Basic Res Cardiol. 1987;82 Suppl 1:63-73 The role of the carnitine system in myocardial fatty acid oxidation: carnitine deficiency, failing mitochondria and cardiomyopathy
    Cardiomyopathy may also be the cause of secondary carnitine deficiency resulting from a mitochondrial defect in acyl-CoA metabolism, or by the mitochondrial defect itself, which may be induced by drugs or viral attack, or be the result of a genetic error. In cardiomyopathic patients with a (subclinical) myopathy, study of isolated mitochondria and homogenate from skeletal muscle may reveal a mitochondrial dysfunction, which, in some patients, is treatable by dietary measures and supplementation with vitamins, CoQ and/or carnitine. When the cause of cardiomyopathy is not known, determination of plasma carnitine and carnitine supplementation of hypocarnitinemic patients is of great therapeutic value.[Abstract]
  12. Kendler BS. J Cardiovasc Nurs. 2006 Jan-Feb;21(1):9-16 Supplemental conditionally essential nutrients in cardiovascular disease therapy
    Conditionally essential nutrients (CENs) are organic compounds that are ordinarily produced by the body in amounts sufficient to meet its physiological requirements. However, in disorders, such as cardiovascular disease (CVD), and in other physiologically stressful conditions, their biosynthesis may be inadequate. Under these circumstances, CENs become essential nutrients, comparable to vitamins. The CENs of primary importance in CVD, based on the quantity and quality of human clinical studies, are l-arginine, l-carnitine, propionyl-l-carnitine, and coenzyme Q10. Limited research has pointed to possible benefits in CVD therapy accruing from supplementation with several CENs in combination. Additional controlled clinical studies of CENs in CVD are urgently needed.[Abstract]
  13. Carnitine bij de behandeling van cardiomyopathie en hartfalen

  14. Rizos I. Am Heart J. 2000 Feb;139(2 Pt 3):S120-3. Three-year survival of patients with heart failure caused by dilated cardiomyopathy and L-carnitine administration
    Survival analysis with the Kaplan-Meier method showed that patients’ survival was statistically significant (P <.04) in favor of the L-carnitine group. L-carnitine appears to possess considerable potential for the long-term treatment of patients with heart failure attributable to dilated cardiomyopathy.[Abstract]
  15. Brevetti G, Chiariello M, Ferulano G, Policicchio A, Nevola E, Rossini A, Attisano T, Ambrosio G, Siliprandi N, Angelini C. Circulation. 1988 Apr;77(4):767-73. Increases in walking distance in patients with peripheral vascular disease treated with L-carnitine: a double-blind, cross-over study
    In conclusion, this study demonstrates that L-carnitine, although not affecting the general or regional hemodynamics, improves the walking capacity of patients with intermittent claudication, probably through a metabolic mechanism.[Article]
  16. Ghidini O, Azzurro M, Vita G, Sartori G. Int J Clin Pharmacol Ther Toxicol. 1988 Apr;26(4):217-20 Evaluation of the therapeutic efficacy of L-carnitine in congestive heart failure
    In the group treated with L-carnitine, a distinct improvement was observed in both subjective and objective conditions; reduced heart rate, edema and dyspnea, increased diuresis and a marked reduction in daily digitalis consumption. L-carnitine treatment also induced a significant reduction in serum cholesterol and triglyceride levels. No adverse reactions attributable to L-carnitine administration were observed in any of the patients.[Abstract]
  17. Gürlek A, Tutar E, Akçil E, Dinçer I, Erol C, Kocatürk PA, Oral D Eur J Heart Fail. 2000 Jun;2(2):189-93 The effects of L-carnitine treatment on left ventricular function and erythrocyte superoxide dismutase activity in patients with ischemic cardiomyopathy
    We conclude that, as a sign of increased free radical production, superoxide dismutase activity was further increased in patients with L-carnitine treatment. L-Carnitine treatment in combination with other traditional pharmacological therapy might have an additive effect for the improvement of left ventricular function in ischemic cardiomyopathy.[Article]
  18. Wilcken DE. J Inherit Metab Dis. 2003;26(2-3):245-57. Overview of inherited metabolic disorders causing cardiovascular disease
    Mutations in several genes have been shown to produce dilated cardiomyopathy in the young, but there is as yet no specific treatment. In fatty acid oxidation disorders, arrhythmias and cardiomyopathy occur during acute decompensation. An important recently established cause of cardiomyopathy is carnitine transporter defect; it is treated effectively with oral carnitine. [Abstract]
  19. Tein I. J Inherit Metab Dis. 2003;26(2-3):147-69. Carnitine transport: pathophysiology and metabolism of known molecular defects
    Early-onset dilatative and/or hypertrophic cardiomyopathy with episodic hypoglycaemic coma and very low serum and tissue concentrations of carnitine should alert the clinician to the probability of the plasmalemmal high-affinity carnitine transporter defect. The institution of high-dose oral carnitine supplementation reverses the pathology in this otherwise lethal autosomal recessive disease of childhood, and carnitine therapy from birth in prospectively screened siblings may altogether prevent the development of the clinical phenotype. [Abstract]
  20. Ferrari R, De Giuli F. J Card Fail. 1997 Sep;3(3):217-24. The propionyl-L-carnitine hypothesis: an alternative approach to treating heart failure
    Administration of PLC in patients with CHF improves skeletal muscle metabolism by increasing pyruvate flux into the Krebs cycle and by decreasing lactate production. These effects occur in the absence of major hemodynamic and neuroendocrinologic changes and may underlie the ability of PLC to increase exercise performance in patients with heart failure. In a randomized study of 50 patients with mild CHF, PLC increased the maximal exercise time, reduced lactate production, and improved left ventricular ejection fraction. [Abstract]
  21. Ferrari R, Merli E, Cicchitelli G, Mele D, Fucili A, Ceconi C.Ann N Y Acad Sci. 2004 Nov;1033:79-91 Therapeutic effects of L-carnitine and propionyl-L-carnitine on cardiovascular diseases: a review
    The results of phase-2 studies in chronic heart failure patients showed that long-term oral treatment with propionyl-L-carnitine improves maximum exercise duration and maximum oxygen consumption over placebo and indicated a specific propionyl-L-carnitine effect on peripheral muscle metabolism. A multicenter trial on 537 patients showed that propionyl-L-carnitine improves exercise capacity in patients with heart failure, but preserved cardiac function.[Abstract]
  22. Pucciarelli G, Mastursi M, Latte S, Sacra C, Setaro A, Lizzadro A, Nolfe G. Clin Ter. 1992 Nov;141(11):379-84. The clinical and hemodynamic effects of propionyl-L-carnitine in the treatment of congestive heart failure
    At the end of six months of treatment maximum exercise time on the treadmill increased 11.1% after 90 days and 16.4% after 180 in the group treated with PLC. rom a hemodynamic standpoint, after 30, 90 and 180 days the ejection fraction increased by 7.3%, 10.7% and 12.1%. At the same time, moreover, the systemic vascular resistances were reduced by 14.9%, 20% and 20.6%.[Abstract]
  23. Mancini M, Rengo F, Lingetti M, Sorrentino GP, Nolfe G. Arzneimittelforschung. 1992 Sep;42(9):1101-4 Controlled study on the therapeutic efficacy of propionyl-L-carnitine in patients with congestive heart failure
    At the stated times the increases in the maximum exercise time were 16.4%, 22.9%, and 25.9%, respectively. The ventricular ejection fraction increased by 8.4%, 11.6% and 13.6%, respectively. On the basis of these results, having studied the particular mechanism of action of propionyl-L-carnitine the authors conclude that it represents a drug of undoubted therapeutic interest in patients with congestive heart failure, in whom it could be efficaciously administered along with a standard pharmacological therapy.[Abstract]
  24. Anand I, Chandrashekhan Y, De Giuli F, Pasini E, Mazzoletti A, Confortini R, Ferrari R. Cardiovasc Drugs Ther. 1998 Jul;12(3):291-9. Acute and chronic effects of propionyl-L-carnitine on the hemodynamics, exercise capacity, and hormones in patients with congestive heart failure
    We conclude that propionyl-L-carnitine increases exercise capacity and reduces ventricular size in patients with congestive heart failure. The drug has no significant effects on hemodynamics or neurohormone levels. The use of a single-blind design reduces the impact of the positive finding on exercise capacity.[Abstract]
  25. Winter S, Jue K, Prochazka J, Francis P, Hamilton W, Linn L, Helton E. J Child Neurol. 1995 Nov;10 Suppl 2:S45-51 The role of L-carnitine in pediatric cardiomyopathy
    Review of reports of L-Carnitine supplementation studies and results from our own trial underscore the importance of its role in cardiac function and demonstrates that there is likely a subpopulation of patients with cardiomyopathy responsive to L-carnitine treatment.[Abstract]
  26. Winter SC, Buist NR. Am Heart J. 2000 Feb;139(2 Pt 3):S63-9. Cardiomyopathy in childhood, mitochondrial dysfunction, and the role of L-carnitine
    Carnitine deficiency can be caused by both genetic and environmental causes with resultant signs and symptoms of metabolic disease, including cardiomyopathy. Administration of L-carnitine can result in improvement or resolution of the cardiomyopathy.[Abstract]
  27. Gesuete V, Ragni L, Picchio FM. G Ital Cardiol (Rome). 2010 Sep;11(9):703-5 The “big heart” of carnitine
    Fat is the primary energy source for heart muscle. In the heart, carnitine is essential for normal fatty acid beta-oxidation and even partial deficiency could lead to organ dysfunction.[Abstract]
  28. Veiligheid carnitine

  29. Hathcock JN, Shao A. Regul Toxicol Pharmacol. 2006 Oct;46(1):23-8. Risk assessment for carnitine
    The OSL risk assessment method indicates that the evidence of safety is strong at intakes up to 2000mg/day l-carnitine equivalents for chronic supplementation, and this level is identified as the OSL. Although much higher levels have been tested without adverse effects and may be safe, the data for intakes above 2000mg/day are not sufficient for a confident conclusion of long-term safety.[Abstract]
  30. Crill CM, Helms RA. Nutr Clin Pract. 2007 Apr;22(2):204-13. The use of carnitine in pediatric nutrition
    Carnitine is synthesized endogenously from methionine and lysine in the liver and kidney and is available exogenously from a meat and dairy diet and from human milk and most enteral formulas. Parenteral nutrition (PN) does not contain carnitine unless it is extemporaneously added. The primary role of carnitine is to transport long-chain fatty acids across the mitochondrial membrane, where they undergo beta-oxidation to produce energy. Although the majority of patients are capable of endogenous synthesis of carnitine, certain pediatric populations, specifically neonates and infants, have decreased biosynthetic capacity and are at risk of developing carnitine deficiency, particularly when receiving PN. [Abstract]
  31. Squarcia U, Agnetti A, Caffarra A, Cavalli C, Marbini A. Pediatr Med Chir. 1986 Mar-Apr;8(2):157-61. Dilated cardiomyopathy due to primary carnitine deficiency
    A case of a 3 and a half years old girl with severe congestive heart failure, and typical picture of dilated cardiomyopathy is presented. L-carnitine (2 gr. three times a day p.o.) was added to anti-congestive therapy. After 8 weeks of therapy, the general and cardiocirculatory conditions are much improved. The physiopathology of dilated cardiomyopathy due to deficit of carnitine are discussed. An early diagnosis, and an early substitutive therapy with L-carnitine dramatically improve the outcome of the disease.[Abstract]
  32. CBG: Carnitene Sigma Tau, drank 1 g/10 ml RVG 11193
    Aanbevolen wordt de volgende dosering per os per dag: Zuigelingen: 100-150 mg/kg lichaamsgewicht Kinderen tot 12 jaar: 50-100 mg/kg lichaamsgewicht. Er is geen toxiciteit gerapporteerd. Hoge doseringen levocarnitine zijn geassocieerd met diarree. [Article]

Q10 and Carnitine

    Synergy between Q10 and Carnitine

  1. Bertelli A, Ronca G. Int J Tissue React. 1990;12(3):183-6. Carnitine and coenzyme Q10: biochemical properties and functions, synergism and complementary action
    The mechanisms by which carnitine and coenzyme Q10 intervene in the energetic metabolism are described. In particular, the metabolic stages in which the action of carnitine is complementary to the action of coenzyme Q10 are illustrated. The synergism of the pharmacological and therapeutic actions that is found when these compounds are administered together is explained on the basis of their biochemical and metabolic complementarity.[Abstract]
  2. Conte A, Palmieri L, Ronca G, Giovannini L, Bertelli A. Int J Tissue React. 1990;12(3):197-201 Synergic and complementary effects of L-carnitine and coenzyme Q on long-chain fatty acid metabolism and on protection against anthracycline damage
    The results obtained suggest that the administration of an association of L-carnitine and CoQ exerts a stronger protection against anthracycline damage and induces a greater utilization of fatty acids as compared to the effects of each compound alone.[Abstract]
  3. Sinatra ST. Altern Ther Health Med. 2009 Mar-Apr;15(2):48-50 Metabolic cardiology: the missing link in cardiovascular disease
    Metabolic therapies that help cardiomyocytes meet their absolute need for ATP fulfill a major clinical challenge of preserving pulsatile cardiac function while maintaining cell and tissue viability. D-ribose, L-carnitine, and coenzyme Q10 work in synergy to help the ischemic or hypoxic heart preserve its energy charge. [Abstract]
  4. Sinatra ST. Altern Ther Health Med. 2009 May-Jun;15(3):44-52. Metabolic cardiology: an integrative strategy in the treatment of congestive heart failure
    The purpose of this communication article is to introduce metabolic cardiology as a vital therapeutic strategy utilizing nutritional biochemical interventions that preserve and promote adenosine triphosphate (ATP) production. Treatment options that incorporate metabolic interventions targeted to preserve energy substrates (D-ribose) or accelerate ATP turnover (L-carnitine and coenzyme Q10) are indicated for at-risk populations or patients at any stage of CHF. [Abstract]
  5. Prevention cardiomyopathy after heart attack using Q10 and Carnitine

  6. Pauly DF, Pepine CJ. Am J Kidney Dis. 2003 Apr;41(4 Suppl 4):S35-43. The role of carnitine in myocardial dysfunction
    Studies on the role of carnitine administration to patients with myocardial infarction (MI), angina, and congestive heart failure generally have been positive. In general, treatment with carnitine (1.5 to 6 g/d for up to 1 year) results in a beneficial effect of fewer deaths and less heart failure when administered to patients after MI.[Abstract]
  7. Iliceto S, Scrutinio D, Bruzzi P, D’Ambrosio G, Boni L, Di Biase M, Biasco G, Hugenholtz PG, Rizzon P. J Am Coll Cardiol. 1995 Aug;26(2):380-7. Effects of L-carnitine administration on left ventricular remodeling after acute anterior myocardial infarction: the L-Carnitine Ecocardiografia Digitalizzata Infarto Miocardico (CEDIM) Trial
    L-Carnitine treatment initiated early after acute myocardial infarction and continued for 12 months can attenuate left ventricular dilation during the first year after an acute myocardial infarction, resulting in smaller left ventricular volumes at 3, 6 and 12 months after the emergent event.[Abstract]
  8. Tarantini G, Scrutinio D, Bruzzi P, Boni L, Rizzon P, Iliceto S. Cardiology. 2006;106(4):215-23. Epub 2006 May 9. Metabolic treatment with L-carnitine in acute anterior ST segment elevation myocardial infarction. A randomized controlled trial
    In CEDIM 2 trial L-carnitine therapy led to a reduction in early mortality (secondary end-point) without affecting the risk of death and heart failure at 6 months in patients with anterior AMI, leading to a non-significant finding with respect to the primary end-point.[Abstract]
  9. Lango R, Smolenski RT, Narkiewicz M, Suchorzewska J, Lysiak-Szydlowska W. Cardiovasc Res. 2001 Jul;51(1):21-9. Influence of L-carnitine and its derivatives on myocardial metabolism and function in ischemic heart disease and during cardiopulmonary bypass
    Carnitine and its derivatives have recently been shown to protect cardiac metabolism and function in ischemic heart disease and other clinical conditions of myocardial ischemia. Potential mechanisms of this effect include an increase in glucose metabolism, a reduction of toxic effects of long-chain acyl-CoA and acyl-carnitine in myocytes, an increase in coronary blood flow and anti-arrhythmic effect. It has also been shown that propionyl-L-carnitine which penetrates faster than carnitine into myocytes is effective in inhibiting production of free radicals. [Article]
  10. Singh RB, Niaz MA, Agarwal P, Beegum R, Rastogi SS, Sachan DS. Postgrad Med J. 1996 Jan;72(843):45-50. A randomised, double-blind, placebo-controlled trial of L-carnitine in suspected acute myocardial infarction
    It is possible that L-carnitine supplementation in patients with suspected acute myocardial infarction may be protective against cardiac necrosis and complications during the first 28 days.[Article]
  11. Davini P, Bigalli A, Lamanna F, Boem A. Drugs Exp Clin Res. 1992;18(8):355-65. Controlled study on L-carnitine therapeutic efficacy in post-infarction
    On the basis of these results, it is concluded that L-carnitine represents an effective treatment in post-infarction ischaemic cardiopathy, since it can improve the clinical evolution of this pathological condition as well as the patient’s quality of life and life expectancy.[Abstract]
  12. Singh RB, Neki NS, Kartikey K, Pella D, Kumar A, Niaz MA, Thakur AS. Mol Cell Biochem. 2003 Apr;246(1-2):75-82. Effect of coenzyme Q10 on risk of atherosclerosis in patients with recent myocardial infarction
    t is possible that treatment with CoQ10 in patients with recent MI may be beneficial in patients with high risk of atherothrombosis, despite optimal lipid lowering therapy during a follow-up of 1 year. Adverse effect of treatments showed that fatigue (40.8 vs. 6.8%, p < 0.01) was more common in the control group than CoQ group.[Abstract]
  13. Singh RB, Wander GS, Rastogi A, Shukla PK, Mittal A, Sharma JP, Mehrotra SK, Kapoor R, Chopra RK. Cardiovasc Drugs Ther. 1998 Sep;12(4):347-53 Randomized, double-blind placebo-controlled trial of coenzyme Q10 in patients with acute myocardial infarction
    These findings suggest that coenzyme Q10 can provide rapid protective effects in patients with AMI if administered within 3 days of the onset of symptoms. More studies in a larger number of patients and long-term follow-up are needed to confirm our results.[Abstract]
  14. Singh RB, Niaz MA. Int J Cardiol. 1999 Jan;68(1):23-9. Serum concentration of lipoprotein(a) decreases on treatment with hydrosoluble coenzyme Q10 in patients with coronary artery disease: discovery of a new role
    Supplementation with hydrosoluble coenzyme Q10 (Q-Gel) decreases lipoprotein(a) concentration in patients with acute coronary disease.[Abstract]
  15. Kuklinski B, Weissenbacher E, Fähnrich A. Mol Aspects Med. 1994;15 Suppl:s143-7. Coenzyme Q10 and antioxidants in acute myocardial infarction
    During the one-year follow-up period after myocardial infarction, six patients (20%) from the control group died from re-infarction whereas one patient from the verum group suffered a non-cardiac death.[Abstract]
  16. Allard ML, Jeejeebhoy KN, Sole MJ. Heart Fail Rev. 2006 Mar;11(1):75-82. The management of conditioned nutritional requirements in heart failure
    L-carnitine, coenzyme Q10, creatine and taurine are reduced in this patient population. Furthermore, deficiencies of taurine, carnitine, and thiamine are established primary causes of dilated cardiomyopathy. [Abstract]
  17. Sole MJ, Jeejeebhoy KN. Herz. 2002 Mar;27(2):174-8. Conditioned nutritional requirements: therapeutic relevance to heart failure
    Deficiencies of carnitine or taurine alone are well documented to result in dilated cardiomyopathy in animals and humans.[Abstract]
all living cells, as well as in RNA-containing viruses. It is not an essential nutrient, since it can be made in the body from other substances, such as glucose.

