Cardiomyopathy (Heart Failure) and Selenium

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Cardiomyopathy (Heart Failure) and Selenium

Bericht door Willy » zo aug 24, 2003 4:32 pm

<H4>Congestive cardiomyopathy and the selenium content of serum</H4><I>
Oster O, Prellwitz W, Kasper W, Meinertz T.</I><BR>
A deficiency of selenium is suspected to be involved in the pathogenesis of congestive cardiomyopathy. Therefore the serum selenium content of 20 patients with proven congestive cardiomyopathy was measured and compared to that of a healthy control group. The serum selenium content of the patients with cardiomyopathy was found to be different from that of the healthy control group. The mean value of selenium in serum for the control group was 80.1 micrograms Se/1 (SD +/- 13.2) within a range of 53 and 117 micrograms Se/1. From the 20 patients with congestive cardiomyopathy six patients showed selenium concentrations in the normal value range of the control group; in the serum of 14 patients a distinct lower selenium content was found (mean value 47.8 micrograms Se/1 (SD +/- 16.2)) within a range of 23 and 70 micrograms Se/1. 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.
Source: http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
<H4>Selenium and Chronic Heart Failure </H4><I>
Michel de Lorgeril, MD; Patricia Salen, BSc Laboratoire du Stress Cardiovasculaire et, Pathologies Associées, Université de Grenoble, Grenoble, France </I><BR>
We read with interest the article by Inoko et al about selenium deficiency,1 but we do not agree with the interpretation of the data.
Selenium deficiency was identified as a factor in the etiology of heart failure syndromes in areas of very low selenium intakes, such as China, where an endemic selenium-responsive cardiomyopathy is called Keshan disease.2 Similar cases of cardiomyopathy were reported in HIV-infected patients3 and in subjects on parenteral nutrition.4 The patient with Crohn’s disease described by Inoko et al falls into the latter category. When the patient developed his first episode of heart failure, the serum selenium level was not very low (62 µg/L). Low selenium was unlikely the single cause of heart failure, although it certainly contributed. Supplementation "improved the condition of the patient but did not normalize the left ventricular dysfunction," and "despite selenium supplementation for 11 years, the echocardiographic findings gradually deteriorated."1 The patient "was free from symptoms of heart failure for 11 years" and died suddenly.1
This discrepancy between the symptoms of heart failure and left ventricular dysfunction emphasizes that the pathophysiology underlying the symptoms of chronic heart failure is complex and poorly understood.5 There is no single cause of the main symptoms of heart failure (dyspnea and muscle fatigue), and treatments that correct the hemodynamics of heart failure do not reliably increase exercise tolerance or reduce the severity of dyspnea.5
The case described by Inoko et al suggests that selenium may have a role in the symptoms of heart failure rather than in the development of left ventricular dysfunction. Yet, selenium deficiency is not the only cause of Keshan disease, and it coincides with the clinical severity rather than the prevalence of the cardiomyopathy as assessed by echocardiography.2 Possible causes of Keshan disease are viral infection and nutritional factors (insufficient zinc or molybdenum, excessive barium or lead). However, when serum selenium levels of residents of an endemic area were raised to the levels found in nonendemic areas, mortality from Keshan disease dramatically decreased, but clinically latent cases were still found, and the echocardiographic prevalence of the disease remained high.2 Therefore, selenium deficiency seems to be a predisposing factor rather than a specific cause of Keshan disease.2 Finally, although the exact cause of Keshan disease remains unknown, numerous agents probably work synergistically.
Thus, if selenium supplementation did improve the condition of the patient described by Inoko et al, the primary cause of his cardiomyopathy remains unknown.1 The hypothesis that "once fully developed, the left ventricular dysfunction may be irreversible even after use of selenium supplements"1 is not supported by either their own case or the relevant literature.
Source: http://circ.ahajournals.org/cgi/content/full/101/5/e74
<H4>Selenium deficiency and fatal cardiomyopathy in a patient receiving long-term home parenteral nutrition</H4><I>
Quercia RA, Korn S, O'Neill D, Dougherty JE, Ludwig M, Schweizer R, Sigman R.</I><BR>
Fatal cardiomyopathy in a patient who received home parenteral nutrition (HPN) for eight years is reported, and the relationship of selenium deficiency to cardiomyopathy and other adverse effects is discussed. A 42-year-old white man with Crohn's disease who was receiving HPN was admitted to the hospital with severe chest pain and dyspnea. During the three days following admission, his symptoms of congestive heart failure and compensated metabolic acidosis persisted despite treatment. On hospital day 6, the patient developed increased ventricular irritability and refractory ventricular fibrillation and died. At autopsy, the heart weighted 500 g, all chambers were dilated, and the myocardium was grossly flabby. Extremely low concentrations of selenium (5-12% of normal) were found in plasma, heart, liver, and kidney tissue samples. The pathological findings in this patient were similar to those in two previously reported cases and strongly suggest that the fatal cardiomyopathy was secondary to selenium deficiency. Selenium is an integral part of the enzyme glutathione peroxidase, which plays an important role in the metabolism of tissues and organs. For metabolically stable patients receiving total parenteral nutrition, the suggested selenious acid dosage is 25-60 micrograms/day for adults and 1.4-30 micrograms/kg/day for pediatric patients. In selenium-depleted adults, a dosage of 100 micrograms/day administered intravenously for 21-31 days has been recommended to reverse symptoms. All HPN patients and hospitalized patients receiving extended parenteral nutrition should be monitored for selenium deficiency and given supplements if necessary.
