Circulation. 2000;101:e74
(Circulation. 2000;101:e74.)
© 2000 American Heart Association, Inc.
Circulation Electronic Pages |
Selenium and Chronic Heart Failure
Michel de Lorgeril, MD;
Patricia Salen, BSc
Laboratoire du Stress Cardiovasculaire et,
Pathologies Associées,
Université de Grenoble,
Grenoble, France
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Introduction
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To the Editor:
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.
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References
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Inoko M, Konishi T, Matsusue S, Kobashi Y.
Midmural fibrosis of left ventricle due to selenium deficiency.
Circulation. 1998;98:2638–2639.[Free Full Text]
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Ge K, Yang G. The epidemiology
of selenium deficiency in the etiological study of endemic diseases in
China. Am J Clin Nutr (Suppl). 1993;57:259S–263S.[Abstract/Free Full Text]
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Lipshultz SE. Dilated
cardiomyopathy in HIV-infected patients.
N Engl J Med. 1998;339:1153–1155.[Free Full Text]
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Huttunen JK. Selenium and
cardiovascular diseases: an update. Biomed
Environ Sci. 1997;10:220–226.[Medline]
[Order article via Infotrieve]
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Coats AJ. Origins of symptoms in heart failure.
Cardiovasc Drugs Ther. 1997;11(suppl 1):265–272.
Response
Moriaki Inoko, MD;
Takashi Konishi, MD;
Satoru Matsusue, MD;
Yoichiro Kobashi, MD
Department of Cardiology, Abdominal Surgery,
and Pathology,
Tenri Hospital,
Tenri, Japan
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Introduction
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We thank Dr Lorgeril and colleagues for their interest in our
article.
R1 The patient we reported in
Circulation could take no food and
almost no water for a
long period of time, so he consequently
experienced zinc deficiency in
the first 1 month and biotin
deficiency in the first 9 months after the
beginning of total
parenteral nutrition and recovered by the
supplementation of
each element.
R2 When he had been
experiencing progressive heart
failure, his serum selenium (Se) level
and his erythrocyte glutathione
peroxidase activity (GSHPx) were low.
After the supplementation
of Se, these levels recovered (serum Se 96
µg/L, erythrocyte
Se 136 µg/L, erythrocyte GSHPx 23.5U/g
hemoglobin), and
the deterioration of heart failure was
stopped.
R3 His clinical
course suggests that the etiology
of his heart failure was Se
deficiency. We agree with Dr Lorgeril and
colleagues that the
cause of Keshan disease may be multifactorial, but
it is plausible
that Se deficiency can cause
cardiomyopathy that is accompanied
by myocardial
loss and fibrous replacement in the left ventricle.
R4 R5 It
is well known that dilatation and systolic dysfunction
of the
left ventricle gradually proceed by remodeling and overload
of the
residual myocardium, once myocardial loss has occurred.
We
regard the first episode of heart failure as having been
caused by
rapidly developing myocardial damage due to Se deficiency,
which was
terminated by the supplementation of Se, and the second
episode of
heart failure as having been the terminal feature
of
cardiomyopathy.
Dr Lorgeril and colleagues pointed out that serum Se was not very low
when the patient developed heart failure and that it was unlikely that
low Se was the single cause of heart failure. The previous reports
about either Keshan disease or Se deficiency in parenteral nutrition
revealed that there is no definite relationship between serum and
erythrocyte Se concentration and erythrocyte GSHPx.R3
Certainly, the serum Se level was not remarkably low in our patient,
but the erythrocyte GSHPx level was very low, and the condition of
heart failure was improved along with the elevation of erythrocyte
GSHPx level after Se supplementation. This clinical course suggests his
heart failure was a result of Se deficiency. So, we consider our
patient to have demonstrated clinical features caused only by Se
deficiency, and this is the first case of Se deficiency that was
observed for a long period after supplementation of Se and with
subsequent autopsy.
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References
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Inoko M, Konishi T, Matsusue S, Kobashi Y.
Midmural fibrosis of left ventricle due to selenium deficiency.
Circulation. 1998;98:2638–2639.
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Matsusue S, Kashihara S, Takeda H, Koizumi S. Biotin
deficiency during total parenteral nutrition: its clinical
manifestations and plasma nonesterified fatty acid level. JPEN J
Parenter Enteral Nutr. 1985;9:760–763.[Abstract]
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Matsusue S, Kashihara S, Tomonaga G. Selenium
deficiency and cardiomyopathy in a patient on
long-term parenteral nutrition. Nippon Geka Gakkai Zasshi. 1987;88:483–488.[Medline]
[Order article via Infotrieve]
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Johnson RA, Baker SS, Fallon JT, Maynard EP III,
Ruskin JN, Wen Z, Ge K, Cohen HJ. An occidental case of
cardiomyopathy and selenium deficiency.
N Engl J Med. 1981;304:1210–1212.[Medline]
[Order article via Infotrieve]
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Fleming CR, Lie JT, McCall JT, O’Brien JF, Baillie
EE, Thistle JL. Selenium deficiency and fatal
cardiomyopathy in a patient on home parenteral
nutrition. Gastroenterology. 1982;83:689–693.[Medline]
[Order article via Infotrieve]
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Introduction
References