D-ribose, however, is very essential for life. Some of the most important biological molecules contain D-ribose, including ATP (adenosine triphosphate), all the nucleotides and nucleotide coenzymes and all forms of RNA (ribonucleic acid). D-ribose, in the form of ribonucleoside diphosphates, is converted to deoxyribonucleoside diphosphates, precursor molecules for DNA. D-ribose in RNA and D-deoxyribose in DNA may be considered genetic sugars.

    D-ribose is onderdeel van metabole cardiologie

  1. Sinatra ST. Altern Ther Health Med. 2009 Mar-Apr;15(2):48-50 Metabolic cardiology: the missing link in cardiovascular disease
    Metabolic therapies that help cardiomyocytes meet their absolute need for ATP fulfill a major clinical challenge of preserving pulsatile cardiac function while maintaining cell and tissue viability. D-ribose, L-carnitine, and coenzyme Q10 work in synergy to help the ischemic or hypoxic heart preserve its energy charge. [Abstract]
  2. Sinatra ST. Altern Ther Health Med. 2009 May-Jun;15(3):44-52. Metabolic cardiology: an integrative strategy in the treatment of congestive heart failure
    The purpose of this communication article is to introduce metabolic cardiology as a vital therapeutic strategy utilizing nutritional biochemical interventions that preserve and promote adenosine triphosphate (ATP) production. Treatment options that incorporate metabolic interventions targeted to preserve energy substrates (D-ribose) or accelerate ATP turnover (L-carnitine and coenzyme Q10) are indicated for at-risk populations or patients at any stage of CHF. [Abstract]
  3. Pauly DF, Pepine CJ. J Cardiovasc Pharmacol Ther. 2000 Oct;5(4):249-58. D-Ribose as a supplement for cardiac energy metabolism
    The heart’s ability to resynthesize ATP is then limited by the supply of D-ribose, which is a necessary component of the adenine nucleotide structure. In support of this hypothesis, recent reports have used D-ribose to increase tolerance to myocardial ischemia. Its use in patients with stable coronary artery disease improves time to exercise-induced angina and electrocardiographic changes.[Abstract]
  4. Wagner S, Herrick J, Shecterle LM, St Cyr JA. Prog Cardiovasc Nurs. 2009 Jun;24(2):59-60. D-ribose, a metabolic substrate for congestive heart failure
    Publications have asserted that the failing heart is energy starved. D-ribose, a naturally occurring pentose carbohydrate and a key component in the adenosine triphosphate (ATP) molecule, has demonstrated an ability to replenish ATP levels and improve diastolic dysfunction following myocardial ischemia, which has been shown to improve the clinical state of patients afflicted with congestive heart failure. D-ribose may provide the necessary metabolic substrate to benefit this energy-deficient state found in heart failure.[Abstract]
  5. Shecterle LM, Terry KR, St Cyr JA. Recent Pat Cardiovasc Drug Discov. 2010 Jun 1;5(2):138-42. The patented uses of D-ribose in cardiovascular diseases
    However, D-ribose, a natural occurring carbohydrate, has demonstrated significant enhancing abilities in replenishing deficient cellular energy levels following myocardial ischemia, as well as improving depressed function in numerous animal investigations. Subsequent clinical trials have further substantiated these benefits of D-ribose in patients afflicted with ischemic cardiovascular disease and those carrying the diagnosis of congestive heart failure. The future of effective therapies for ischemic heart disease and congestive heart failure must strongly consider novel pharmaceuticals directed at replenishing cellular energy levels. [Abstract]
  6. Het gebruik van D-ribose bij cardiomyopathie en hartfalen

  7. Omran H, Illien S, MacCarter D, St Cyr J, Lüderitz B. Eur J Heart Fail. 2003 Oct;5(5):615-9. D-Ribose improves diastolic function and quality of life in congestive heart failure patients: a prospective feasibility study
    The administration of D-ribose resulted in an enhancement of atrial contribution to left ventricular filling (40±11 vs. 45±9%, P=0.02), a smaller left atrial dimension (54±20 vs. 47±18 ml, P=0.02) and a shortened E wave deceleration (235±64 vs. 196±42, P=0.002) by echocardiography. Both supplements were supplied as a dry powder, 5 g/dose, dissolved in 8 oz of water, and administered three times a day with meals.[Article]
  8. Wikipedia Diastolic heart failure
    iastolic heart failure or diastolic dysfunction refers to decline in performance of one or both ventricles of the heart during the time phase of diastole. Diastole is that phase of the cardiac cycle when the heart is not contracting to propel blood out systole to the body, brain and lungs but instead is relaxed and filling with incoming blood that is being returned from the body through the inferior vena cava IVC from the lungs through the pulmonary veins and from the brain through the superior vena cava SVC.[Article]
  9. MacCarter D, Vijay N, Washam M, Shecterle L, Sierminski H, St Cyr JA. Int J Cardiol. 2009 Sep 11;137(1):79-80. D-ribose aids advanced ischemic heart failure patients
    All patients had a significant improvement in ventilatory parameters at anaerobic threshold, along with a 44% Weber class improvement. Ribose improved the ventilatory exercise status in advanced heart failure patients.[Abstract]
  10. De veiligheid van D-ribose

  11. Griffiths JC, Borzelleca JF, St Cyr J. Food Chem Toxicol. 2007 Jan;45(1):144-52 Sub-chronic (13-week) oral toxicity study with D-ribose in Wistar rats
    Analysis of microscopic histopathology revealed no evidence of changes that could be attributed to the DR treatment. It is scientifically reasonable to conclude that the present study supports a concentration of 5% DR in the diet, corresponding to an average daily intake of DR of 3.6 and 4.4 g/kg body weight/day in male and female rats, respectively, as being the absolute no observed adverse effect level (NOAEL) for this substance.[Abstract]

  12. .[Abstract]

Taurine

Taurine, a lesser known amino acid, is not part of our muscle protein yet is important in metabolism, especially in the brain. It is essential in newborns, as they cannot make it. Adults can produce sulfur-containing taurine from cysteine with the help of pyridoxine, B6. It is possible that if not enough taurine is made in the body, especially if cysteine or B6 is deficient, it might be further required in the diet. Animal protein is a good source of taurine, as it is not found in vegetable protein. Vegetarians with an unbalanced protein intake, and therefore deficient in methionine or cysteine may have difficulty manufacturing taurine. Dietary intake is thought to be more important in women as the female hormone estradiol depresses the formation of taurine in the liver.

Taurine is a non-essential amino acid that functions electrically active tissues such as the brain and heart to help stabilize cell membranes. Supplements decrease the tendency to develop abnormal heart arrythmias after heart attacks. People with congestive heart failure have also responded to supplementation with improved cardiac and respiratory function.

    Taurine is een veelzijdig aminozuur

  1. Lourenço R, Camilo ME. Nutr Hosp. 2002 Nov-Dec;17(6):262-70. Taurine: a conditionally essential amino acid in humans? An overview in health and disease
    Taurine, a sulphur containing amino acid, is the most abundant intracellular amino acid in humans, and is implicated in numerous biological and physiological functions. This comprehensive overview explores areas, from its characterisation to its potential clinical benefit as a conditionally essential amino acid and a pharmaconutrient. Taurine is an essential amino acid for preterm neonates and is assured by breast milk. Specific groups of individuals are at risk for taurine deficiency and may benefit from supplementation, e.g. patients requiring long-term parenteral nutrition (including premature and newborn infants); those with chronic hepatic, heart or renal failure. [Abstract]
  2. Birdsall TC. Altern Med Rev. 1998 Apr;3(2):128-36. Therapeutic applications of taurine
    Taurine is a conditionally-essential amino acid which is not utilized in protein synthesis, but rather is found free or in simple peptides. Taurine has been shown to be essential in certain aspects of mammalian development, and in vitro studies in various species have demonstrated that low levels of taurine are associated with various pathological lesions, including cardiomyopathy, retinal degeneration, and growth retardation, especially if deficiency occurs during developmen.[Article]
  3. Functionele tekorten van het “zieke hart”

  4. Allard ML, Jeejeebhoy KN, Sole MJ. Heart Fail Rev. 2006 Mar;11(1):75-82. The management of conditioned nutritional requirements in heart failur
    myocyte calcium overload and increased oxidative stress. Nutritional factors known to be important for myocardial energy production, calcium homeostasis and the reduction of oxidative stress, such as thiamine, riboflavin, pyridoxine, L-carnitine, coenzyme Q10, creatine and taurine are reduced in this patient population. Furthermore, deficiencies of taurine, carnitine, and thiamine are established primary causes of dilated cardiomyopathy. [Abstract]
  5. Sole MJ, Jeejeebhoy KN. Curr Opin Clin Nutr Metab Care. 2000 Nov;3(6):417-24. Conditioned nutritional requirements and the pathogenesis and treatment of myocardial failure
    Several specific deficiencies have been found in the failing myocardium: a reduction in the content of L-carnitine, coenzyme Q10, creatine and thiamine, nutrient cofactors that are important for myocardial energy production; a relative deficiency of taurine, an amino acid that is integral to the modulation of intracellular calcium levels; and an increase in myocardial oxidative stress, and a reduction of both endogenous and exogenous antioxidant defences. [Abstract]
  6. Sole MJ, Jeejeebhoy KN. Herz. 2002 Mar;27(2):174-8. Conditioned nutritional requirements: therapeutic relevance to heart failure
    The advent of disease, genetic predisposition or certain drug therapies may significantly alter the nutritional demands of specific organs. Several specific metabolic deficiencies have been found in the failing myocardium: (1) a reduction in L-carnitine, coenzyme Q10, creatine, and thiamine–nutrient cofactors important for myocardial energy production; (2) a relative deficiency of taurine, an amino acid integral to intracellular calcium homeostasis; (3) increased myocardial oxidative stress and a reduction of antioxidant defenses. These experiments suggest that a comprehensive restoration of adequate myocyte nutrition may be important to any therapeutic strategy designed to benefit patients suffering from congestie heart failure. Future studies in this area are of clinical importance.[Abstract]
  7. Het gebruik van taurine bij cardiomyopathie en hartfalen

  8. Azuma J, Sawamura A, Awata N, Ohta H, Hamaguchi T, Harada H, Takihara K, Hasegawa H, Yamagami T, Ishiyama T, et al. Clin Cardiol. 1985 May;8(5):276-82. Therapeutic effect of taurine in congestive heart failure: a double-blind crossover trial
    The results indicate that addition of taurine to conventional therapy is safe and effective for the treatment of patients with congestive heart failure.[Abstract]
  9. Schaffer SW, Lombardini JB, Azuma J. Amino Acids. 2000;18(4):305-18. Interaction between the actions of taurine and angiotensin II
    One disease that responds favorably to taurine therapy is congestive heart failure. In this review, we discuss three mechanisms that might underlie the beneficial effect of taurine in heart failure. First, taurine promotes natriuresis and diuresis, presumably through its osmoregulatory activity in the kidney, its modulation of atrial natriuretic factor secretion and its putative regulation of vasopressin release. Second, taurine mediates a modest positive inotropic effect by regulating [Na+]i and Na+/Ca2+ exchanger flux. Although this effect of taurine has not been examined in human tissue, it is significant that it bypasses the major calcium transport defects found in the failing human heart. Third, taurine attenuates the actions of angiotensin II on Ca2+ transport, protein synthesis and angiotensin II signaling. Through this mechanism taurine would be expected to minimize many of the adverse actions of angiotensin II, including the induction of cardiac hypertrophy, volume overload and myocardial remodeling. [Abstract]
  10. Jeejeebhoy F, Keith M, Freeman M, Barr A, McCall M, Kurian R, Mazer D, Errett L. Am Heart J. 2002 Jun;143(6):1092-100. Nutritional supplementation with MyoVive repletes essential cardiac myocyte nutrients and reduces left ventricular size in patients with left ventricular dysfunction
    Supplementation results in higher myocardial CoQ10, taurine, and carnitine levels and is associated with a reduction in left ventricular end-diastolic volume in patients with left ventricular dysfunction before revascularization. Because the risk of death for surgical revascularization is related to preoperative left ventricular end-diastolic volume, supplementation could improve outcomes.[Abstract]
  11. De veiligheid Taurine

  12. Gaull GE. Pediatrics. 1989 Mar;83(3):433-42. Taurine in pediatric nutrition: review and update
    Taurine is now added to many infant formulas as a measure of prudence to provide improved nourishment with the same margin of safety for its newly identified physiologic functions as that found in human milk.[Abstract]
  13. Shao A, Hathcock JN. egul Toxicol Pharmacol. 2008 Apr;50(3):376-99 Risk assessment for the amino acids taurine, L-glutamine and L-arginine
    The OSL risk assessments indicate that based on the available published human clinical trial data, the evidence for the absence of adverse effects is strong for Tau at supplemental intakes up to 3 g/d,.[Abstract]

  14. .[Abstract]

  15. .[Abstract]

Magnesium

    Magnesium en metabole cardiologie

  1. Fox C, Ramsoomair D, Carter C. South Med J. 2001 Dec;94(12):1195-201. Magnesium: its proven and potential clinical significance
    Magnesium is the fourth most abundant cation in the body and is present in more than 300 enzymatic systems, where it is crucial for adenosine triphosphate (ATP) metabolism.[Abstract]
  2. Shechter M. Am J Cardiovasc Drugs. 2003;3(4):231-9. Does magnesium have a role in the treatment of patients with coronary artery disease?
    Hypomagnesemia is common in hospitalized patients, especially in elderly patients with coronary artery disease (CAD) and/or those with chronic heart failure. Hypomagnesemia is associated with increased all cause mortality and mortality from CAD. Magnesium supplementation improves myocardial metabolism, inhibits calcium accumulation and myocardial cell death; it improves vascular tone, peripheral vascular resistance, afterload and cardiac output, reduces cardiac arrhythmias and improves lipid metabolism. Nevertheless, the theoretical benefits of magnesium supplementation as a cardio-protective agent in CAD patients, promising results from animal and human studies, its relatively low-cost and ease of handling requiring no special expertise, together with its excellent tolerability, gives magnesium a place in treating CAD patients, especially in those at high risk, such as CAD patients with heart failure, the elderly and hospitalized patients with hypomagnesemia. Furthermore, magnesium therapy is indicated in life-threatening ventricular arrhythmias such as torsades de pointes and intractable ventricular tachycardia.[Abstract]
  3. Shechter M. Harefuah. 2011 Jan;150(1):41-5, 67. Body magnesium–the spark of life
    Magnesium supplementation improves myocardial metabolism, inhibits calcium accumulation and myocardial cell death; it improves vascular tone, peripheral vascular resistance, afterload and cardiac output, reduces cardiac arrhythmias and improves lipid metabolism.[Abstract]
  4. Magnesium deficiëntie komt vaak voor

  5. Ohtsuka S, Yamaguchi I. Clin Calcium. 2005 Feb;15(2):181-6. Magnesium in congestive heart failure
    Magnesium deficit and other electrolyte abnormalities is a frequent disorder in patients with congestive heart failure. Overstimulation of the renin-angiotensin-aldosterone system, long-term administration of diuretics, digoxin, poor oral intake and impaired absorption contribute to these electrolytes abnormalities. Nevertheless, since magnesium depletion may be prevalent in congestive heart failure and magnesium has anti-arrhythmic and beneficial cardiovascular effects, magnesium should be supplemented to the patients suspected to have its deficiency.[Abstract]
  6. Douban S, Brodsky MA, Whang DD, Whang R. Am Heart J. 1996 Sep;132(3):664-71 Significance of magnesium in congestive heart failure
    Electrolyte balance has been regarded as a factor important to cardiovascular stability, particularly in congestive heart failure. Among the common electrolytes, the significance of magnesium has been debated because of difficulty in accurate measurement and other associated factors, including other electrolyte abnormalities. The serum magnesium level represents < 1% of total body stores and does not reflect total-body magnesium concentration, a clinical situation very similar to that of serum potassium. Typical therapy for heart failure (digoxin, diuretic agents, and ACE inhibitors) are influenced by or associated with significant alteration in magnesium balance. Magnesium therapy, both for deficiency replacement and in higher pharmacologic doses, has been beneficial in improving hemodynamics and in treating arrhythmias. Magnesium toxicity rarely occurs except in patients with renal dysfunction. In conclusion, the intricate role of magnesium on a biochemical and cellular level in cardiac cells is crucial in maintaining stable cardiovascular hemodynamics and electrophysiologic function.[Abstract]
  7. Sueta CA, Patterson JH, Adams KF Jr. Magnes Res. 1995 Dec;8(4):389-401. Antiarrhythmic action of pharmacological administration of magnesium in heart failure: a critical review of new data
    Patients with congestive heart failure are predisposed to magnesium deficit for many reasons, including neurohormonal activation, poor gastrointestinal absorption, and drug therapy. Hypomagnesaemia is common in these patients and has been linked to an increased frequency of complex ventricular ectopy. Magnesium administration is well tolerated and serious adverse effects are rare. The potential mechanisms of the antiarrhythmic action of magnesium and limitations of the available data are discussed. The evidence reviewed suggests that serum magnesium concentrations should be monitored and corrected in patients with congestive heart failure.[Abstract]
  8. Ceremuzy?ski L, Gebalska J, Wolk R, Makowska E. J Intern Med. 2000 Jan;247(1):78-86. Hypomagnesemia in heart failure with ventricular arrhythmias. Beneficial effects of magnesium supplementation
    Hypomagnesemia, probably related to increased urine magnesium excretion, is an essential feature of heart failure associated with complex ventricular arrhythmias. These arrhythmias can be alleviated/abolished by magnesium supplementation.[Article]
  9. Lin XY, Xiao LZ, Gao LJ, Zhang HF. Zhonghua Xin Xue Guan Bing Za Zhi. 2005 Nov;33(11):995-7. Effects of carvedilol on neurohormone and magnesium metabolism in patients with chronic heart failure
    Carvedilol decreases significantly plasma concentrations of neurohormone and urine magnesium excretion, and increases cell magnesium content in patients with CHF.[Abstract]
  10. Wester PO. Am J Cardiol. 1992 Oct 8;70(10):44C-49C. Electrolyte balance in heart failure and the role for magnesium ions
    It is well established that clinically significant changes in a number of electrolytes occur in patients with congestive heart failure (CHF). Magnesium ions are an essential requirement for many enzyme systems, and evidence is rapidly emerging that magnesium deficiency is a major risk factor for survival of CHF patients. [Abstract]
  11. Extra magnesium vermindert de kans op hartritmestoornissen