Source: http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
<H4>Dietary and blood antioxidants in patients with chronic heart failure. Insights into the potential importance of selenium in heart failure</H4><I>
de Lorgeril M, Salen P, Accominotti M, Cadau M, Steghens JP, Boucher F, de Leiris J. Laboratoire du Stress Cardiovasculaire et Pathologies Associees, UFR de Medecine et Pharmacie, Universite Joseph Fourier de Grenoble, Domaine de la Merci, 38706 La Tronche, Grenoble, France. michel.delorgeril@ujf-grenoble.fr</I><BR>
BACKGROUND: Chronic heart failure (CHF) seems to be associated with increased oxidative stress. However, the hypothesis that antioxidant nutrients may contribute to the clinical severity of the disease has never been investigated. AIMS: To examine whether antioxidant nutrients influence the exercise capacity and left ventricular function in patients with CHF.
METHODS: Dietary intake and blood levels of major antioxidant nutrients were evaluated in 21 consecutive CHF patients and in healthy age- and sex-matched controls. Two indexes of the severity of CHF, peak exercise oxygen consumption (peak VO2) and left ventricular ejection fraction (LVEF), were measured and their relations with antioxidants were analysed.
RESULTS: Whereas plasma alpha-tocopherol and retinol were in the normal range, vitamin C (P=0.005) and beta-carotene (P=0.01) were lower in CHF. However, there was no significant association between vitamins and either peak VO2 or LVEF. Dietary intake (P<0.05) and blood levels of selenium (P<0.0005) were lower in CHF. Peak VO2 (but not LVEF) was strongly correlated with blood selenium: r=0.76 by univariate analysis (polynomial regression) and r=0.87 (P<0.0005) after adjustment for age, sex and LVEF.
CONCLUSIONS: Antioxidant defences are altered in patients with CHF. Selenium may play a role in the clinical severity of the disease, rather than in the degree of left ventricular dysfunction. Further studies are warranted to confirm the data in a large sample size and to investigate the mechanisms by which selenium and other antioxidant nutrients are involved in CHF.
Source: http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
<H4>Dietary and blood antioxidants in patients with chronic heart failure. Insights into the potential importance of selenium in heart failure</H4><I>
de Lorgeril M, Salen P, Accominotti M, Cadau M, Steghens JP, Boucher F, de Leiris J. Laboratoire du Stress Cardiovasculaire et Pathologies Associees, UFR de Medecine et Pharmacie, Universite Joseph Fourier de Grenoble, Domaine de la Merci, 38706 La Tronche, Grenoble, France. michel.delorgeril@ujf-grenoble.fr</I><BR>
BACKGROUND: Chronic heart failure (CHF) seems to be associated with increased oxidative stress. However, the hypothesis that antioxidant nutrients may contribute to the clinical severity of the disease has never been investigated. AIMS: To examine whether antioxidant nutrients influence the exercise capacity and left ventricular function in patients with CHF. METHODS: Dietary intake and blood levels of major antioxidant nutrients were evaluated in 21 consecutive CHF patients and in healthy age- and sex-matched controls. Two indexes of the severity of CHF, peak exercise oxygen consumption (peak VO2) and left ventricular ejection fraction (LVEF), were measured and their relations with antioxidants were analysed.
RESULTS: Whereas plasma alpha-tocopherol and retinol were in the normal range, vitamin C (P=0.005) and beta-carotene (P=0.01) were lower in CHF. However, there was no significant association between vitamins and either peak VO2 or LVEF. Dietary intake (P<0.05) and blood levels of selenium (P<0.0005) were lower in CHF. Peak VO2 (but not LVEF) was strongly correlated with blood selenium: r=0.76 by univariate analysis (polynomial regression) and r=0.87 (P<0.0005) after adjustment for age, sex and LVEF.
CONCLUSIONS: Antioxidant defences are altered in patients with CHF. Selenium may play a role in the clinical severity of the disease, rather than in the degree of left ventricular dysfunction. Further studies are warranted to confirm the data in a large sample size and to investigate the mechanisms by which selenium and other antioxidant nutrients are involved in CHF.
