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Cardiovascular Research 1997 35(1):6-12; doi:10.1016/S0008-6363(97)00076-X
© 1997 by European Society of Cardiology
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Copyright © 1997, European Society of Cardiology

Cardiac hypertrophy, arrhythmogenicity and the new myocardial phenotype. II. The cellular adaptational process

Bernard Swynghedauwa,*, Brigitte Chevaliera, Daniéle Charlemagnea, Pascale Mansiera and François Carréb

aU127-INSERM, Hôpital Lariboisière, 41 Bd de la Chapelle, 75475, Paris CEDEX, France
bDépartement de Physiologie, Faculté de Médecine, Rennes, France

* Corresponding author. Tel.: +33 (1) 42858065; fax: +33 (1) 48742315.

Ventricular fibrosis is not the only structural determinant of arrhythmias in left ventricular hypertrophy. In an experimental model of compensatory cardiac hypertrophy (CCH) the degree of cardiac hypertrophy is also independently linked to ventricular arrhythmias. Cardiac hypertrophy reflects the level of adaptation, and matches the adaptational modifications of the myocardial phenotype. We suggest that these modifications have detrimental aspects. The increased action potential (AP) and QT duration and the prolonged calcium transient both favour spontaneous calcium oscillations, and both are potentially arrhythmogenic and linked to phenotypic changes in membrane proteins. To date, only two ionic currents have been studied in detail: Ito is depressed (likely the main determinant in AP duration), and If, the pacemaker current, is induced in the overloaded ventricular myocytes. In rat CCH, the two components of the sarcoplasmic reticulum, namely Ca2+-ATPase and ryanodine receptors, are down-regulated in parallel. Nevertheless, while the inward calcium current is unchanged, the functionally linked duo composed of the Na+/Ca2+ exchanger and (Na+, K+)-ATPase, is less active. Such an imbalance may explain the prolonged calcium transient. The changes in heart rate variability provide information about the state of the autonomic nervous system and has prognostic value even in CCH. Transgenic studies have demonstrated that the myocardial adrenergic and muscarinic receptor content is also a determining factor. During CCH, several phenotypic membrane changes participate in the slowing of contraction velocity and are thus adaptational. They also have a detrimental counterpart and, together with fibrosis, favour arrhythmias.

KEYWORDS Arrhythmias; Heart rate, variability; Cardiac hypertrophy, compensatory; Calcium transients; Na+/Ca2+ exchange; Phenotype


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