  12. Bashir Y, Sneddon JF, Staunton HA, Haywood GA, Simpson IA, McKenna WJ, Camm AJ. Am J Cardiol. 1993 Nov 15;72(15):1156-62. Effects of long-term oral magnesium chloride replacement in congestive heart failure secondary to coronary artery disease
    In conclusion, magnesium supplementation reduced the frequency of asymptomatic ventricular arrhythmias, possibly due to secondary changes in potassium homeostasis, and produced a minor degree of vasodilation.[Abstract]
  13. Zehender M, Meinertz T, Faber T, Caspary A, Jeron A, Bremm K, Just H. J Am Coll Cardiol. 1997 Apr;29(5):1028-34. Antiarrhythmic effects of increasing the daily intake of magnesium and potassium in patients with frequent ventricular arrhythmias. Magnesium in Cardiac Arrhythmias (MAGICA) Investigators
    To our knowledge, this study is the first to provide controlled data on the antiarrhythmic effect of oral administration of magnesium and potassium salts when directed to patients with frequent and stable ventricular tachyarrhythmias. A 50% increase in the recommended minimum daily dietary intake of the two minerals for 3 weeks results in a moderate but significant antiarrhythmic effect. However, with the given therapeutic regimen, repetitive tachyarrhythmias and patient symptoms remain unchanged.[Abstract]
  14. J Intern Med. 2000 Jan;247(1):78-86 Ceremuzy?ski L, Gebalska J, Wolk R, Makowska E. Hypomagnesemia in heart failure with ventricular arrhythmias. Beneficial effects of magnesium supplementation
    Hypomagnesemia, probably related to increased urine magnesium excretion, is an essential feature of heart failure associated with complex ventricular arrhythmias. These arrhythmias can be alleviated/abolished by magnesium supplementation.[Article]
  15. Sueta CA, Clarke SW, Dunlap SH, Jensen L, Blauwet MB, Koch G, Patterson JH, Adams KF Jr. Circulation. 1994 Feb;89(2):660-6. Effect of acute magnesium administration on the frequency of ventricular arrhythmia in patients with heart failure
    Intravenous magnesium chloride administration reduces the frequency of ventricular arrhythmia in patients with symptomatic heart failure.[Article]
  16. Gullestad L, Birkeland K, Mølstad P, Høyer MM, Vanberg P, Kjekshus J. Clin Cardiol. 1993 May;16(5):429-34. The effect of magnesium versus verapamil on supraventricular arrhythmias
    Magnesium appears to be an effective and safe drug for the treatment of supraventricular arrhythmias. The overall efficacy for conversion to sinus rhythm is at least as effective as with verapamil, and its action is more rapid.[Abstract]
  17. Magnesium bij de behandeling van cardiomyopathie en hartfalen

  18. Stepura OB, Martynow AI. Int J Cardiol. 2009 May 1;134(1):145-7. Magnesium orotate in severe congestive heart failure (MACH)
    Magnesium orotate may be used as adjuvant therapy in patients on optimal treatment for severe congestive heart failure, increasing survival rate and improving clinical symptoms and patient’s quality of life.[Abstract]
  19. Almoznino-Sarafian D, Berman S, Mor A, Shteinshnaider M, Gorelik O, Tzur I, Alon I, Modai D, Cohen N. Eur J Nutr. 2007 Jun;46(4):230-7. Magnesium and C-reactive protein in heart failure: an anti-inflammatory effect of magnesium administration?
    Oral Mg supplementation to HF patients significantly attenuates blood levels of CRP, a biomarker of inflammation. Targeting the inflammatory cascade by Mg administration might prove a useful tool for improving the prognosis in HF.[Abstract]
  20. De veiligheid van magnesium

  21. European Guidelines may 2003 Safe Upper levels for Vitamins en Minerals
    .[Article]
  22. Magnesiumoxide ratiopharm 500 mg, kauwtabletten
    Symptomatische behandeling van klachten als gevolg van hyperaciditeit, bijvoorbeeld bij indigestie, zuurbranden, ulcus pepticum, gastritis, lichte reflux-oesophagitis.[Article]

  23. .[Abstract]

Visolie

    VISOLIE EN HART EN VAATZIEKTEN
  1. Lee KW, Lip GY. QJM. 2003 Jul;96(7):465-80 The role of omega-3 fatty acids in the secondary prevention of cardiovascular disease
    It has long been recognized from epidemiological studies that Greenland Eskimos have substantially reduced rates of acute myocardial infarction (MI) compared with Western controls. From these epidemiological observations, the benefits of fatty fish consumption have been explored in cell culture and animal studies, as well as randomized controlled trials investigating the cardioprotective effects of omega-3 fatty acids. Dietary omega-3 fatty acids seem to stabilize the myocardium electrically, resulting in reduced susceptibility to ventricular arrhythmias, thereby reducing the risk of sudden death. These fatty acids also have potent anti-inflammatory effects, and may also be antithrombotic and anti-atherogenic. Furthermore, the recent GISSI-Prevention study of 11 324 patients showed a marked decrease in risk of sudden cardiac death as well as a reduction in all-cause mortality in the group taking a highly purified form of omega-3 fatty acids, despite the use of other secondary prevention drugs, including beta-blockers and lipid-lowering therapy. The use of omega-3 fatty acids should be considered as part of a comprehensive secondary prevention strategy post-myocardial infarction.[Article]
  2. Ishikawa Y, Yokoyama M, Saito Y, Matsuzaki M, Origasa H, Oikawa S, Sasaki J, Hishida H, Itakura H, Kita T, Kitabatake A, Nakaya N, Sakata T, Shimada K, Shirato K, Matsuzawa Y; Circ J. 2010 Jul;74(7):1451-7. Preventive effects of eicosapentaenoic acid on coronary artery disease in patients with peripheral artery disease
    Subanalysis of the JELIS trial demonstrated that in patients with PAD the incidence of CAD was higher than in controls, and that EPA markedly reduced the occurrence of CAD in those patients.[Abstract]
  3. Gezondheidsraad Richtlijnen goede voeding 2006
    De hoeveelheid visolie vetzuren in de voeding zal daarentegen aanzienlijk moeten toenemen om te kunnen voldoen aan de voedingsnorm voor deze vetzuren van 450 mg per dag. Deze inname kan worden gerealiseerd door tweemaal per week een portie vis te gebruiken waarvan ten minste eenmaal een portie vette vis.[Article]
  4. Itakura H, Yokoyama M, Matsuzaki M, Saito Y, Origasa H, Ishikawa Y, Oikawa S, Sasaki J, Hishida H, Kita T, Kitabatake A, Nakaya N, Sakata T, Shimada K, Shirato K, Matsuzawa Y; J Atheroscler Thromb. 2011;18(2):99-107 Relationships between plasma fatty acid composition and coronary artery disease
    The higher plasma level of EPA (hazard ratio=0.83, p=0.049, in all participants and hazard ratio=0.71, p=0.018, in the EPA intervention group), but not of DHA, was inversely associated with the risk of major coronary events.[Article]
  5. Harris WS, Von Schacky C. Prev Med. 2004 Jul;39(1):212-20. The Omega-3 Index: a new risk factor for death from coronary heart disease?
    The Omega-3 Index was inversely associated with risk for CHD mortality.The Omega-3 Index may represent a novel, physiologically relevant, easily modified, independent, and graded risk factor for death from CHD that could have significant clinical utility.[Abstract]
  6. VISOLIE AND HF
  7. Gissi-HF Investigators, Tavazzi L, Maggioni AP, Marchioli R, Barlera S, Franzosi MG, Latini R, Lucci D, Nicolosi GL, Porcu M, Tognoni G Lancet. 2008 Oct 4;372(9645):1223-30 Effect of n-3 polyunsaturated fatty acids in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial
    A simple and safe treatment with n-3 PUFA can provide a small beneficial advantage in terms of mortality and admission to hospital for cardiovascular reasons in patients with heart failure in a context of usual care.[Abstract]
  8. Moertl D, Hammer A, Steiner S, Hutuleac R, Vonbank K, Berger R. Am Heart J. 2011 May;161(5):915.e1-9. Dose-dependent effects of omega-3-polyunsaturated fatty acids on systolic left ventricular function, endothelial function, and markers of inflammation in chronic heart failure of nonischemic origin: a double-blind, placebo-controlled, 3-arm study
    Treatment with n3-PUFA for 3 months exerts a dose-dependent increase of LVEF in patients with CHF. In parallel, a significant improvement of endothelial function and decrease of interleukin 6 is found with high-dose n3-PUFA intervention.[Abstract]
  9. Ghio S, Scelsi L, Latini R, Masson S, Eleuteri E, Palvarini M, Vriz O, Pasotti M, Gorini M, Marchioli R, Maggioni A, Tavazzi L; Eur J Heart Fail. 2010 Dec;12(12):1345-53 Effects of n-3 polyunsaturated fatty acids and of rosuvastatin on left ventricular function in chronic heart failure: a substudy of GISSI-HF trial
    n-3 PUFA can provide a small but statistically significant advantage in terms of LV function in patients with symptomatic HF of any aetiology, already treated with recommended therapies.[Abstract]
  10. Nodari S, Triggiani M, Campia U, Manerba A, Milesi G, Cesana BM, Gheorghiade M, Dei Cas L. J Am Coll Cardiol. 2011 Feb 15;57(7):870-9. Effects of n-3 polyunsaturated fatty acids on left ventricular function and functional capacity in patients with dilated cardiomyopathy
    In patients with NICM and minimal symptoms in response to evidence-based medical therapy, n-3 PUFAs treatment increases LV systolic function and functional capacity and may reduce hospitalizations for HF. Given these promising results, larger studies are in order to confirm our findings.[Abstract]
  11. Mehra MR, Lavie CJ, Ventura HO, Milani RV. J Heart Lung Transplant. 2006 Jul;25(7):834-8 Fish oils produce anti-inflammatory effects and improve body weight in severe heart failure
    Fish oils decrease TNF-alpha production in heart failure and improve body weight. Fish oil therapy may represent a novel therapeutic approach in late-stage heart failure characterized by cardiac cachexia.[Abstract]
  12. Witte KK, Clark AL. Eur J Cardiovasc Prev Rehabil. 2004 Aug;11(4):267-74. Fish oils–adjuvant therapy in chronic heart failure?
    Despite advances in medical management and device therapy, chronic heart failure (CHF) remains a condition of high mortality and poor quality of life. Many of the effects of PUFAs could be of benefit in CHF patients. They can improve endothelial function, reduce vascular tone, reduce platelet aggregability, improve myocardial relaxation, stabilize myocardial cells by prolonging the refractory period, and lead to increased appetite and weight gain. They also have potentially important immune-modulating effects, reducing cytokine production and release and altering prostaglandin metabolism.[Abstract]
  13. Marchioli R, Silletta MG, Levantesi G, Pioggiarella R. Curr Atheroscler Rep. 2009 Nov;11(6):440-7. Omega-3 fatty acids and heart failure
    During the past three decades, the protective role of omega (n)-3 polyunsaturated fatty acids (PUFA), mainly eicosapentaenoic acid and docosahexaenoic acid, in patients with coronary heart disease has been widely reported. The Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico-Heart Failure (GISSI-HF) study, a large-scale clinical trial, recently showed that n-3 PUFA (850-882 mg/d) reduced mortality and admission to the hospital for cardiovascular reasons in patients with chronic heart failure (HF) who were already receiving recommended therapies. [Abstract]
  14. ARRHYTHMIAS
  15. Singer P, Wirth M. Prostaglandins Leukot Essent Fatty Acids. 2004 Sep;71(3):153-9. Can n-3 PUFA reduce cardiac arrhythmias? Results of a clinical trial
    The data indicate an antiarrhythmic action of n-3 PUFA under conditions of clinical practice which might help to explain the reduced incidence of fatal myocardial infarction and sudden cardiac death in cohorts on a fish-rich diet or supplemented with n-3 PUFA. [Abstract]
  16. Virtanen JK, Mursu J, Voutilainen S, Tuomainen TP. Circulation. 2009 Dec 8;120(23):2315-21 Serum long-chain n-3 polyunsaturated fatty acids and risk of hospital diagnosis of atrial fibrillation in men
    An increased concentration of long-chain n-3 PUFAs in serum, a marker of fish or fish oil consumption, may protect against AF. Serum docosahexaenoic acid concentration had the greatest impact.[Article]
  17. Kumar S, Sutherland F, Rosso R, Teh AW, Lee G, Heck PM, Feldman A, Medi C, Watt S, Garg ML, Sparks PB. Heart Rhythm. 2011 Apr;8(4):562-8 Effects of chronic omega-3 polyunsaturated fatty acid supplementation on human atrial electrophysiology
    Chronic fish oil supplementation in humans prolongs atrial refractoriness and reduces vulnerability to inducible AF. These EP changes may explain the antifibrillatory effect of chronic fish oil ingestion.[Abstract]
  18. Nodari S, Metra M, Milesi G, Manerba A, Cesana BM, Gheorghiade M, Dei Cas L. Cardiovasc Drugs Ther. 2009 Feb;23(1):5-15. The role of n-3 PUFAs in preventing the arrhythmic risk in patients with idiopathic dilated cardiomyopathy
    N-3 PUFAs administration is associated with favorable effects on parameters related to arrhythmic risk in patients with idiopathic dilated cardiomyopathy. These results are consistent with antiarrhythmic activity independent from their antiischemic effects.[Abstract]
  19. Finzi AA, Latini R, Barlera S, Rossi MG, Ruggeri A, Mezzani A, Favero C, Franzosi MG, Serra D, Lucci D, Bianchini F, Bernasconi R, Maggioni AP, Nicolosi G, Porcu M, Tognoni G, Tavazzi L, Marchioli R. Am Heart J. 2011 Feb;161(2):338-343.e1 Effects of n-3 polyunsaturated fatty acids on malignant ventricular arrhythmias in patients with chronic heart failure and implantable cardioverter-defibrillators: A substudy of the Gruppo Italiano per lo Studio della Sopravvivenza nell’Insufficienza Cardiaca (GISSI-HF) trial
    The results of this study, though not statistically significant, support prior evidences of an antiarrhythmic effect of n-3PUFA in patients with ICD, although they leave open the issue of whether this effect leads to a survival benefit.[Abstract]
  20. Kumar S, Sutherland F, Wheeler M, Heck PM, Lee G, Teh AW, Garg ML, Morgan JG, Sparks PB. Heart Rhythm. 2011 May;8(5):643-9. Effects of chronic omega-3 polyunsaturated fatty acid supplementation on human atrial mechanical function after reversion of atrial arrhythmias to sinus rhythm: reversal of tachycardia-mediated atrial cardiomyopathy with fish oils
    Chronic fish oil ingestion in humans attenuates atrial mechanical stunning after reversion of atrial arrhythmias to sinus rhythm. This suggests that fish oils may target or even reverse underlying cellular and/or structural remodeling that occurs in response to persistent atrial arrhythmias.[Abstract]
  21. Heidt MC, Vician M, Stracke SK, Stadlbauer T, Grebe MT, Boening A, Vogt PR, Erdogan A. Thorac Cardiovasc Surg. 2009 Aug;57(5):276-80 Beneficial effects of intravenously administered N-3 fatty acids for the prevention of atrial fibrillation after coronary artery bypass surgery: a prospective randomized study
    Perioperative intravenous infusion of PUFA reduces the incidence of AF after CABG and leads to a shorter stay in the ICU and in hospital. Our data suggest that perioperative intravenous infusion of PUFA should be recommended for patients undergoing CABG.[Abstract]

  22. .[Abstract]

Selenium

    SELENIUM TEKORTEN
  1. Jackson MJ, Dillon SA, Broome CS, McArdle A, Hart CA, McArdle F. Proc Nutr Soc. 2004 Nov;63(4):513-7. Are there functional consequences of a reduction in selenium intake in UK subjects?
    Dietary Se levels in the UK have fallen over the last 20 years and recent surveys indicate that average Se intakes are 30-40 microg/d, which is well below the current UK reference nutrient intake for adult men (75 microg/d) or women (60 microg/d). [Abstract]
  2. Shortt CT, Duthie GG, Robertson JD, Morrice PC, Nicol F, Arthur JR. Eur J Clin Nutr. 1997 Jun;51(6):400-4. Selenium status of a group of Scottish adults
    The results of the present study suggest that selenium status of certain Scottish individuals may be compromised and that further studies are warranted.[Abstract]
  3. Rayman MP Lancet. 2000 Jul 15;356(9225):233-41. The importance of selenium to human health
    The essential trace mineral, selenium, is of fundamental importance to human health. As a constituent of selenoproteins, selenium has structural and enzymic roles, in the latter context being best-known as an antioxidant and catalyst for the production of active thyroid hormone. Selenium is needed for the proper functioning of the immune system, and appears to be a key nutrient in counteracting the development of virulence and inhibiting HIV progression to AIDS. It is required for sperm motility and may reduce the risk of miscarriage. Deficiency has been linked to adverse mood states. Findings have been equivocal in linking selenium to cardiovascular disease risk although other conditions involving oxidative stress and inflammation have shown benefits of a higher selenium status. An elevated selenium intake may be associated with reduced cancer risk. Large clinical trials are now planned to confirm or refute this hypothesis. In the context of these health effects, low or diminishing selenium status in some parts of the world, notably in some European countries, is giving cause for concern.[Abstract]
  4. Broadley MR, White PJ, Bryson RJ, Meacham MC, Bowen HC, Johnson SE, Hawkesford MJ, McGrath SP, Zhao FJ, Breward N, Harriman M,Tucker M. Proc Nutr Soc. 2006 May;65(2):169-81. Biofortification of UK food crops with selenium
    Se is an essential element for animals. In man low dietary Se intakes are associated with health disorders including oxidative stress-related conditions, reduced fertility and immune functions and an increased risk of cancers. Although the reference nutrient intakes for adult females and males in the UK are 60 and 75 microg Se/d respectively, dietary Se intakes in the UK have declined from >60 microg Se/d in the 1970s to 35 microg Se/d in the 1990s, with a concomitant decline in human Se status. An immediate solution to low dietary Se intake and status is to enrich UK-grown food crops using Se fertilisers (agronomic biofortification). Such a strategy has been adopted with success in Finland. It may also be possible to enrich food crops in the longer term by selecting or breeding crop varieties with enhanced Se-accumulation characteristics (genetic biofortification). The present paper will review the potential for biofortification of UK food crops with Se. [Abstract]
  5. SELENIUM EN HART EN VAATZIEKTEN
  6. Neve J. Pathol Biol (Paris). 1989 Dec;37(10):1102-6. Selenium and cardiovascular pathology
    Selenium deficiency has established implications in cardiovascular diseases, particularly on cardiac muscle integrity. [Abstract]
  7. Huttunen JK. Biomed Environ Sci. 1997 Sep;10(2-3):220-6 Selenium and cardiovascular diseases–an update
    Dietary deficiency of selenium has been incriminated in the etiology of cardiovascular diseases. Thus, cardiomyopathy associated with low selenium intake has been described in areas of exceptionally low selenium intake and in patients receiving total parenteral nutrition. Epidemiological studies have provided some evidence for the role of selenium deficiency in the etiology of atherosclerotic disease. [Abstract]
  8. Bogye G, Fehér J, Georg A, Antti A Orv Hetil. 1994 Jan 16;135(3):115-8. Relationship between selenium deficiency and high mortality and morbidity of cardiovascular diseases
    The authors consider the role of selenium deficiency to be of the utmost importance in the deteriorating health status of the Hungarian population. The pathophysiological processes occurring in selenium deficiency and possibly leading to cardio- and cerebrovascular diseases are discussed in detail. The results of human studies investigating the relationship between vascular diseases and selenium deficiency are summarized. It is concluded that selenium deficiency together with other harmful (prooxidant) effects may be responsible for the poor health status of the Hungarian population and therefore the importance of long term selenium supplementation in the prevention of such diseases is stressed.[Abstract]
  9. SELENIUM TEKORTEN EN CARDIOMYOPATHIE / HARTFALEN
  10. de Lorgeril M, Salen P. Heart Fail Rev. 2006 Mar;11(1):13-7. Selenium and antioxidant defenses as major mediators in the development of chronic heart failure
    Increased oxidative stress is involved in the pathogenesis of chronic heart failure (CHF), the common end result of most cardiac diseases. Selenium is an “essential” trace element, which means that it must be supplied by our daily diet and that its blood and tissue concentrations are extremely low. The best known of these are the antioxidant glutathione peroxidase (GPx) enzymes, which remove hydrogen peroxide and the harmful lipid hydroperoxides generated in vivo by oxygen-derived species. GPx deficiency exacerbates endothelial dysfunction, a major contributing factor in the severity of CHF symptoms, in various conditions such as hyperhomocysteinemia.[Abstract]
  11. Alsafwah S, Laguardia SP, Arroyo M, Dockery BK, Bhattacharya SK, Ahokas RA, Newman KP. Clin Med Res. 2007 Dec;5(4):238-43 Congestive heart failure is a systemic illness: a role for minerals and micronutrients
    Aberrations in minerals and micronutrient homeostasis that includes Ca(2+), Mg(2+), vitamin D, zinc and selenium appear to be an integral component of pathophysiologic expressions of CHF that contributes to its systemic and progressive nature.[Article]
  12. Burke MP, Opeskin K. Med Sci Law. 2002 Jan;42(1):10-3. Fulminant heart failure due to selenium deficiency cardiomyopathy (Keshan disease)
    Selenium deficiency is a rare cause of cardiomyopathy that may be encountered by the forensic pathologist. Selenium deficiency is associated with a cardiomyopathy, myopathy and osteoarthropathy.[Abstract]
  13. Witte KK, Clark AL, Cleland JG. J Am Coll Cardiol. 2001 Jun 1;37(7):1765-74. Chronic heart failure and micronutrients
    Selective deficiency of selenium, calcium and thiamine can directly lead to the HF syndrome. [Article]
  14. Oster O, Prellwitz W, Kasper W, Meinertz T. Clin Chim Acta. 1983 Feb 28;128(1):125-32. Congestive cardiomyopathy and the selenium content of serum
    A deficiency of selenium is suspected to be involved in the pathogenesis of congestive cardiomyopathy. A positive correlation was found between serum selenium content and the left ventricular ejection fraction. Our results suggest that a deficiency of selenium may be present in a number of patients with congestive cardiomyopathy.[Abstract]
  15. BEHANDELING MET EXTRA SELENIUM
  16. Witte KK, Nikitin NP, Parker AC, von Haehling S, Volk HD, Anker SD, Clark AL, Cleland JG. Eur Heart J. 2005 Nov;26(21):2238-44. The effect of micronutrient supplementation on quality-of-life and left ventricular function in elderly patients with chronic heart failure
    Thirty CHF patients [age 75.4 (0.7), mean (SEM), LV ejection fraction (LVEF) < or =35%] were randomized to receive capsules containing a combination of high-dose micronutrients (calcium, magnesium, zinc, copper, selenium, vitamin A, thiamine, riboflavin, vitamin B(6), folate, vitamin B(12), vitamin C, vitamin E, vitamin D, and Coenzyme Q10) or placebo for 9 months in a double-blind fashion. Long-term multiple micronutrient supplementation can improve LV volumes and LVEF and QoL scores in elderly patients with heart failure due to LV systolic dysfunction.[Article ]
  17. VEILIGHEID
  18. Whanger P, Vendeland S, Park YC, Xia Y. Ann Clin Lab Sci. 1996 Mar-Apr;26(2):99-113. Metabolism of subtoxic levels of selenium in animals and humans
    Low adverse effect level of dietary (mean LOAEL) selenium was calculated to be about 1540 +/- 653 micrograms per day (or 28 micrograms/kg body weight) and the maximum safe dietary (mean NOAEL) selenium was calculated to be 819 +/- 126 micrograms per day (or 15 micrograms/kg body weight).[Abstract]
  19. Reid ME, Stratton MS, Lillico AJ, Fakih M, Natarajan R, Clark LC, Marshall JR. J Trace Elem Med Biol. 2004;18(1):69-74. A report of high-dose selenium supplementation: response and toxicities
    Concerns about the toxicity of selenium has limited the doses used in chemoprevention. Based on previous studies, intakes of 400 microg/day and plasma selenium of 1000 ng/ml (Dietary Reference Intakes, Academy Press, New York, 2000, p. 384) were established as the no observed adverse effect level (NOAEL). his investigation summarizes the plasma response and toxicity reports from 24 men with biopsy-proven prostate cancer who were randomized to either 1600 or 3200 microg/day of selenized yeast as part of a controlled clinical trial testing selenium as a chemopreventive agent for prostate cancer progression. We observed no obvious selenium-related serious toxicities. As selenium is used in more chemoprevention and therapeutic settings, additional information on selenium species, sequestration of selenium in specific organs, excretion, and toxicities is needed.[Abstract]
  20. Schrauzer GN. J Am Coll Nutr. 2001 Feb;20(1):1-4. Nutritional selenium supplements: product types, quality, and safety
    Current evidence favors selenomethionine over the other forms of selenium. Extradietary supplementation of selenium at the dosage of 200 micrograms per day is generally considered safe and adequate for an adult of average weight subsisting on the typical American diet.[Article]

