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European Heart Journal 1994 15(3):328-334;
Copyright © 1994 by the European Society of Cardiology.
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© 1994 The European Society of Cardiology

Chrome congestive heart failure

Red blood cell sodium heteroexchange in familial primary hypertrophic cardiomyopathy

A. SEMPLICINI, M. G. MOZZATO, S. BONGLOVI, M. MARZOLA, F. MACOR, G. CEOLOTTO, L. SERENA and A. C. PESSINA

Institute of Clinical Medicine, University of Padova Italy

Received 24 February 1993; revised 12 October 1993; .

Correspondence: Dr Marie Stugaard, Medical Department B. Rikshospitalet, The National Hospital, N-0027 Oslo. Norway

Abstract

The hallmark of primary hypertrophic cardiomyopathy is an inappropriate myocardial hypertrophy, linked to myofibril disarray of the left ventricle. Its variable clinical expression may be due to genetic heterogeneity and variable penetrance. Since we have recently shown that abnormalities of cation transport in the erythrocytes are associated with cardiac hypertrophy in essential hypertensives and insulin-dependent diabetics, we have investigated the relationship between cardiac anatomy and function and red cell Li+lNa+ and Na+ exchange in 33 relatives of a patient who died of cardiac failure and was found to have a primary hypertrophic cardiomyopathy at autopsy.

According to echocardiographic examination, 11 members of the family also had a hypertrophic cardiomyopathy, with a family distribution compatible with autosomal dominant genetic transmission and variable penetrance. Red cell Li+lNa+ and Na+ exchange were not significantly different in the affected members as compared to the unaffected, but in the former, after correction for potentially confounding variables, interventricular septum thickness was positively correlated to Na+lH+ exchange and diastolic function (Area ElArea A and Vmax ElVmax A) negatively correlated to Li+lNa+ exchange.

Since a generalized overactivity of the cell membrane Na+lH+ exchange, reflected by increased Na+lH+ and Li+lNa+ exchanges in the red cells, could favour cellular growth and diastolic dysfunction, our data suggest that abnormalities of cell membrane cation transport could play a role in the phenotypic expression of hypertrophic cardiomyopathy.

Key Words: Countertransport • echocardiography • erythrocytes • lithium • familiar hypertrophic cardiomyopathy • Sodium


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