Source: http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
<H4>Fulminant heart failure due to selenium deficiency cardiomyopathy (Keshan disease)</H4><I>
Burke MP, Opeskin K. Victorian Institute of Forensic Medicine, Department of Forensic Medicine, Monash University, Southbank, Australia.</I><BR>
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. In Asia and Africa, dietary selenium deficiency is associated with a cardiomyopathy known as Keshan disease and an osteoarthropathy called Kashin-Beck disease. Chronic selenium deficiency may also occur in individuals with malabsorption and long term selenium-deficient parenteral nutrition. Selenium deficiency causes myopathy as a result of the depletion of selenium-associated enzymes which protect cell membranes from damage by free radicals. We present a case of fulminant heart failure in a middle aged woman with a complex medical and surgical history including documented malabsorption and selenium deficiency. Pathological examination of the heart showed features consistent with Keshan disease.
Source: http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
<H4>Selenium status, kwashiorkor and congestive heart failure</H4><I>
Manar MJ, MacPherson GD, Mcardle F, Jackson MJ, Hart CA. College of Medicine, University of Malawi, Blanthre. manary@kids.wustl.edu</I><BR>
Selenium deficiency is associated with congestive heart failure (CHF) in geographic areas where dietary selenium intake is low and in individuals receiving total parenteral nutrition. Among 66 children with kwashiorkor (including marasmic-kwashiorkor), those who developed CHF had lower serum selenium concentrations than those who did not (32.9 +/- 8.3 vs 41.1 +/- 11.9 microg/L, mean +/- SD, p = 0.03). This association was independent of serum albumin and selenium status was not associated with severity of symptoms, anthropometric indices or HIV infection.
CONCLUSION: This association raises the possibility that selenium may contribute to CHF in washiorkor.
Source: http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
<H4>Dilated cardiomyopathy and selenium deficiency in AIDS. Apropos of a case</H4><I>
Constans J, Sire S, Sergeant C, Simonoff M, Ragnaud JM. Clinique de medecine interne et des maladies vasculaires, hopital Saint-Andre, Bordeaux, France.</I><BR>
Cardiac-related death of HIV-positive patients is not rare. The etiology of AIDS-associated dilated cardiomyopathies often remains unknown, even at autopsy. We report an observation associated to a severe deficit in selenium. The patient had been diagnosed as HIV-positive 2 years before. He presented Pneumocystis carinii pneumonia then Cryptococcus meningitis. Two months later he was hospitalized for pancreatitis and cachexia. He presented global heart failure that lead to death. No microorganism was found in myocardium at autopsy but plasma selenium was dramatically decreased (24 micrograms/L). The deficit in selenium has been associated to a dilated cardiomyopathy in non-AIDS patients. HIV-positive patients have an early decrease in plasma selenium, this concentration is dramatically decreased in malnourished patients. Selenium deficit might be the cause of some of the AIDS-related dilated cardiomyopathies and selenium supplementation might be useful in these patients.
Source: http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
<H4>Selenium deficiency and fatal cardiomyopathy in a patient receiving long-term home parenteral nutrition</H4><I>
Quercia RA, Korn S, O'Neill D, Dougherty JE, Ludwig M, Schweizer R, Sigman R.</I><BR>
Fatal cardiomyopathy in a patient who received home parenteral nutrition (HPN) for eight years is reported, and the relationship of selenium deficiency to cardiomyopathy and other adverse effects is discussed. A 42-year-old white man with Crohn's disease who was receiving HPN was admitted to the hospital with severe chest pain and dyspnea. During the three days following admission, his symptoms of congestive heart failure and compensated metabolic acidosis persisted despite treatment. On hospital day 6, the patient developed increased ventricular irritability and refractory ventricular fibrillation and died. At autopsy, the heart weighted 500 g, all chambers were dilated, and the myocardium was grossly flabby. Extremely low concentrations of selenium (5-12% of normal) were found in plasma, heart, liver, and kidney tissue samples. The pathological findings in this patient were similar to those in two previously reported cases and strongly suggest that the fatal cardiomyopathy was secondary to selenium deficiency. Selenium is an integral part of the enzyme glutathione peroxidase, which plays an important role in the metabolism of tissues and organs. For metabolically stable patients receiving total parenteral nutrition, the suggested selenious acid dosage is 25-60 micrograms/day for adults and 1.4-30 micrograms/kg/day for pediatric patients. In selenium-depleted adults, a dosage of 100 micrograms/day administered intravenously for 21-31 days has been recommended to reverse symptoms. All HPN patients and hospitalized patients receiving extended parenteral nutrition should be monitored for selenium deficiency and given supplements if necessary.
Source: http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
<H4>An etiologic basis for congestive heart failure on the molecular level</H4><I>
Peterson DA.</I><BR>
It is here proposed that disordered redox balance leads to congestive heart failure in a variety of diverse clinical situations. These conditions include those associated with an excess of reducing agents, such as catecholamines and thyroid hormone, or impaired oxidant defenses, such as in selenium deficiency. The clinical situations include hypertension, hyperthyroidism, progressive congestive heart failure, amphetamine overdose and hemochromatosis. The molecular damage to the cardiac muscle is postulated to be mediated via reaction oxygen radicals.
Source: http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

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