  21. .[Abstract]

Vitamine C

    ENDOTHEEL DYSFUNCTIE BIJ CARDIOMYOPATHIE EN HARTFALEN
  1. From Wikipedia, the free encyclopedia Endothelial dysfunction
    Endothelial dysfunction is a systemic pathological state of the endothelium (the inner lining of blood vessels) and can be broadly defined as an imbalance between vasodilating and vasoconstricting substances produced by (or acting on) the endothelium.[1] Normal functions of endothelial cells include mediation ofcoagulation, platelet adhesion, immune function and control of volume and electrolyte content of the intravascular and extravascular spaces. [Article]
  2. From Wikipedia, the free encyclopedia Endothelium
    The endothelium is the thin layer of cells that lines the interior surface of blood vessels,[1] forming an interface between circulating blood in the lumen and the rest of the vessel wall. These cells are calledendothelial cells. Endothelial cells line the entire circulatory system, from the heart to the smallest capillary. These cells reduce turbulence of the flow of blood, allowing the fluid to be pumped farther.[Article]
  3. Roura S, Bayes-Genis A. Nat Rev Cardiol. 2009 Sep;6(9):590-8.  Vascular dysfunction in idiopathic dilated cardiomyopathy
    However, cardiac endothelial dysfunction has also been shown to be associated with progression and poor prognosis of IDCM. [Abstract]
  4. Farhangkhoee H, Khan ZA, Kaur H, Xin X, Chen S, Chakrabarti S. Pharmacol Ther. 2006 Aug;111(2):384-99. Vascular endothelial dysfunction in diabetic cardiomyopathy: pathogenesis and potential treatment targets
    Pathogenesis of diabeticcardiomyopathy involves vascular endothelial cell dysfunction, as well as myocyte necrosis.[Abstract]
  5. Rössig L, Haendeler J, Mallat Z, Hugel B, Freyssinet JM, Tedgui A, Dimmeler S, Zeiher AM. J Am Coll Cardiol. 2000 Dec;36(7):2081-9. Congestive heart failure induces endothelial cell apoptosis: protective role of carvedilol
    Congestive heart failure is associated with impaired endothelial function in the peripheral systemic vasculature and with systemic release of inflammatory cytokines. Pro-inflammatory cytokines have been shown to induce endothelial cell apoptosis in vitro. Therefore, we hypothesized that CHF is associated with enhanced apoptosis of endothelial cells. These findings indicate that endothelial cell apoptosis may play a role in the pathophysiology of heart failure. Inhibition of endothelial cell apoptosis by carvedilol may contribute to the beneficial effects of carvedilol in patients with heart failure.[Article]
  6. Rössig L, Hoffmann J, Hugel B, Mallat Z, Haase A, Freyssinet JM, Tedgui A, Aicher A, Zeiher AM, Dimmeler S. Circulation. 2001 Oct 30;104(18):2182-7. Vitamin C inhibits endothelial cell apoptosis in congestive heart failure
    Administration of vitamin C to CHF patients suppresses EC apoptosis in vivo, which might contribute to the established functional benefit of vitamin C supplementation on endothelial function.[Article]
  7. Ellis GR, Anderson RA, Chirkov YY, Morris-Thurgood J, Jackson SK, Lewis MJ, Horowitz JD, Frenneaux MP. J Cardiovasc Pharmacol. 2001 May;37(5):564-70. Acute effects of vitamin C on platelet responsiveness to nitric oxide donors and endothelial function in patients with chronic heart failure
    In patients with CHF acute intravenous administration of vitamin C enhances platelet responsiveness to the anti-aggregatory effects of NO donors and improves endothelial function, suggesting a potential role for vitamin C as a therapeutic agent in CHF.[Abstract]
  8. Richartz BM, Werner GS, Ferrari M, Figulla HR. Am J Cardiol. 2001 Nov 1;88(9):1001-5. Reversibility of coronary endothelial vasomotor dysfunction in idiopathic dilated cardiomyopathy: acute effects of vitamin C
    Thus, patients with idiopathic dilated cardiomyopathy had endothelial dysfunction, and administration of vitamin C reversed endothelium-dependent dysfunction.[Abstract]
  9. Ellis GR, Anderson RA, Chirkov YY, Morris-Thurgood J, Jackson SK, Lewis MJ, Horowitz JD, Frenneaux MP. J Cardiovasc Pharmacol. 2001 May;37(5):564-70. Acute effects of vitamin C on platelet responsiveness to nitric oxide donors and endothelial function in patients with chronic heart failure
    Chronic heart failure (CHF) is characterized by a prothrombotic state, which may relate to increased platelet aggregability, endothelial dysfunction, and increased oxidative stress. In patients with CHF acute intravenous administration of vitamin C enhances platelet responsiveness to the anti-aggregatory effects of NO donors and improves endothelial function, suggesting a potential role for vitamin C as a therapeutic agent in CHF.[Abstract]
  10. ATRIUMFIBRILLEREN
  11. Akoum N, Hamdan MH. Curr Heart Fail Rep. 2007 Jun;4(2):78-83. Atrial fibrillation and congestive heart failure: a two-way street
    Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia encountered in clinical cardiology, particularly in patients with heart failure. Its prevalence increases with the degree of left ventricular dysfunction and severity of heart failure symptoms. The development of AF in the setting of heart failure has been shown to result in increased mortality.[Abstract]
  12. Lubitz SA, Benjamin EJ, Ellinor PT. Heart Fail Clin. 2010 Apr;6(2):187-200. Atrial fibrillation in congestive heart failure
    Atrial fibrillation and congestive heart failure are morbid conditions that have common risk factors and frequently coexist. Each condition predisposes to the other, and the concomitant presence of the two identifies individuals at increased risk for mortality.[Article]
  13. Rodrigo R, Vinay J, Castillo R, Cereceda M, Asenjo R, Zamorano J, Araya J, Castillo-Koch R, Espinoza J, Larraín E. Int J Cardiol. 2010 Feb 4;138(3):221-8. Epub 2009 May 15. Use of vitamins C and E as a prophylactic therapy to prevent postoperative atrial fibrillation
    Oxidative stress has been strongly involved in the underlying mechanism of atrial fibrillation, particularly in the arrhythmia occurring in patients undergoing cardiac surgery with extracorporeal circulation (postoperative atrial fibrillation). The clinical and experimental evidence supporting the view that the pharmacological use of antioxidant vitamins could contribute to prevent postoperative atrial fibrillation is presented.[Abstract]
  14. Korantzopoulos P, Kolettis TM, Kountouris E, Dimitroula V, Karanikis P, Pappa E, Siogas K, Goudevenos JA. Int J Cardiol. 2005 Jul 10;102(2):321-6. Oral vitamin C administration reduces early recurrence rates after electrical cardioversion of persistent atrial fibrillation and attenuates associated inflammation
    These findings suggest that vitamin C reduces the early recurrence rates after cardioversion of persistent AF and attenuates the associated low-level inflammation. These effects indicate that therapeutic approaches targeting at inflammation and oxidative stress may exert favourable effects on atrial electrical remodeling.[Abstract]
  15. Eslami M, Badkoubeh RS, Mousavi M, Radmehr H, Salehi M, Tavakoli N, Avadi MR. Tex Heart Inst J. 2007;34(3):268-74. Oral ascorbic acid in combination with beta-blockers is more effective than beta-blockers alone in the prevention of atrial fibrillation after coronary artery bypass grafting
    We conclude that ascorbic acid is effective, in addition to being well-tolerated and relatively safe. Therefore, it can be prescribed as an adjunct to beta-blockers for the prophylaxis of post-bypass atrial fibrillation.[Article]
  16. NITRAAT INTOLLERANTIE
  17. Wikipedia Angina pectoris
    Angina pectoris is een drukkend, respectievelijk zwaar gevoel en/of pijn midden op de borst (angineuze pijn) dat ontstaat als dehartspier niet voldoende bloed toegevoerd krijgt om het hart zijn werk te laten doen. Meestal wordt dit veroorzaakt door vernauwing van dekransslagaders, vaak in combinatie met lichamelijke inspanning of emotie waardoor het hart krachtiger gaat kloppen en dus meerzuurstof nodig heeft. Bij afnemende zuurstofbehoefte van het hart verdwijnt de angina pectoris dan weer.[Article]
  18. Wikipedia Nitroglycerin
    Angina pectoris is due to an inadequate flow of blood and oxygen to the heart. It is believed that nitroglycerin corrects the imbalance between the flow of oxygen and blood to the heart.[16] The principal action of nitroglycerin is vasodilation—widening of the blood vessels. Nitroglycerin will dilate veins more than arteries. It also lowers the pressure in the arteries against which the heart must pump.[14] Dilating the veins decreases cardiac preload and leads to the following therapeutic effects during episodes of angina pectoris:[Article]
  19. Gori T, Parker JD. Circulation. 2002 Oct 29;106(18):2404-8. The puzzle of nitrate tolerance: pieces smaller than we thought?
    Nitroglycerin (GTN) and other organic nitrates are important drugs commonly used in cardiovascular medicine, and, more recently, in obstetrics as tocolytic agents.1The development of tolerance, ie, the reduction in effect or the requirement for higher doses that appears after continuous use,2 is a major factor limiting the efficacy of these drugs. Despite their clinical importance in the therapy of ischemic heart disease and heart failure, many aspects of the pharmacology of organic nitrates, including the mechanism(s) of tolerance, remain unclear.[Article]
  20. Watanabe H, Kakihana M, Ohtsuka S, Sugishita Y. Circulation. 1998 Mar 10;97(9):886-91 Randomized, double-blind, placebo-controlled study of ascorbate on the preventive effect of nitrate tolerance in patients with congestive heart failure
    These findings indicate that ascorbate, an antioxidant, may prevent the development of nitrate tolerance during continuous nitrate therapy in patients with congestive heart failure.[Article]
  21. VEILIGHEID
  22. Bendich A, Langseth L. J Am Coll Nutr. 1995 Apr;14(2):124-36. The health effects of vitamin C supplementation: a review
    A comprehensive review of the literature indicates that populations with long-term consumption of higher than RDA levels of vitamin C (> or = 60 mg/day) from foods and/or supplements have reduced risks of cancer at several sites, cardiovascular disease, and cataracts.The safety of higher than RDA intakes of vitamin C is confirmed in eight placebo-controlled, double-blind studies and six non-placebo clinical trials in which up to 10,000 mg of vitamin C was consumed daily for up to 3 years. There are no clinical data which suggest that vitamin C’s enhancement of non-heme iron absorption in individuals with low iron status could be a critical factor in the possible increased risk of heterozygous hemochromatosis-related cardiovascular disease. In fact, the cumulative data do not confirm that iron status is related to risk of cardiovascular disease. Moreover, higher than RDA intakes of vitamin C have been associated with several indices of lowered cardiovascular disease risk including increases in HDL, and decreases in LDL oxidation, blood pressure and cardiovascular mortality.[Abstract]
  23. Voedingscentrum – vitamine c aanbevolen dagelijkse hoeveelheid
    22-50 jaar 70mg [Article]
  24. Weber P, Bendich A, Schalch W. Int J Vitam Nutr Res. 1996;66(1):19-30 Vitamin C and human health–a review of recent data relevant to human requirements
    The recent scientific literature indicates that beyond merely protecting against scurvy vitamin C contributes to many aspects of human health. The main areas of research reviewed include: 1. Vitamin C requirements of smokers. The data indicate that the vitamin C requirement of smokers is higher by at least 60 mg per day (up to 140 mg per day) than that of nonsmokers. 2. Important functions of the body, such as immune response, pulmonary function, and iron absorption are related to vitamin C intakes. Daily vitamin C intake of at least 150-200 mg per day enhance these functions. 3. Vitamin C may play critical roles in the prevention of CHD, cancer and cataract. Based on the available data, vitamin C intakes of at least 80-120 mg per day are associated with lowering the risk of these chronic diseases. 4. The literature documents that these and much higher intake levels of vitamin C are safe.[Abstract]
  25. Carr AC, Frei B. Am J Clin Nutr. 1999 Jun;69(6):1086-107. Toward a new recommended dietary allowance for vitamin C based on antioxidant and health effects in humans
    The totality of the reviewed data suggests that an intake of 90-100 mg vitamin C/d is required for optimum reduction of chronic disease risk in nonsmoking men and women. This amount is about twice the amount on which the current RDA for vitamin C is based, suggesting a new RDA of 120 mg vitamin C/d.[Article]
  26. Jacob RA, Sotoudeh G. Nutr Clin Care. 2002 Mar-Apr;5(2):66-74. Vitamin C function and status in chronic disease
    High intakes of the vitamin are generally well tolerated; a Tolerable Upper Level was recently set at 2 g based on gastrointestinal upset that sometimes accompanies excessive intakes.[Abstract]
  27. Bendich A, Cohen M. Toxicol Lett. 1990 Apr;51(2):189-201. Ascorbic acid safety: analysis of factors affecting iron absorption
    Ascorbic acid did not increase the incidence of ‘high’ iron absorbers (greater than 2 SD from population mean) above control levels; limited data for ascorbic acid doses greater than 100 mg/d indicated no change in the distribution of iron absorption values.[Abstract]

  28. .[Abstract]

Alfa Liponzuur


  1. .[Abstract]

  2. .[Abstract]

  3. .[Abstract]

Vitamine D3

    Vitamine D is belangrijk voor het immuunsysteem

  1. Beard JA, Bearden A, Striker R. J Clin Virol. 2011 Mar;50(3):194-200. Vitamin D and the anti-viral state
    Vitamin D has long been recognized as essential to the skeletal system. Newer evidence suggests that it also plays a major role regulating the immune system, perhaps including immune responses to viral infection. Interventional and observational epidemiological studies provide evidence that vitamin D deficiency may confer increased risk of influenza and respiratory tract infection. Vitamin D deficiency is also prevalent among patients with HIV infection.[Abstract]
  2. Bikle DD. Exp Dermatol. 2011 Jan;20(1):7-13. Vitamin D: an ancient hormone
    Vitamin D has been produced by plants and animals almost from the time life began. The ability to transport and metabolize vitamin D to more active forms evolved as the structures of plants and animals became more complex, and the cells within these organisms took on more specialized functions. In higher-order animals, the vitamin D receptor (VDR) is found in nearly every cell, and the ability of the cell to produce the active hormone, 1,25(OH)2D, is also widely distributed. Furthermore, the physiological functions with which vitamin D signalling is now associated are as diverse as the tissues in which the VDR is located. Why is this, and is there a common theme? This viewpoint article argues that there is. All cells maintain a fairly constant and submicromolar concentration of free calcium. Calcium is an important regulator of many processes within the cell. The ebb and flow of calcium within cells is controlled by calcium pumps, antiporters and channels. Animals with calcified exo- or endoskeletons have an additional need for calcium, a need that changes during the life cycle of the organism. In this article, I make the case that vitamin D signalling evolved to enable the organism to effectively regulate calcium flux, storage and signalling and that such regulation is critical for the evolutionary process.[Article]
  3. Schwalfenberg GK. Mol Nutr Food Res. 2011 Jan;55(1):96-108. doi: 10.1002/mnfr.201000174. A review of the critical role of vitamin D in the functioning of the immune system and the clinical implications of vitamin D deficiency
    This review looks at the critical role of vitamin D in improving barrier function, production of antimicrobial peptides including cathelicidin and some defensins, and immune modulation. The function of vitamin D in the innate immune system and in the epithelial cells of the oral cavity, lung, gastrointestinal system, genito-urinary system, skin and surface of the eye is discussed. [Article]
  4. Ginde AA, Mansbach JM, Camargo CA Jr. Curr Allergy Asthma Rep. 2009 Jan;9(1):81-7. Vitamin D, respiratory infections, and asthma
    Over the past decade, interest has grown in the role of vitamin D in many nonskeletal medical conditions, including respiratory infection. Emerging evidence indicates that vitamin D-mediated innate immunity, particularly through enhanced expression of the human cathelicidin antimicrobial peptide (hCAP-18), is important in host defenses against respiratory tract pathogens. Observational studies suggest that vitamin D deficiency increases risk of respiratory infections. [Abstract]
  5. Oduwole AO, Renner JK, Disu E, Ibitoye E, Emokpae E. West Afr J Med. 2010 Nov-Dec;29(6):373-8 Relationship between Vitamin D Levels and Outcome of Pneumonia in Children
    The study showed that Vitamin D insufficiency, and not solely its deficiency, may have an important role to play in the immune and haemopoetic system. It may therefore affect the response of a child to infections especially pneumonia.[Abstract]
  6. Leow L, Simpson T, Cursons R, Karalus N, Hancox RJ. Respirology. 2011 May;16(4):611-6. doi: 10.1111/j.1440-1843.2011.01924.x Vitamin D, innate immunity and outcomes in community acquired pneumonia
    25-hydroxyvitamin D deficiency is associated with increased mortality in patients admitted to hospital with community acquired pneumonia during winter.[Abstract]
  7. Gilbert CR, Arum SM, Smith CM. Can Respir J. 2009 May-Jun;16(3):75-80. Vitamin D deficiency and chronic lung disease
    Vitamin D deficiency is increasingly being recognized as a prevalent problem in the general population. Patients with chronic lung diseases such as asthma, cystic fibrosis, chronic obstructive lung disease and interstitial pneumonia appear to be at increased risk for vitamin D deficiency for reasons that are not clear.[Article]
  8. Walker VP, Modlin RL. Pediatr Res. 2009 May;65(5 Pt 2):106R-113R. The vitamin D connection to pediatric infections and immune function
    This knowledge is particularly relevant and timely, because infants and children seem more susceptible to viral rather than bacterial infections in the face of vitamin D deficiency. The connection among vitamin D, infections, and immune function in the pediatric population indicates a possible role for vitamin D supplementation in potential interventions and adjuvant therapies.[Article]
  9. Vitamine D tekorten bij cardiomyopathie en hartfalen

  10. Gezondheidsraad:’Naar een toerijkende inname van vitamine D’;Samenvatting, 30 september 2008
    Naar een toereikende inname van vitamine D. Een onvoldoende vitamine D-status komt onder alle lagen van de Nederlandse bevolking voor. Het percentage is daarbij hoger aan het einde van de winter dan aan het einde van de zomer (tabel 1).[Article]
  11. Zittermann A, Schleithoff SS, Koerfer R. Heart Fail Rev. 2006 Mar;11(1):25-33. Vitamin D insufficiency in congestive heart failure: why and what to do about it?
    This article gives an overview of the current knowledge on vitamin D status in patients with congestive heart failure (CHF). A serum 25-hydroxyvitamin D level below 50 nmol/l (20 ng/ml) is generally regarded as insufficient. Available data indicate that the majority of CHF patients have 25-hydroxyvitamin D levels in the insufficiency range. At present, daily oral intake of 50-100 microg vitamin D seems to be the most effective way to improve vitamin D status in CHF patients.[Abstract]
  12. Pilz S, Tomaschitz A, Drechsler C, Dekker JM, März W. Mol Nutr Food Res. 2010 Aug;54(8):1103-13. Vitamin D deficiency and myocardial diseases
    Vitamin D deficiency is common among patients with myocardial diseases because sun-induced vitamin D production in the skin and dietary intake of vitamin D is often insufficient. In our opinion, the current knowledge of the beneficial effects of vitamin D on myocardial and overall health strongly argue for vitamin D supplementation in all vitamin D-deficient patients with or at high risk for myocardial diseases.[Article]
  13. Zittermann A, Schleithoff SS, Tenderich G, Berthold HK, Körfer R, Stehle P. J Am Coll Cardiol. 2003 Jan 1;41(1):105-12. Low vitamin D status: a contributing factor in the pathogenesis of congestive heart failure?
    The low vitamin D status can explain alterations in mineral metabolism as well as myocardial dysfunction in the CHF patients, and it may therefore be a contributing factor in the pathogenesis of CHF.[Abstract]
  14. Vitamine D bij de behandeling van cardiomyopathie en hartfalen

  15. Mascitelli L, Goldstein MR, Pezzetta F. Recenti Prog Med. 2010 May;101(5):202-11. Vitamin D deficiency and cardiovascular diseases
    The increasing worldwide displacement from the natural outdoor environment of human beings to an indoor sedentary lifestyle, along with the recommendation to avoid any direct sun exposure because of the risk of skin cancer, has resulted in a global pandemic of vitamin D insufficiency. Vitamin D insufficiency seems to predispose to hypertension, diabetes and the metabolic syndrome, left ventricular hypertrophy, heart failure, and chronic vascular inflammation. [Abstract]
  16. Cioffi G, Gatti D, Adami S G Ital Cardiol (Rome). 2010 Sep;11(9):645-53. Vitamin D deficiency, left ventricular dysfunction and heart failure
    Epidemiologic data indicate that about one million people worldwide suffer from and should be treated for vitamin D deficiency. Although many cardiovascular diseases such as arterial hypertension, myocardial ischemia, diabetic cardiomyopathy and heart failure, may arise from a low vitamin D status, cardiologists do not routinely search for this disease in clinical practice.[Abstract]
  17. Lee W, Kang PM. Curr Opin Investig Drugs. 2010 Mar;11(3):309-14. Vitamin D deficiency and cardiovascular disease: Is there a role for vitamin D therapy in heart failure?
    Accumulating evidence suggests that vitamin D deficiency is associated with cardiovascular disease, and that vitamin D therapy may have significant mortality and morbidity benefits in the treatment of congestive heart failure. [Abstract]
  18. Meems LM, van der Harst P, van Gilst WH, de Boer RA. Curr Drug Targets. 2011 Jan;12(1):29-41. Vitamin D biology in heart failure: molecular mechanisms and systematic review
    Vitamin D has recently been suggested as an important mediator of blood pressure and cardiovascular disease, including heart failure. The steroid hormone vitamin D regulates gene expression of many genes that play a prominent role in the progression of heart failure, such as cytokines and hormones. Specifically, vitamin D is a negative regulator of the hormone renin, the pivotal hormone of the renin-angiotensin system. [Abstract]
  19. Schleithoff SS, Zittermann A, Tenderich G, Berthold HK, Stehle P, Koerfer R. Am J Clin Nutr. 2006 Apr;83(4):754-9. Vitamin D supplementation improves cytokine profiles in patients with congestive heart failure: a double-blind, randomized, placebo-controlled trial
    Vitamin D(3) reduces the inflammatory milieu in CHF patients and might serve as a new antiinflammatory agent for the future treatment of the disease. Our data provide evidence for the involvement of an impaired vitamin D-parathyroid hormone axis in the progression of CHF.[Article]
  20. De veiligheid van vitamine D

  21. Voedingscentrum / vitamine D
    Vitamine D is nodig om calcium uit de voeding in het lichaam te kunnen opnemen en daarom belangrijk voor de groei en het handhaven van stevige botten en tanden. De belangrijkste vorm is cholecalciferol (vitamine D3).[Article]
  22. Hathcock JN, Shao A, Vieth R, Heaney R. Am J Clin Nutr. 2007 Jan;85(1):6-18. Risk assessment for vitamin D
    The objective of this review was to apply the risk assessment methodology used by the Food and Nutrition Board (FNB) to derive a revised safe Tolerable Upper Intake Level (UL) for vitamin D. New data continue to emerge regarding the health benefits of vitamin D beyond its role in bone. The intakes associated with those benefits suggest a need for levels of supplementation, food fortification, or both that are higher than current levels. A prevailing concern exists, however, regarding the potential for toxicity related to excessive vitamin D intakes. The UL established by the FNB for vitamin D (50 microg, or 2000 IU) is not based on current evidence and is viewed by many as being too restrictive, thus curtailing research, commercial development, and optimization of nutritional policy. Human clinical trial data published subsequent to the establishment of the FNB vitamin D UL published in 1997 support a significantly higher UL. We present a risk assessment based on relevant, well-designed human clinical trials of vitamin D. Collectively, the absence of toxicity in trials conducted in healthy adults that used vitamin D dose > or = 250 microg/d (10,000 IU vitamin D3) supports the confident selection of this value as the UL.[Article]
  23. Vieth R. Am J Clin Nutr. 1999 May;69(5):842-56 Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety
    Total-body sun exposure easily provides the equivalent of 250 microg (10000 IU) vitamin D/d, suggesting that this is a physiologic limit. The assembled data from many vitamin D supplementation studies reveal a curve for vitamin D dose versus serum 25-hydroxyvitamin D [25(OH)D] response that is surprisingly flat up to 250 microg (10000 IU) vitamin D/d. To ensure that serum 25(OH)D concentrations exceed 100 nmol/L, a total vitamin D supply of 100 microg (4000 IU)/d is required. Except in those with conditions causing hypersensitivity, there is no evidence of adverse effects with serum 25(OH)D concentrations <140 nmol/L, which require a total vitamin D supply of 250 µg (10000 IU)/d to attain [Article]
  24. Hathcock JN, Shao A, Vieth R, Heaney R. Am J Clin Nutr. 2007 Jan;85(1):6-18. Risk assessment for vitamin D
    The present a risk assessment based on relevant, well-designed human clinical trials of vitamin D. Collectively, the absence of toxicity in trials conducted in healthy adults that used vitamin D dose > or = 250 microg/d (10,000 IU vitamin D3) supports the confident selection of this value as the UL. [Article]
  25. Bischoff-Ferrari HA, Shao A, Dawson-Hughes B, Hathcock J, Giovannucci E, Willett WC. Osteoporos Int. 2010 Jul;21(7):1121-32 Benefit-risk assessment of vitamin D supplementation
    Our analysis suggests that mean serum 25(OH)D levels of about 75 to 110 nmol/l provide optimal benefits for all investigated endpoints without increasing health risks. These levels can be best obtained with oral doses in the range of 1,800 to 4,000 IU vitamin D per day; further work is needed, including subject and environment factors, to better define the doses that will achieve optimal blood levels in the large majority of the population.[Article]
  26. Vieth R. J Bone Miner Res. 2007 Dec;22 Suppl 2:V64-8Vitamin D toxicity, policy, and science
    However, because sunshine can provide an adult with vitamin D in an amount equivalent to daily oral consumption of 250 mug (10,000 IU)/d, this is intuitively a safe dose. The incremental consumption of 1 mug (40 IU)/day of vitamin D(3) raises serum 25(OH)D by approximately 1 nM (0.4 ng/ml). [Article]

  27. .[Abstract]

Hawthorn

    Meidoornextract bij de behandeling van cardiomyopathie en hartfalen

  1. Pittler MH, Guo R, Ernst E. Hawthorn extract for treating chronic heart failure. Cochrane Database Syst Rev. 2008 Jan 23;(1):CD005312.
    These results suggest that there is a significant benefit in symptom control and physiologic outcomes from hawthorn extract as an adjunctive treatment for chronic heart failure.[Abstract]
  2. Pittler MH, Schmidt K, Ernst E. Am J Med. 2003 Jun 1;114(8):665-74.Hawthorn extract for treating chronic heart failure: meta-analysis of randomized trials
    The aim of this meta-analysis was to assess the evidence from rigorous clinical trials of the use of hawthorn extract to treat patients with chronic heart failure. In conclusion, these results suggest that there is a significant benefit from hawthorn extract as an adjunctive treatment for chronic heart failure.[Abstract]
  3. Habs M. Prospective, comparative cohort studies and their contribution to the benefit assessments of therapeutic options: heart failure treatment with and without Hawthorn special extract WS 1442. Forsch Komplementarmed Klass Naturheilkd. 2004 Aug;11 Suppl 1:36-9.
    The data show a clear benefit for patients with heart failure stage NYHA II treated with WS 1442. The single or add-on administration in addition to a chemical-synthetic medication resulted in objective improvements at comparable costs.[Abstract]
  4. Tauchert M, Gildor A, Lipinski J. Herz. 1999 Oct;24(6):465-74; discussion 475. High-dose Crataegus extract WS 1442 in the treatment of NYHA stage II heart failure
    The efficacy and tolerance of the standardized hawthorn (crataegus) extract WS 1442 were tested in a multicenter utilization observational study. We monitored 1,011 patients with cardiac insufficiency stage NYHA II, treated with this extract (Crataegutt novo 450, 1 tablet b.i.d.) over a period of 24 weeks. Almost 2/3 of the patients felt better or much better following the 24 weeks of treatment. More than 3/4 of the participating physicians noted a good or a very good efficacy, and 98.7% noted a good or a very good tolerance. High-dose hawthorn therapy is an efficient, well-tolerated and easily regulated therapeutic alternative for patients suffering from cardiac insufficiency stage NYHA II.[Abstract]
  5. Zapfe jun G. Phytomedicine. 2001 Jul;8(4):262-6. Clinical efficacy of crataegus extract WS 1442 in congestive heart failure NYHA class II
    Recording of laboratory parameters and adverse events showed that WS 1442 was safe and well tolerated. The data show that Crataegus extract WS 1442 is clinically effective in patients with congestive heart failure corresponding to NYHA class II.[Abstract]
  6. Degenring FH, Suter A, Weber M, Saller R. Phytomedicine. 2003;10(5):363-9. A randomised double blind placebo controlled clinical trial of a standardised extract of fresh Crataegus berries (Crataegisan) in the treatment of patients with congestive heart failure NYHA II
    The significant improvement, due to the fact that dyspnoea and fatigue do not occur until a significantly higher wattage has been reached in the bicycle exercise testing allows the conclusion that the recruited NYHA II patients may expect an improvement in their heart failure condition under long term therapy with the standardised extract of fresh Crataegus berries. [Abstract]
  7. Leuchtgens H. Fortschr Med. 1993 Jul 20;111(20-21):352-4. Crataegus Special Extract WS 1442 in NYHA II heart failure. A placebo controlled randomized double-blind study
    The active substance group showed a statistically significant advantage over placebo in terms of changes in PRP (at a load of 50 W) and the score, but also in the secondary parameter heart rate. In both groups, systolic and diastolic blood pressure was mildly reduced. No adverse reactions occurred. [Abstract]
  8. De veiligheid van Meidoornextract

  9. Tauchert M. Efficacy and safety of crataegus extract WS 1442 in comparison with placebo in patients with chronic stable New York Heart Association class-III heart failure. Am Heart J. 2002 May;143(5):910-5.
    A total of 209 patients were randomized to treatment with 1800 mg of WS 1442, 900 mg of WS 1442, or with placebo. After 16 weeks of therapy with 1800 mg of WS 1442 per day, maximal tolerated workload during bicycle exercise showed a statistically significant increase in comparison with both placebo and 900 mg of WS 1442. The data from this study confirm that there is a dose-dependent effect of WS 1442 on the exercise capacity of patients with heart failure and on typical heart failure-related clinical signs and symptoms. The drug was shown to be well tolerated and safe.[Abstract]
  10. Weikl A, Assmus KD, Neukum-Schmidt A, Schmitz J, Zapfe G, Noh HS, Siegrist J. Fortschr Med. 1996 Aug 30;114(24):291-6. Crataegus Special Extract WS 1442. Assessment of objective effectiveness in patients with heart failure (NYHA II)
    All in all, the results of the present clinical investigation confirm those of previous studies showing that Crataegus-Specialextrakt WS 1442 is an effective and low-risk phytotherapeutic form of treatment in patients with NYHA II cardiac insufficiency.[Abstract]
  11. Daniele C, Mazzanti G, Pittler MH, Ernst E. Drug Saf. 2006;29(6):523-35. Adverse-event profile of Crataegus spp.: a systematic review
    A total of 7311 patients were enrolled, and data from 5,577 patients were available for analysis. The daily dose and duration of treatment with hawthorn monopreparations ranged from 160 to 1,800 mg and from 3 to 24 weeks, respectively. The extracts most used in the clinical trials were WS 1,442 (extract of hawthorn standardised to 18.75% oligomeric procyanidins) and LI 132 (extract of hawthorn standardised to 2.25% flavonoids). Overall, 166 adverse events were reported. Most of these adverse events were, in general, mild to moderate; eight severe adverse events have been reported with the LI 132 extract. The most frequent adverse events were dizziness/vertigo (n = 15), gastrointestinal complaints (n = 24), headache (n = 9), migraine (n = 8) and palpitation (n = 11). The WHO spontaneous reporting scheme received 18 case reports. In the identified trials, the most frequent adverse events were dizziness (n = 6), nausea (n = 5), fall (n = 2), gastrointestinal haemorrhage (n = 2), circulation failure (n = 2) and erythematous rash (n = 2). There were no reports of drug interactions.[Abstract]
  12. Crataegutt novo 450mg gebrauchsinformation [Article]
  13. EXTRA
  14. Rietbrock N, Hamel M, Hempel B, Mitrovic V, Schmidt T, Wolf G Arzneimittelforschung. 2001 Oct;51(10):793-8. Actions of standardized extracts of Crataegus berries on exercise tolerance and quality of life in patients with congestive heart failure
    The present study proves the efficacy and safety of a standardized extract of fresh Crataegus berries (Rob 10) in patients with congestive heart failure (NYHA II) regarding the parameters evaluated.[Abstract]
  15. Holubarsch CJ, Colucci WS, Meinertz T, Gaus W, Tendera M; Survival and Prognosis: Investigation of Crataegus Extract WS 1442 in CHF (SPICE) trial study group. Eur J Heart Fail. 2008 Dec;10(12):1255-6 The efficacy and safety of Crataegus extract WS 1442 in patients with heart failure: the SPICE trial.
    2681 patients (WS 1442: 1338; placebo: 1343) were randomised. Average time to first cardiac event was 620 days for WS 1442 and 606 days for placebo. In this study, WS 1442 had no significant effect on the primary endpoint. WS 1442 was safe to use in patients receiving optimal medication for heart failure. In addition, the data may indicate that WS 1442 can potentially reduce the incidence of sudden cardiac death, at least in patients with less compromised left ventricular function.[Article]
  16. Hwang HS, Bleske BE, Ghannam MM, Converso K, Russell MW, Hunter JC, Boluyt MO. Cardiovasc Drugs Ther. 2008 Feb;22(1):19-28. Effects of hawthorn on cardiac remodeling and left ventricular dysfunction after 1 month of pressure overload-induced cardiac hypertrophy in rats
    Hawthorn treatment modifies left ventricular remodeling and counteracts myocardial dysfunction in early pressure overload-induced cardiac hypertrophy.[Abstract]

Berberine

    HEART FAILURE
  1. Zeng XH, Zeng XJ, Li YY. Am J Cardiol. 2003 Jul 15;92(2):173-6. Efficacy and safety of berberine for congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy
    This study was designed to assess the efficacy and safety of berberine for chronic congestive heart failure (CHF). One hundred fifty-six patients with CHF and >90 ventricular premature complexes (VPCs) and/or nonsustained ventricular tachycardia (VT) on 24-hour Holter monitoring were randomly divided into 2 groups. After treatment with berberine, there was a significantly greater increase in LVEF, exercise capacity, improvement of the dyspnea-fatigue index, and a decrease of frequency and complexity of VPCs compared with the control group. There was a significant decrease in mortality in the berberine-treated patients during long-term follow-up (7 patients receiving treatment died vs 13 on placebo, p <0.02). Proarrhythmia was not observed, and there were no apparent side effects. Thus, berberine improved quality of life and decreased VPCs and mortality in patients with CHF.[Abstract]
  2. Marin-Neto JA, Maciel BC, Secches AL, Gallo Júnior L. Clin Cardiol. 1988 Apr;11(4):253-60. Cardiovascular effects of berberine in patients with severe congestive heart failure
    Berberine, an alkaloid of the protoberberine family, has been shown to have strong positive inotropic and peripheral resistance-lowering effects in dogs with and without heart failure. [Abstract]
  3. ARRYTHMIAS HUMANS
  4. Hartstichting – Hartoverslagen: geen echte ritmestoornis, maar wat dan wel?
    Soms worden de extrasystolen veroorzaakt door een hartaandoening. Heeft u veel klachten? Bespreek ze dan met uw huisarts. Hij onderzoekt of er een onderliggende oorzaak is en bepaalt of er een behandeling nodig is.[Article]
  5. Wikipedia – Ventricular tachycardia
    Ventricular tachycardia (V-tach or VT) is a tachycardia, or fast heart rhythm, that originates in one of the ventricles of the heart. This is a potentially life-threatening arrhythmia because it may lead to ventricular fibrillation, asystole, and sudden death.[Article]
  6. Lau CW, Yao XQ, Chen ZY, Ko WH, Huang Y. Cardiovasc Drug Rev. 2001 Fall;19(3):234-44. Cardiovascular actions of berberine
    Both derivatives of berberine have antiarrhythmic activity. Some cardiovascular effects of berberine and its derivatives are attributed to the blockade of K+ channels (delayed rectifier and K(ATP)) and stimulation of Na+ -Ca(2+) exchanger. Berberine has been shown to prolong the duration of ventricular action potential. Its vasodilator activity has been attributed to multiple cellular mechanisms. The cardiovascular effects of berberine suggest its possible clinical usefulness in the treatment of arrhythmias and/or heart failure.[Abstract]
  7. Huang W Zhonghua Xin Xue Guan Bing Za Zhi. 1990 Jun;18(3):155-6, 190. Ventricular tachyarrhythmias treated with berberine
    These results revealed that berberine is effective for ventricular tachyarrhythmias. There were no severe side effects, only mild gastroenterologic symptoms were observed in some patients.[Abstract]
  8. ARRYTHMIAS ANIMALS
  9. Dai DZ. Cardiovasc Drug Rev. 2006 Summer;24(2):101-15. CPU86017: a novel Class III antiarrhythmic agent with multiple actions at ion channels
    CPU86017 is a novel Class III antiarrhythmic agent derived from berberine and with an improved pharmacological profile, solubility and bioavailability. It is active in suppressing arrhythmias in several animal models. CPU86017 appears to be a promising antiarrhythmic agent with a cardioprotective action. It can be expected to protect from malignant arrhythmias and sudden cardiac death by suppressing molecular events caused by channelopathies.[Article]
  10. Wang YX, Yao XJ, Tan YH. J Cardiovasc Pharmacol. 1994 May;23(5):716-22. Effects of berberine on delayed afterdepolarizations in ventricular muscles in vitro and in vivo
    In rabbit left ventricular (LV) muscles in vivo,berberine 1 mg/kg intravenously (i.v.) decreased the amplitude of delayed afterdepolarizations evoked by ouabain and calcium gluconate from 9.6 +/- 1.9 to 6.8 +/- 0.8 mV and left stellate ganglion stimulation from 9.4 +/- 2.1 to 6.2 +/- 0.7 mV and blocked ventricular arrhythmias. [Abstract]
  11. Xu Z, Cao HY, Li Q. Zhongguo Yao Li Xue Bao. 1989 Jul;10(4):320-4. Protective effects of berberine on spontaneous ventricular fibrillation in dogs after myocardial infarction
    The results suggest that Ber may be effective in preventing the onset of reentrant ventricular tachyarrhythmias and sudden coronary death after myocardial ischemic damage.[Abstract]
  12. SAFETY
  13. Kheir MM, Wang Y, Hua L, Hu J, Li L, Lei F, Du L. Food Chem Toxicol. 2010 Apr;48(4):1105-10. Acute toxicity of berberine and its correlation with the blood concentration in mice
    However, we discovered an interesting phenomenon indicating that the absorption of BBR by oral administration has a limit, therefore, explaining the difficulty in obtaining an LD(50) of BBR.[Abstract]
  14. Yang P, Song DQ, Li YH, Kong WJ, Wang YX, Gao LM, Liu SY, Cao RQ, Jiang JD. Bioorg Med Chem Lett. 2008 Aug 15;18(16):4675-7. Synthesis and structure-activity relationships of berberine analogues as a novel class of low-density-lipoprotein receptor up-regulators
    Because of the unique mode of action and good safety record, BBR provoked our interest to do structure modification at different domains for its cholesterol-lowering activity.[Abstract]
  15. Kong WJ, Wei J, Zuo ZY, Wang YM, Song DQ, You XF, Zhao LX, Pan HN, Jiang JD Metabolism. 2008 Aug;57(8):1029-37. Combination of simvastatin with berberine improves the lipid-lowering efficacy
    Our results display the rationale, effectiveness, and safety of the combination therapy for hyperlipidemia using BBR and SIMVA. It could be a new regimen for hypercholesterolemia.[Abstract]
  16. Zhang Y, Li X, Zou D, Liu W, Yang J, Zhu N, Huo L, Wang M, Hong J, Wu P, Ren G, Ning G. J Clin Endocrinol Metab. 2008 Jul;93(7):2559-65. Treatment of type 2 diabetes and dyslipidemia with the natural plant alkaloid berberine
    Berberine is effective and safe in the treatment of type 2 diabetes and dyslipidemia.[Article]
  17. Guo Y, Li F, Ma X, Cheng X, Zhou H, Klaassen CD. Xenobiotica. 2011 Jul 25. CYP2D plays a major role in berberine metabolism in liver of mice and humans
    CYP2D plays a major role in berberine biotransformation, therefore, CYP2D6 pharmacogenetics and potential drug-drug interactions should be considered when berberine is used.[Abstract]
  18. Zhao Y, Hellum BH, Liang A, Nilsen OG. Phytother Res. 2011 Jun 16. doi: 10.1002/ptr.3554 The In Vitro Inhibition of Human CYP1A2, CYP2D6 and CYP3A4 by Tetrahydropalmatine, Neferine and Berberine
    No clinical significant metabolic interaction seems likely to occur between the CYP enzymes and herbal constituents tested, with a possible exception for the CYP2D6 inhibition by Tet and Ber.[Abstract]

MSM

  1. DMSO and MSM The Biochemical Oxygen Transport Pair Once it is understood that DMSO (& MSM) acts as a profoundly effective oxygen transport system, this opens up the opportunity to use this information to treat a multitude of medical disorders, immediate and long term that are caused by a deficiency of oxygen transport.
  2. Parcell S. Altern Med Rev. 2002 Feb;7(1):22-44. Sulfur in human nutrition and applications in medicine
    Other sulfur compounds such as SAMe, dimethylsulfoxide (DMSO), taurine, glucosamine or chondroitin sulfate, and reduced glutathione may also have clinical applications in the treatment of a number of conditions such as depression, fibromyalgia, arthritis, interstitial cystitis, athletic injuries, congestive heart failure, diabetes, cancer, and AIDS. [Article]

  3. .[Abstract]

Kinderen

    PROGNOSIS
  1. Wikipedia – Hartfalen
    Hartfalen is een chronische aandoening, en de vooruitzichten zijn op langere termijn meestal vrij slecht. Als de oorzaak niet kan worden behandeld (bijvoorbeeld door vervanging van een hartklep) is de levensverwachting statistisch gezien maar enkele jaren – slechter dan bij de meeste vormen van kanker. De behandeling met geneesmiddelen leidt tot een vermindering van klachten en een vertraging van de progressie van de ziekte, maar kan de patiënt nooit meer helemaal genezen. Wanneer bij iemand hartfalen is geconstateerd wordt er naast medicamenteuze therapie aangeraden om zo gezond mogelijk te leven door bijvoorbeeld te stoppen met roken. De dood treedt soms in door geleidelijke verslechtering van het hartfalen tot op het punt dat deze onbehandelbaar wordt, soms ook plotseling door een fatale hartritmestoornis.[Article]
  2. Schmaltz AA. Z Kardiol. 2001 Apr;90(4):263-8. Dilated cardiomyopathy in childhood
    Abstract In childhood, dilative cardiomyopathy (DCM) has a prevalence of 2.6 patients in 100,000 inhabitants. Manifestation age is, in 75%, the first two years of life. There are no specific symptoms. Diagnosis is often made, when congestive heart failure occurs. Despite intensive therapy with digitalis, diuretics and ACE inhibitors, DCM is the main indication for heart transplantation. The prognosis is critical: 11 studies with approximately 450 children showed a mean 1-year survival rate of 75% and a 5-year survival rate of 60%. In most cases etiology of DCM remains unclear (“idiopathic”). In the second position (approximately 40%) is inflammatory pathogenesis. While familiar DCM is manifested mainly during the 3rd and 4th decade, specific cardiomyopathy is often found during infancy: inborn errors of metabolism, neuromuscular diseases or malformation syndromes are the causes of a cardiomyopathy, which can appear as dilative or hypertrophic cardiomyopathy. A causal therapy exists only in a few cases.[Abstract]
  3. Bostan OM, Cil E. Acta Cardiol. 2006 Apr;61(2):169-74. Dilated cardiomyopathy in childhood: prognostic features and outcome
    The natural history of dilated cardiomyopathy in children is difficult to predict due to the heterogeneous character of the disease. The outcome in infants and children is highly variable from complete recovery to death. In conclusion, in this study, the rate of recovery and survival is higher than in previous studies. A good outcome is related to age at presentation (< or = two years old), a history of viral disease within three months of presentation and improvement in ventricular function during the first 6 months after diagnosis. Intractable heart failure has an adverse effect on the outcome.[Abstract]
  4. Gesuete V, Ragni L, Prandstraller D, Oppido G, Formigari R, Gargiulo GD, Picchio FM. Cardiol Young. 2010 Dec;20(6):680-5. Dilated cardiomyopathy presenting in childhood: aetiology, diagnostic approach, and clinical course
    In children, dilated cardiomyopathy is a diverse disorder with outcomes that depend on cause, age, and cardiac failure status at presentation. Overt cardiac failure at presentation is a major prognostic factor for death or cardiac transplantation. Older age at presentation and metabolic aetiology may be associated with a poorer prognosis.[Article]
  5. LVAD
  6. Adachi I, Fraser CD Jr. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu. 2011;14(1):38-44. Mechanical circulatory support for infants and small children
    The development of mechanical circulatory support devices for infants and small children with heart failure has significantly lagged behind the development of devices for adults. In the United States, there was really very little activity focused on the development and implementation of durable mechanical assist devices for small children until the early part of this millennium. At present, the Berlin Heart EXCOR Pediatric ventricular assist device (Berlin Heart Inc., The Woodlands, TX) is currently the only device available to provide long-term support to small children awaiting cardiac transplantation; this device is only available through either compassionate use solicitation or within the confines of an ongoing investigation device exemption trial. There are several other devices being developed at this time, but it will be years before they are tested in clinical trials. In this article, we will review the current status of mechanical circulatory support devices and therapy strategies for infants and small children presenting in acute heart failure.[Abstract]
  7. Jaquiss RD, Imamura M. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu. 2011;14(1):120-5. Implantation of a Berlin Heart ventricular assist device
    Until recently the only mode of mechanical circulatory support available in North America for use as bridge to cardiac transplantation in small children was extra-corporeal membrane oxygenation. However, since 2005 the Berlin Heart pediatric ventricular assist device has been increasingly widely used for both biventricular and left ventricular support. The device is available in a wide range of sizes, allowing its use in children as small as 5 kg and as large as 60 kg. It has been applied in end-stage heart failure of both structural/congenital and myopathic etiology (including myocarditis). In the article the technique for implantation of the device will be described, with focus on certain details that facilitate safe implantation and subsequent explantation, whether in the setting of a heart transplant operation or in the setting of recovery of native heart function.[Abstract]
  8. Amodeo A, Brancaccio G, Michielon G, Filippelli S, Ricci Z, Morelli S, Gagliardi MG, Iacobelli R, Pongiglione G, Di Donato RM. Artif Organs. 2010 Nov;34(11):1017-22. doi: 10.1111/j.1525-1594.2010.01144.x. Pneumatic pulsatile ventricular assist device as a bridge to heart transplantation in pediatric patients
    Despite the remarkable advances with the use of ventricular assist devices (VAD) in adults, pneumatic pulsatile support in children is still limited. We report on our experience in the pediatric population. A retrospective review of 17 consecutive children offered mechanical support with Berlin Heart as a bridge to heart transplant from February 2002 to April 2010 was conducted. The median patient age was 3.9 years (75 days to 13.3 years). The median patient weight was 14.1?kg (2.9-43kg). Before VAD implantation, all children were managed by multiple intravenous inotropes and mechanical ventilation (14) or extracorporeal membrane oxygenation (3). All patients had right ventricular dysfunction. Nine patients required biventricular mechanical support (BVAD), but in all other cases a single left ventricular assist device proved sufficient (47%). The median duration of VAD support was 47 days (1-168 days). The median pre-VAD pulmonary vascular resistance index (Rpi) was 5.7?WU/m(2) (3.5 to 14.4WU/m(2) ). Eleven patients (65%) were successfully bridged to heart transplantation after a median duration of mechanical support of 68 days (6-168 days). Six deaths occurred (35%), three for neurological complications, one for sepsis, and two others for device malfunctioning. Since 2007, the survival rate of our patients has increased from 43% to 80%, and the need for BVAD has decreased from 86% to 30%. In two patients with Rpi >10WU/m(2) , unresponsive to pulmonary vasodilatator therapy, Rpi dropped to 2.2 and 2WU/m(2) after 40 and 23 days of BVAD support, respectively. Seven patients (41%) required at least one pump change. Of 11 patients undergoing heart transplant, four developed an extremely elevated (>60%) panel reactive antibody by enzyme-linked immunosorbent assay, confirmed by Luminex. All of them experienced at least one acute episode of rejection in the first month after heart transplant, needing plasmapheresis. The survival rate after heart transplantation was 100% with a median follow-up of 25.4 months (6 days to 7.7 years). Mechanical support in children with end-stage heart failure is an effective strategy as a bridge to heart transplantation with a reasonable morbidity and mortality. BVAD support may offer an additional means to reverse extremely elevated pulmonary vascular resistance.[Abstract]
  9. Milanesi O, Cerutti A, Biffanti R, Salvadori S, Gambino A, Stellin G. J Cardiovasc Med (Hagerstown). 2007 Jan;8(1):67-71 Heart transplantation in pediatric age
    Heart transplantation, formerly the final option for terminally ill children, has now become the treatment of choice for a number of serious acquired or congenital cardiac conditions, which cannot be treated conservatively. Nevertheless, several problems remain unsolved. First of all the shortage of donors, mainly in the first months and years of life, which has become more and more significant with time, regardless of the country, religious belief or culture of the people. Secondly, the long-term impact of immunosuppression in a developing organism, and its possible inter-relation with the primary disorder, which leads to intractable heart failure.[Abstract]
  10. Berg A. Crit Care Nurs Q. 2002 Nov;25(3):79-87. Pediatric heart transplantation: a clinical overview
    The International Society for Heart and Lung Transplantation reports a 79% survival at 1 year. 70% survival at 2 years. and 67% at 5 years for all ages and diagnoses. This article provides an overview of pediatric heart transplantation.[Abstract]
  11. Dayton JD, Kanter KR, Vincent RN, Mahle WT.`J Heart Lung Transplant. 2006 Apr;25(4):409-15 Cost-effectiveness of pediatric heart transplantation
    The mean cost of initial hospitalization and organ procurement was $221,897 per patient for primary transplant and $285,296 per patient for re-transplant. Annual follow-up costs were estimated to be $18,141 in the first year (excluding the first 90 days post-transplant) and $18,480 per year thereafter. Under base-case assumptions, costs per QALY gained were $49,679 for primary transplantation and $87,883 for re-transplantation. Sensitivity analysis yielded a cost-utility range of $44,943 to $57,628 per QALY gained for primary transplantation and $70,834 to $103,661 per QALY gained for re-transplantation.[Abstract]
  12. Crudele V, Picascia A, Infante T, Grimaldi V, Maiello C, Napoli C. Immunol Lett. 2011 Jul 22. Repeated immune and non immune insults to the graft after heart transplantation
    The clinical transplantation outcome is related to both effects of immunological and non immunological factors degenerating into hyperacute, acute and chronic rejection. Modern immunosuppressive treatments have resolved most events linked to acute rejection while long-term survival still remains the major problem after heart transplantation. The goal of personalized immunosuppressive therapy is to prevent rejection without inducing toxic effects. The aim of future studies could be to clarify the pathogenesis of chronic rejection and develop new and less toxic therapeutic approaches to induce “tolerance” to the graft without major side effects.[Abstract]
  13. METABOLIC CARDIOLOGY
  14. Sinatra ST. Altern Ther Health Med. 2009 Mar-Apr;15(2):48-50 Metabolic cardiology: the missing link in cardiovascular disease
    Metabolic therapies that help cardiomyocytes meet their absolute need for ATP fulfill a major clinical challenge of preserving pulsatile cardiac function while maintaining cell and tissue viability. D-ribose, L-carnitine, and coenzyme Q10 work in synergy to help the ischemic or hypoxic heart preserve its energy charge. [Abstract]
  15. Sinatra ST. Altern Ther Health Med. 2009 May-Jun;15(3):44-52. Metabolic cardiology: an integrative strategy in the treatment of congestive heart failure
    The purpose of this communication article is to introduce metabolic cardiology as a vital therapeutic strategy utilizing nutritional biochemical interventions that preserve and promote adenosine triphosphate (ATP) production. Treatment options that incorporate metabolic interventions targeted to preserve energy substrates (D-ribose) or accelerate ATP turnover (L-carnitine and coenzyme Q10) are indicated for at-risk populations or patients at any stage of CHF. [Abstract]
  16. THE USE OF Q10
  17. Bhagavan HN, Chopra RK. Clin Nutr. 2005 Jun;24(3):331-8. Potential role of ubiquinone (coenzyme Q10) in pediatric cardiomyopathy
    Based upon the biochemical rationale and a large body of data on patients with adult cardiomyopathy, heart failure, and mitochondrial diseases with heart involvement, a role for coenzyme Q10 therapy in PCM patients is indicated, and preliminary results are promising. Additional studies on the potential usefulness of coenzyme Q10 supplementation as an adjunct to conventional therapy in PCM, particularly in children with dilated cardiomyopathy, are therefore warranted.[Abstract]
  18. Kocharian A, Shabanian R, Rafiei-Khorgami M, Kiani A, Heidari-Bateni G. Cardiol Young. 2009 Sep;19(5):501-6. Coenzyme Q10 improves diastolic function in children with idiopathic dilated cardiomyopathy
    Our results, therefore, indicate that administration of coenzyme Q10 is useful in ameliorating cardiac failure in patients with idiopathic dilated cardiomyopathy through its significant effect on improving diastolic function.[Abstrat]
  19. Bhagavan HN, Chopra RK. Clin Nutr. 2005 Jun;24(3):331-8. Potential role of ubiquinone (coenzyme Q10) in pediatric cardiomyopathy
    Based upon the biochemical rationale and a large body of data on patients with adult cardiomyopathy, heart failure, and mitochondrial diseases with heart involvement, a role for coenzyme Q10 therapy in PCM patients is indicated, and preliminary results are promising. [Abstract]
  20. Kocharian A, Shabanian R, Rafiei-Khorgami M, Kiani A, Heidari-Bateni G. Cardiol Young. 2009 Sep;19(5):501-6. Coenzyme Q10 improves diastolic function in children with idiopathic dilated cardiomyopathy
    .Our results, therefore, indicate that administration of coenzyme Q10 is useful in ameliorating cardiac failure in patients with idiopathic dilated cardiomyopathy through its significant effect on improving diastolic function.[Abstract]
  21. VITAMINE D
  22. Schwalfenberg GK. Mol Nutr Food Res. 2011 Jan;55(1):96-108. doi: 10.1002/mnfr.201000174. A review of the critical role of vitamin D in the functioning of the immune system and the clinical implications of vitamin D deficiency
    This review looks at the critical role of vitamin D in improving barrier function, production of antimicrobial peptides including cathelicidin and some defensins, and immune modulation. The function of vitamin D in the innate immune system and in the epithelial cells of the oral cavity, lung, gastrointestinal system, genito-urinary system, skin and surface of the eye is discussed. [Article]
  23. Ginde AA, Mansbach JM, Camargo CA Jr. Curr Allergy Asthma Rep. 2009 Jan;9(1):81-7. Vitamin D, respiratory infections, and asthma
    Over the past decade, interest has grown in the role of vitamin D in many nonskeletal medical conditions, including respiratory infection. Emerging evidence indicates that vitamin D-mediated innate immunity, particularly through enhanced expression of the human cathelicidin antimicrobial peptide (hCAP-18), is important in host defenses against respiratory tract pathogens. Observational studies suggest that vitamin D deficiency increases risk of respiratory infections. [Abstract]
  24. Oduwole AO, Renner JK, Disu E, Ibitoye E, Emokpae E. West Afr J Med. 2010 Nov-Dec;29(6):373-8 Relationship between Vitamin D Levels and Outcome of Pneumonia in Children
    The study showed that Vitamin D insufficiency, and not solely its deficiency, may have an important role to play in the immune and haemopoetic system. It may therefore affect the response of a child to infections especially pneumonia.[Abstract]
  25. Leow L, Simpson T, Cursons R, Karalus N, Hancox RJ. Respirology. 2011 May;16(4):611-6. doi: 10.1111/j.1440-1843.2011.01924.x Vitamin D, innate immunity and outcomes in community acquired pneumonia
    25-hydroxyvitamin D deficiency is associated with increased mortality in patients admitted to hospital with community acquired pneumonia during winter.[Abstract]
  26. Gilbert CR, Arum SM, Smith CM. Can Respir J. 2009 May-Jun;16(3):75-80. Vitamin D deficiency and chronic lung disease
    Vitamin D deficiency is increasingly being recognized as a prevalent problem in the general population. Patients with chronic lung diseases such as asthma, cystic fibrosis, chronic obstructive lung disease and interstitial pneumonia appear to be at increased risk for vitamin D deficiency for reasons that are not clear.[Article]
  27. Walker VP, Modlin RL. Pediatr Res. 2009 May;65(5 Pt 2):106R-113R. The vitamin D connection to pediatric infections and immune function
    This knowledge is particularly relevant and timely, because infants and children seem more susceptible to viral rather than bacterial infections in the face of vitamin D deficiency. The connection among vitamin D, infections, and immune function in the pediatric population indicates a possible role for vitamin D supplementation in potential interventions and adjuvant therapies.[Article]
  28. Bischoff-Ferrari HA, Shao A, Dawson-Hughes B, Hathcock J, Giovannucci E, Willett WC. Osteoporos Int. 2010 Jul;21(7):1121-32 Benefit-risk assessment of vitamin D supplementation
    Our analysis suggests that mean serum 25(OH)D levels of about 75 to 110 nmol/l provide optimal benefits for all investigated endpoints without increasing health risks. These levels can be best obtained with oral doses in the range of 1,800 to 4,000 IU vitamin D per day; further work is needed, including subject and environment factors, to better define the doses that will achieve optimal blood levels in the large majority of the population.[Article]

  29. .[Abstract]

DHEA

    DHEA DEFICIENTIE BIJ CARDIOMYOPATHIE EN HARTFALEN
  1. Kawano H, Nagayoshi Y, Soejima H, Tanaka Y, Yamabe H, Kinoshita Y, Ogawa H. Int J Cardiol. 2008 Apr 10;125(2):277-9. Dehydroepiandrosterone levels vary according as heart failure condition in patients with idiopathic dilated cardiomyopathy
    DHEAS levels were significantly lower in patients with congestive heart failure than in controls (82.2+/-9.9 vs. 122.7+/-18.6 microg/dL, respectively, p<0.01), whereas there was no difference in cortisol levels between the 2 groups. After 3 months of treatment, NYHA functional class improved in all patients, and DHEAS levels increased (from 82.2+/-9.9 to 106.2+/-21.1 microg/dL, p<0.01). DHEAS levels vary according as heart failure condition in patients with idiopathic dilated cardiomyopathy.[Abstract]
  2. Moriyama Y, Yasue H, Yoshimura M, Mizuno Y, Nishiyama K, Tsunoda R, Kawano H, Kugiyama K, Ogawa H, Saito Y, Nakao K. J Clin Endocrinol Metab. 2000 May;85(5):1834-40. The plasma levels of dehydroepiandrosterone sulfate are decreased in patients with chronic heart failure in proportion to the severity
    These results indicate that the plasma levels of DHEAS are decreased in patients with CHF in proportion to its severity and that oxidative stress is associated with decreased levels of DHEAS in patients with CHF.[Article]
  3. Thijs L, Fagard R, Forette F, Nawrot T, Staessen JA. Acta Cardiol. 2003 Oct;58(5):403-10. Are low dehydroepiandrosterone sulphate levels predictive for cardiovascular diseases? A review of prospective and retrospective studies
    The present findings suggest that, in men, low serum levels of DHEAS may be associated with coronary heart disease. However, whether DHEA supplementation has any cardiovascular benefit is not clear. Data from prospective randomised trials are needed.[Abstract]
  4. Shufelt C, Bretsky P, Almeida CM, Johnson BD, Shaw LJ, Azziz R, Braunstein GD, Pepine CJ, Bittner V, Vido DA, Stanczyk FZ, Bairey Merz CN. J Clin Endocrinol Metab. 2010 Nov;95(11):4985-92 DHEA-S levels and cardiovascular disease mortality in postmenopausal women: results from the National Institutes of Health–National Heart, Lung, and Blood Institute (NHLBI)-sponsored Women’s Ischemia Syndrome Evaluation (WISE)
    Among postmenopausal women with coronary risk factors undergoing coronary angiography for suspected myocardial ischemia, lower DHEA-S levels were linked with higher CVD mortality and all-cause mortality. Our study provides valuable feasibility data useful for future investigations and possible mechanistic pathways.[Abstract]
  5. Khaw KT. J Endocrinol. 1996 Sep;150 Suppl:S149-53. Dehydroepiandrosterone, dehydroepiandrosterone sulphate and cardiovascular disease
    High dehyroepiandrosterone (DHEA) or dehydroepiandrosterone sulphate (DHEAS) levels have been suggested to be protective for cardiovascular disease. DHEA supplementation is reported to lower low-density levels of cholesterol in humans and to reduce atherosclerotic plaques in rabbits. [Abstract]
  6. Johnson MD, Bebb RA, Sirrs SM. Ageing Res Rev. 2002 Feb;1(1):29-41. Uses of DHEA in aging and other disease states
    Dehydro-3-epiandrosterone is a steroid hormone synthesized in large quantities by the adrenal gland whose physiologic role remains unclear. The effects of DHEA could be estrogenic or androgenic, depending on the hormonal milieu. Low levels of DHEA are associated with aging, cardiovascular disease in men, and an increased risk of pre-menopausal breast and ovarian cancer. High levels of DHEA might increase the risk of postmenopausal breast cancer. Therapeutically DHEA might be useful for improving psychological well-being in the elderly, reducing disease activity in people with mild to moderate systemic lupus erythematosus and myotonic dystrophy, improving mood in those clinically depressed, and improving various parameters in women with adrenal insufficiency. Although many other claims have been made for DHEA in diverse conditions, such as aging, dementia, and AIDS, no well-designed clinical trials have clearly substantiated the utility and safety of long-term DHEA supplementation.[Abstract]
  7. VOORDELEN VAN DHEA
  8. Genazzani AR, Pluchino N. Climacteric. 2010 Aug;13(4):314-6. DHEA therapy in postmenopausal women: the need to move forward beyond the lack of evidence
    Postulated consequences of low DHEA levels include insulin resistance, obesity, cardiovascular disease, cancer, reduction of the immune defence system as well as psychosocial problems such as depression and a general deterioration in the sensation of well-being and cognitive function. [Abstract]
  9. Cameron DR, Braunstein GD. Treat Endocrinol. 2005;4(2):95-114 The use of dehydroepiandrosterone therapy in clinical practice
    Clinical trials suggest that 50mg of oral DHEA, but not <30mg, can increase serum androgen levels to within the physiologic range for young adults with primary and secondary adrenal insufficiency, possibly improve sexual function, improve mood and self-esteem, and decrease fatigue/exhaustion. [Abstract]

  10. .[Abstract]

  11. .[Abstract]

  12. .[Abstract]
  13. VEILIGHEID
  14. Buvat J. World J Urol. 2003 Nov;21(5):346-55 Androgen therapy with dehydroepiandrosterone
    However, it must be realized that DHEA is also converted into estradiol, which may be a risk factor for breast or endometrial cancer in postmenopausal women.[Abstract]
  15. Stoll BA. Eur J Clin Nutr. 1999 Oct;53(10):771-5. Dietary supplements of dehydroepiandrosterone in relation to breast cancer risk
    Late promotion of breast cancer in postmenopausal women may be stimulated by prolonged intake of DHEA, and the risk may be increased by the endocrine abnormality associated with pre-existing abdominal obesity. Caution is advised in the use of dietary supplements of DHEA particularly by obese postmenopausal women.[Abstract]
  16. Raven PW, Hinson JP. Menopause Int. 2007 Jun;13(2):75-8 Dehydroepiandrosterone (DHEA) and the menopause: an update
    In fact, the benefits and adverse effects of DHEA administration in postmenopausal women increasingly resemble those of conventional hormone replacement therapy. Overall, we conclude that DHEA is not currently to be recommended for therapeutic use in the majority of postmenopausal women. However, DHEA supplementation may be of benefit in two specific groups of women: those with the lowest circulating levels of DHEA; and those for whom osteoporosis is a particular problem.[Article]

  17. .[Abstract]

  18. .[Abstract]

  19. .[Abstract]

Testosteron

    TESTOSTERON DEFICIENCIE
  1. Tenover JS. Int J Impot Res. 2003 Aug;15 Suppl 4:S3-8. Declining testicular function in aging men
    Age-related decline in male sex hormones, particularly testosterone, is referred to as andropause. Like menopause, andropause is associated with physical and emotional changes that may be alleviated by hormone replacement therapy. Hypogonadism in aging men, as defined by a low free testosterone index, is due to declining testosterone production and increased sex hormone-binding globulin levels. About 30% of men in their 60s and more than 80% of men over 80 y may have a low free testosterone index. Diagnosis of hypogonadism is based on clinical symptoms (eg, decreased muscle mass, fractures, loss of libido) and laboratory determinations of serum testosterone-usually total testosterone levels. Measuring bioavailable testosterone, or free testosterone, is expensive and time-consuming, but may more accurately detect hypogonadism. Testosterone replacement therapy is generally safe in aging men and may improve libido, cognition, bone mineral density, body mass composition, and serum lipoproteins. Although contraindicated in men with prostate or breast cancer, testosterone replacement therapy in aging men warrants examination. Any of the available testosterone formulations can be used, but injectable forms have certain advantages, including excellent dose adjustability, lack of skin irritation, and low cost.[Article]
  2. Smith KW, Feldman HA, McKinlay JB. Clin Endocrinol (Oxf). 2000 Dec;53(6):703-11. Construction and field validation of a self-administered screener for testosterone deficiency (hypogonadism) in ageing men
    All subjects provided blood samples for endocrine testing. Survey data from 1660 men aged 40-79 years participating in the Massachusetts Male Ageing Study (MMAS) were analysed in the first phase. The prevalence of testosterone deficiency was 20.4% in the MMAS and 42.1% in the clinic sample.[Abstract]
  3. Kalinchenko SIu, Vorslov LO, Aglamazian NL, Morgunov LIu Urologiia. 2007 Jan-Feb;(1):57, 59-61. Efficacy and safety of hormonal therapy with androgens (androgel) in men with erectile dysfunction, partial androgen deficiency of aging male and cardiovascular diseases
    After the age of 30-40 a testosterone level falls 1-2% a year. The number of men with testosterone deficiency grows from 8% in 40-60-year-olds to 85% at the age over 80 years. Low testosterone correlates with such risk factors of cardiovascular diseases as dyslipidemia, atherosclerosis, low fibrinolysis, insulin resistance and abdominal obesity. [Abstract]
  4. Dillon EL, Durham WJ, Urban RJ, Sheffield-Moore M. Clin Nutr. 2010 Dec;29(6):697-700. Hormone treatment and muscle anabolism during aging: androgens
    Aging is associated with a gradual decline in circulating testosterone concentrations and decreased musculature in men. The definition of hypogonadism in men remains obscure but is generally indicated by total testosterone concentrations less than a threshold value of 300-500 ng/dL. Androgen administration, either alone or in combination with other treatments, can be successful in improving muscle mass by increasing protein anabolism and reducing protein catabolism in men and women. Further research is necessary to optimize the anabolic and anticatabolic properties of androgens for treatment and prevention of muscle loss in men and women.[Abstract]
  5. Lazarou S, Reyes-Vallejo L, Morgentaler A. J Sex Med. 2006 Nov;3(6):1085-9. Wide variability in laboratory reference values for serum testosterone
    The low reference value for total testosterone ranged from 130 to 450 ng/dL (350% difference), and the upper value ranged from 486 to 1,593 ng/dL (325% difference). Age-adjusted reference values were applied in four centers for total testosterone and in seven labs for free testosterone. All reference values were based on a standard statistical model without regard for clinical aspects of hypogonadism. Twenty-three of the 25 lab directors responded that clinically relevant testosterone reference ranges would be preferable to current standards. Laboratory reference values for testosterone vary widely, and are established without clinical considerations.[Abstract]
  6. Bhasin S, Pencina M, Jasuja GK, Travison TG, Coviello A, Orwoll E, Wang PY, Nielson C, Wu F, Tajar A, Labrie F, Vesper H, Zhang A, Ulloor J, Singh R, D’Agostino R, Vasan RS. J Clin Endocrinol Metab. 2011 Aug;96(8):2430-9 Reference ranges for testosterone in men generated using liquid chromatography tandem mass spectrometry in a community-based sample of healthy nonobese young men in the Framingham Heart Study and applied to three geographically distinct cohorts
    In a reference sample of 456 men, mean (sd), median (quartile), and 2.5th percentile values were 723.8 (221.1), 698.7 (296.5), and 348.3 ng/dl for TT and 141. 8 (45.0), 134.0 (60.0), and 70.0 pg/ml for FT, respectively. In all three samples, men with low TT and FT were more likely to have slow walking speed, difficulty climbing stairs, or frailty and diabetes than those with normal levels. In EMAS, men with low TT and FT were more likely to report sexual symptoms than men with normal levels. Men with low TT and FT were more likely to have at least one of the following: sexual symptoms (EMAS only), physical dysfunction, or diabetes.[Abstract]
  7. Centrum voor Andrologie – Universitair Ziekenhuis Gent
    herstel van een “normale” testosteron concentratie in het bloed (waarde tijdens de voormiddag hoger dan 375 ng/dL, streefwaarde 500-600 ng/dL).[Article]
  8. STOORNISSEN DOOR EEN TESTOSTERON DEFICIENCIE
  9. Jones TH. Trends Endocrinol Metab. 2010 Aug;21(8):496-503. Testosterone deficiency: a risk factor for cardiovascular disease?
    This manuscript reviews the current evidence supporting a link between low testosterone and cardiovascular disease, highlighting the need for larger, longer-term studies.[Abstract]
  10. Traish AM, Saad F, Feeley RJ, Guay A. J Androl. 2009 Sep-Oct;30(5):477-94 The dark side of testosterone deficiency: III. Cardiovascular disease
    A considerable body of evidence exists suggesting that androgen deficiency contributes to the onset, progression, or both of cardiovascular disease (CVD). [Article]
  11. Traish AM, Miner MM, Morgentaler A, Zitzmann M. Am J Med. 2011 Jul;124(7):578-87 Testosterone deficiency
    Testosterone deficiency (TD) afflicts approximately 30% of men aged 40-79 years, with an increase in prevalence strongly associated with aging and common medical conditions including obesity, diabetes, and hypertension.[Abstract]
  12. Traish AM, Guay A, Feeley R, Saad F. J Androl. 2009 Jan-Feb;30(1):10-22. Epub 2008 Jul 17. The dark side of testosterone deficiency: I. Metabolic syndrome and erectile dysfunction
    MetS has been associated with hypogonadism and erectile dysfunction (ED), and MetS may be considered a risk factor for ED.[Article]
  13. Traish AM, Saad F, Guay A. J Androl. 2009 Jan-Feb;30(1):23-32. The dark side of testosterone deficiency: II. Type 2 diabetes and insulin resistance
    A considerable body of evidence exists suggesting a link among reduced testosterone plasma levels, type 2 diabetes (T2D), and insulin resistance (IR). [Article]
  14. Derby CA, Zilber S, Brambilla D, Morales KH, McKinlay JB. Clin Endocrinol (Oxf). 2006 Jul;65(1):125-31. Body mass index, waist circumference and waist to hip ratio and change in sex steroid hormones: the Massachusetts Male Ageing Study
    Obesity was associated with decreased levels of total and free testosterone, and of SHBG at follow-up relative to baseline. For any given baseline concentration of TT, FT or SHBG, follow-up levels were lowest among men who remained obese or who became obese during follow-up. This was true for all three indices of obesity. Central adiposity was associated with lower DHEAS levels at follow-up, while elevated body mass index was not. Obesity may predict greater decline in testosterone and SHBG levels with age. Central adiposity may be a more important predictor of decline in DHEAS than is body mass index.[Abstract]
  15. TESTOSTERON THERAPIE BIJ STOORNISSEN DOOR EEN DEFICIENCIE
  16. Guay AT, Traish A. Urol Clin North Am. 2011 May;38(2):175-83. Testosterone deficiency and risk factors in the metabolic syndrome: implications for erectile dysfunction
    Hypogonadism, or testosterone deficiency (TD), is an integral component of the pathology underlying endothelial dysfunction and MetS, with insulin resistance (IR) at its core. Testosterone replacement therapy for TD has been shown to ameliorate some of the components of the MetS, improve IR, and may serve as treatment for decreasing cardiovascular and ED risk.[Abstract]
  17. Kapoor D, Goodwin E, Channer KS, Jones TH. Eur J Endocrinol. 2006 Jun;154(6):899-906 Testosterone replacement therapy improves insulin resistance, glycaemic control, visceral adiposity and hypercholesterolaemia in hypogonadal men with type 2 diabetes
    Testosterone replacement therapy reduces insulin resistance and improves glycaemic control in hypogonadal men with type 2 diabetes. Improvements in glycaemic control, insulin resistance, cholesterol and visceral adiposity together represent an overall reduction in cardiovascular risk.[Article]
  18. TESTOSTERON DEFICIENCIE EN HARTFALEN
  19. Wu HY, Wang XF, Wang JH, Li JY. Asian J Androl. 2011 Sep;13(5):759-63. doi: 10.1038/aja.2011.26. Testosterone level and mortality in elderly men with systolic chronic heart failure
    Our study showed that levels of TT and eFT are commonly decreased in elderly patients with systolic CHF and related to disease severity, but they are not independent predictors for mortality.[Abstract]
  20. Jankowska EA, Biel B, Majda J, Szklarska A, Lopuszanska M, Medras M, Anker SD, Banasiak W, Poole-Wilson PA, Ponikowski P. Circulation. 2006 Oct 24;114(17):1829-37. Anabolic deficiency in men with chronic heart failure: prevalence and detrimental impact on survival
    In male CHF patients, anabolic hormone depletion is common, and a deficiency of each anabolic hormone is an independent marker of poor prognosis. Deficiency of >1 anabolic hormone identifies groups with a higher mortality.[Article]
  21. Naghi JJ, Philip KJ, DiLibero D, Willix R, Schwarz ER. J Cardiovasc Pharmacol Ther. 2011 Mar;16(1):14-23. Testosterone therapy: treatment of metabolic disturbances in heart failure
    Recent attention to the catabolic state found in patients with chronic heart failure has sparked interest in new potential targets for medical therapy. In particular, as many as 26% to 37% of men affected with HF have been found to be testosterone deficient. The severity of androgen deficiency has been shown to correlate with symptoms, functional class, and prognosis in patients with heart failure. [Abstract]
  22. J Card Fail. 2009 Jun;15(5):442-50. Reduction in circulating testosterone relates to exercise capacity in men with chronic heart failure
    In men with CHF, low circulating testosterone independently relates to exercise intolerance. The greater the reduction of serum TT in the course of disease, the more severe the progression of exercise intolerance. Whether testosterone supplementation would improve exercise capacity in hypogonadal men with CHF requires further studies.[Abstract]
  23. Jankowska EA, Drohomirecka A, Ponikowska B, Witkowska A, Lopuszanska M, Szklarska A, Borodulin-Nadzieja L, Banasiak W, Poole-Wilson PA, Ponikowski P. Eur J Heart Fail. 2010 Sep;12(9):966-73. Deficiencies in circulating testosterone and dehydroepiandrosterone sulphate, and depression in men with systolic chronic heart failure
    TT and DHEAS deficiencies predict severity of depression in men with CHF. Depression and combined androgen deficiencies are independently related to poor outcome in these patients.[Article]
  24. Iellamo F, Rosano G, Volterrani M. Curr Heart Fail Rep. 2010 Jun;7(2):59-65 Testosterone deficiency and exercise intolerance in heart failure: treatment implications
    Chronic heart failure (CHF) is characterized by a metabolic shift favoring catabolism with impairment in skeletal muscle bulk and function. There is evidence that low plasma levels of testosterone play a role in this shift, and that hypotestosteronemia could be involved in the impairment of skeletal muscle function and exercise tolerance, which characterize CHF syndrome. Recent studies have indeed indicated that testosterone supplementation increases functional capacity and muscle performance in patients with CHF. [Abstract]
  25. TESTOSTERON THERAPIE BIJ HARTFALEN
  26. Caminiti G, Volterrani M, Iellamo F, Marazzi G, Massaro R, Miceli M, Mammi C, Piepoli M, Fini M, Rosano GM. J Am Coll Cardiol. 2009 Sep 1;54(10):919-27. Effect of long-acting testosterone treatment on functional exercise capacity, skeletal muscle performance, insulin resistance, and baroreflex sensitivity in elderly patients with chronic heart failure a double-blind, placebo-controlled, randomized study
    These results suggest that long-acting testosterone therapy improves exercise capacity, muscle strength, glucose metabolism, and BRS in men with moderately severe CHF. Testosterone benefits seem to be mediated by metabolic and peripheral effects.[Article]
  27. Malkin CJ, Channer KS, Jones TH. Curr Opin Endocrinol Diabetes Obes. 2010 Jun;17(3):262-8. Testosterone and heart failure
    Testosterone replacement therapy appears to improve metabolism and endurance in patients with CHF; further trials will be necessary before widespread use. Physicians who regularly treat patients with CHF may consider testosterone therapy but it is likely that they will require the advice and support from endocrine specialists.[Abstract]
  28. Pugh PJ, Jones RD, West JN, Jones TH, Channer KS. Heart. 2004 Apr;90(4):446-7. Testosterone treatment for men with chronic heart failure
    Chronic heart failure (CHF) is a disabling disease characterised by exercise intolerance and dyspnoea. Disease progression arises from prolonged neurohormonal and pro-inflammatory cytokine activation and is associated with a metabolic shift favouring catabolism, vasodilator incapacity, and loss of skeletal muscle bulk and function. In men, androgens are important determinants of anabolic function and physical strength. Androgens also possess anti-inflammatory and vasodilatory properties. In addition, testosterone has been shown to augment cardiac output acutely in men with CHF. Low plasma concentrations of testosterone have been described in men with CHF, and correlate positively with cardiac output. [Article]
  29. Pugh PJ, Jones TH, Channer KS. Eur Heart J. 2003 May;24(10):909-15. Acute haemodynamic effects of testosterone in men with chronic heart failure
    Anabolic therapy with testosterone may be useful in the treatment of wasting associated with chronic heart failure but little is known about its cardiovascular actions. The aim of this study was to determine the acute haemodynamic effects of testosterone administration in men with heart failure.Administration of testosterone increases cardiac output acutely, apparently via reduction of left ventricular afterload.[Article]
  30. Nguyen CT, Aaronson A, Morrissey RP, Agarwal M, Willix RD, Schwarz ER. Expert Rev Cardiovasc Ther. 2011 Jun;9(6):711-20. Myths and truths of growth hormone and testosterone therapy in heart failure
    It has been observed that low levels of growth hormone and testosterone have been associated with increased mortality and morbidity in patients with heart failure. Likewise, testosterone has been shown to improve hemodynamic parameters via reduction in peripheral vascular resistance and increased coronary blood flow through vasodilation, thereby improving functional and symptomatic status. To date, growth hormone and testosterone therapy have shown some positive benefits, albeit with some concerns over adverse effects. However, large randomized controlled trials are still needed to assess the long-term safety and efficacy.[Abstract]
  31. Iellamo F, Volterrani M, Caminiti G, Karam R, Massaro R, Fini M, Collins P, Rosano GM. J Am Coll Cardiol. 2010 Oct 12;56(16):1310-6. Testosterone therapy in women with chronic heart failure: a pilot double-blind, randomized, placebo-controlled study
    Testosterone supplementation improves functional capacity, insulin resistance, and muscle strength in women with advanced CHF. Testosterone seems to be an effective and safe therapy for elderly women with CHF. [Abstract]
  32. Malkin CJ, Pugh PJ, West JN, van Beek EJ, Jones TH, Channer KS. Eur Heart J. 2006 Jan;27(1):57-64. Testosterone therapy in men with moderate severity heart failure: a double-blind randomized placebo controlled trial
    Chronic heart failure is associated with maladaptive and prolonged neurohormonal and pro-inflammatory cytokine activation causing a metabolic shift favouring catabolism, vasodilator incapacity, and loss of skeletal muscle bulk and function. Testosterone replacement therapy improves functional capacity and symptoms in men with moderately severe heart failure. [Article]
  33. Malkin CJ, Jones TH, Channer KS. Front Horm Res. 2009;37:183-96. Testosterone in chronic heart failure
    There is developing evidence that of all morbid populations, patients with chronic heart failure in particular are likely to benefit from testosterone treatment since the natural history is that of progressive disordered metabolism with catabolic excess and androgen imbalance.[Abstract]
  34. TESTOSTERON THERAPIE EN HET RISICO OP PROSTAATKANKER
  35. Morgentaler A. J Sex Med. 2008 Aug;5(8):1834-40 Guilt by association: a historical perspective on Huggins, testosterone therapy, and prostate cancer
    INTRODUCTION: A long-standing belief is that higher testosterone (T) will increase the risk of prostate cancer (PCa), yet recent studies do not support this view.AIM: To identify the key historical and scientific events leading to the establishment and persistence of the belief in a T-dependent model of PCa growth, despite evidence to the contrary.METHODS: Review of key historical scientific articles regarding T and PCa.RESULTS: The T-dependent model of PCa growth arose from the work of Huggins and coworkers, who in 1941 demonstrated dramatic responses to castration among men with advanced PCa. These authors and others also reported a rapid clinical progression with T administration. This led to the concept that T was like “food for a hungry tumor” for men with PCa.Fowler and Whitmore recognized in 1981 that the negative effect of T administration did not occur unless men had been previously castrated. However, this critical observation was either forgotten or dismissed amid major changes in PCa diagnosis and management during the 1980s.More recent studies have failed to provide clinical evidence supporting the belief that higher T represents a risk for PCa. Factors contributing to the persistence of the T-dependent model included dramatic effects of castration, continued use of androgen deprivation for treatment of PCa, an influential spokesperson (Huggins), groupthink (failure to acknowledge evidence inconsistent with the prevalent ideology), and an imprecise formulation of the model (“more T, more cancer growth”), making refutation difficult.CONCLUSIONS: The fear that higher T will increase PCa growth stems from a theory of T-dependent PCa growth that originated with observations in a special population (castrated men) that is not particularly relevant to T therapy in hypogonadal men. The negative view of T with regard to PCa should be recognized for what it is–guilt by association. .[Abstract]
  36. Morgentaler A. Can J Urol. 2006 Feb;13 Suppl 1:40-3. Testosterone replacement therapy and prostate risks: where’s the beef?
    It has been part of the conventional medical wisdom for six decades that higher testosterone in some way increases the risk of prostate cancer. This belief is derived largely from the well-documented regression of prostate cancer in the face of surgical or pharmacological castration. However, there is an absence of scientific data supporting the concept that higher testosterone levels are associated with an increased risk of prostate cancer. Specifically, no increased risk of prostate cancer was noted in 1) clinical trials of testosterone supplementation, 2) longitudinal population-based studies, or 3) in a high-risk population of hypogonadal men receiving testosterone treatment. Moreover, hypogonadal men have a substantial rate of biopsy-detectableprostate cancer, suggesting that low testosterone has no protective effect against development of prostate cancer. These results argue against an increased risk of prostate cancer with testosterone replacement therapy.[Abstract]
  37. Morgentaler A. Urol Clin North Am. 2011 May;38(2):119-24. Testosterone and prostate cancer: what are the risks for middle-aged men?
    With increased recognition of the benefits of testosterone (T) therapy for middle-aged men, there has been a concomitant reexamination of the historical fear that raising T will result in more prostate cancer (PCa). Studies have failed to show increased risk of PCa in men with higher serum T, and supraphysiologic T fails to increase prostate volume or prostate-specific antigen in healthy men. This apparent paradox is explained by the Saturation Model, which posits a finite capacity of androgen to stimulate PCa growth. Modern studies indicate no increased risk of PCa among men with serum T in the therapeutic range.[Abstract]
  38. Umbas R, Sugiono M. Acta Med Indones. 2010 Jul;42(3):171-5. Testosterone replacement therapy in prostate cancer patients: is it safe?
    The increasing population of elderly men means there is also an increase in those suffering from late-onset hypogonadism and testosterone deficiency, with all its attending consequences such as reduced libido, erectile dysfunction, metabolic disturbances, cardiovascular disease, decreased bone density and reduced quality of life. The use of testosterone replacement therapy may benefit such patients but remains controversial, especially with regard to the risk it may have on prostate cancer. However, there is no conclusive evidence that testosterone therapy increases the risk of developing prostate cancer nor is there any evidence to suggest that it can convert subclinical or indolent prostate cancer into a clinically significant one. In fact, a number of recent reports have shown that it is safe to give testosterone therapy in patients who have been successfully treated for early prostate cancer. Therefore, the purpose of this review is to discuss the role of testosterone replacement therapy, focusing on those with prostate cancer, as well as the risks and benefits that every physician must consider before commencing treatment.[Article]
  39. Rhoden EL, Averbeck MA. Arq Bras Endocrinol Metabol. 2009 Nov;53(8):956-62 Prostate carcinoma and testosterone: risks and controversies
    Hypogonadism is a clinical and biochemical syndrome which may cause significant detriment in the quality of life. With the increase in life expectancy and prostate cancer survival a significant increase in the number of men with hypogonadism who have undergone presumably curative treatment for PCa is anticipated. Despite the widespread contraindication of testosterone in men with known or suspected prostate cancer, there is no convincing evidence that the normalization of testosterone serum levels in men with low, but not castrate levels, is deleterious. Although further studies are necessary before definitive conclusions can be drawn, the available evidence suggests that testosterone replacement therapy can be cautiously considered in selected hypogonadal men treated with curative intent for low risk prostate cancer and without evidence of active disease.[Abstract]
  40. Rhoden EL, Averbeck MA. Curr Urol Rep. 2009 Nov;10(6):453-9. Testosterone therapy and prostate carcinoma
    Hypogonadism is a clinical and biochemical syndrome associated with a range of disease states that has significant effects on morbidity and mortality and also affects quality of life. Because of the increase in life expectancy and prostate carcinoma (PCa) survival, a significant increase in the number of men with hypogonadism who have undergone presumably curative treatment of PCa is anticipated. Despite the widespread belief regarding contraindication of testosterone administration to men with known or suspected PCa, there is no convincing evidence that the normalization of testosterone serum levels in men with low levels presents a deleterious effect on the evolution of the disease. In the few available case series describing testosterone replacement therapy (TRT) after treatment of PCa, no case of clinical or biochemical progression was observed. The available data suggest that TRT can be cautiously considered in selected hypogonadal men previously treated for curative intent of low-risk PCa and without evidence of active disease.[Abstract]
  41. Morgentaler A, Rhoden EL. Urology. 2006 Dec;68(6):1263-7. Prevalence of prostate cancer among hypogonadal men with prostate-specific antigen levels of 4.0 ng/mL or less
    Prostate cancer was present in more than 1 of 7 hypogonadal men with PSA of 4.0 ng/mL or less. An increased risk of prostate cancer was associated with more severe reductions in testosterone.[Abstract]
  42. Rhoden EL, Morgentaler A. J Urol. 2003 Dec;170(6 Pt 1):2348-51. Testosterone replacement therapy in hypogonadal men at high risk for prostate cancer: results of 1 year of treatment in men with prostatic intraepithelial neoplasia
    After 1 year of TRT men with PIN do not have a greater increase in PSA or a significantly increased risk of cancer than men without PIN. These results indicate that TRT is not contraindicated in men with a history of PIN[Abstract]
  43. TESTOSTERON THERAPIE EN HET RISICO OP BORSTKANKER
  44. Schover LR. Fertil Steril. 2008 Jul;90(1):129-40. Androgen therapy for loss of desire in women: is the benefit worth the breast cancer risk?
    Epidemiological findings agree that higher endogenous serum androgen levels confer increased breast cancer risk both before and after menopause. Androgenic hormonal replacement regimens also increase the risk of breast cancer.[Abstract]
  45. Somboonporn W, Davis SR. Maturitas. 2004 Dec 10;49(4):267-75. Postmenopausal testosterone therapy and breast cancer risk
    However, in postmenopausal women, who are oestrogen deplete and have increased adipose aromatase activity, higher testosterone has been associated with greater breast cancer risk.[Abstract]
  46. Krapf JM, Simon JA Maturitas. 2009 Jul 20;63(3):213-9. The role of testosterone in the management of hypoactive sexual desire disorder in postmenopausal women
    Although some fear an increased risk of breast cancer with exogenous testosterone administration, recent studies support the idea that androgens can play a role in suppressing the proliferative effects of estrogen and progesterone.[Abstract]
  47. Shufelt CL, Braunstein GD. Maturitas. 2009 May 20;63(1):63-6. Safety of testosterone use in women
    Data is mixed with outcomes of breast cancer risk, with some experimental studies suggesting a decrease in estrogen-induced breast epithelial proliferation with low dose testosterone. Additionally, models of superphysiologic testosterone levels, such as polycystic ovarian disease, have not shown an increased risk of breast cancer. As with all hormone therapy in postmenopausal women, testosterone therapy should be individualized and requires that each woman weigh the risk and benefits. [Abstract]
  48. Somboonporn W, Davis SR; National Health and Medical Research Council. Endocr Rev. 2004 Jun;25(3):374-88 Testosterone effects on the breast: implications for testosterone therapy for women
    In experimental studies, androgens exhibit growth-inhibitory and apoptotic effects in some, but not all, breast cancer cell lines.[Article]

  49. .[Abstract]

Nog niet gebruikt onderzoek

    REVIEW
  1. Brown JM1, Hazen SL. Curr Opin Lipidol. 2014 Feb;25(1):48-53. doi: 10.1097/MOL.0000000000000036. Metaorganismal nutrient metabolism as a basis of cardiovascular disease
    Microbial metabolism of TMA containing nutrients can lead to formation of the proatherogenic compound TMAO. Recent insights into this diet-microbe-host interaction provide new clues surrounding the pathogenesis of atherosclerosis, and may serve as a framework for new CVD therapies.[Abstract]
  2. COMPERATIVE
  3. Hartiala J, Bennett BJ, Tang WH, Wang Z, Stewart AF, Roberts R, McPherson R, Lusis AJ1, Hazen SL1, Allayee H2; CARDIoGRAM Consortium. Arterioscler Thromb Vasc Biol. 2014 Jun;34(6):1307-13. doi: 10.1161/ATVBAHA.114.303252. Comparative genome-wide association studies in mice and humans for trimethylamine N-oxide, a proatherogenic metabolite of choline and L-carnitine
    he results of these limited observational studies indicate that, at least in humans, genes play a marginal role in determining TMAO levels and that any genetic effects are relatively weak and complex. Variation in diet or the repertoire of gut microbiota may be more important determinants of plasma TMAO levels in mice and humans, which should be investigated in future studies.[Abstract]
  4. OTHER
  5. Trøseid M1, Ueland T, Hov JR, Svardal A, Gregersen I, Dahl CP, Aakhus S, Gude E, Bjørndal B, Halvorsen B, Karlsen TH, Aukrust P, Gullestad L, Berge RK, Yndestad A. J Intern Med. 2014 Nov 8. doi: 10.1111/joim.12328 Microbiota-dependent metabolite trimethylamine-N-oxide is associated with disease severity and survival of patients with chronic heart failure
    TMAO levels were elevated in patients with HF, and associated with NYHA class, ischaemic aetiology and adverse outcomes. Future studies should focus on gut microbiota, dietary composition and intestinal dysfunction in relation to TMAO levels and clinical outcome in HF. This article is protected by copyright. All rights reserved.[Abstract]
  6. REVIEW
  7. Sandek A1, Rauchhaus M, Anker SD, von Haehling S. Curr Opin Clin Nutr Metab Care. 2008 Sep;11(5):632-9. doi: 10.1097/MCO.0b013e32830a4c6e. The emerging role of the gut in chronic heart failure
    It remains unclear whether increased adherent bacteria in patients with chronic heart failure are a primary or secondary event and whether they contribute to systemic inflammation. Both lack of mucosal integrity with consecutive local and systemic inflammation and dysfunction of transport proteins may worsen the clinical symptoms of chronic heart failure. Therefore, future studies need to address the pathophysiology of the intestinal barrier whose reactivity seems to be crucial for heart function.[Abstract]
  8. REVIEW
  9. Krack A1, Sharma R, Figulla HR, Anker SD. Eur Heart J. 2005 Nov;26(22):2368-74. The importance of the gastrointestinal system in the pathogenesis of heart failure
    There is an increasing evidence to suggest that a ‘leaky’ bowel wall may lead to translocation of bacteria and/or endotoxin, which may be an important stimulus for inflammatory cytokine activation in CHF.[Article]

  10. .[Abstract]

  11. .[Abstract]
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