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European Heart Journal 1992 13(Supplement D):2-8; doi:10.1093/eurheartj/13.suppl_D.2
Copyright © 1992 by the European Society of Cardiology.
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© 1992 The European Society of Cardiology

Biological basis of diastolic dysfunction of hypertensive heart

B. Swynghedauw, C. Delcayre, S. L. Cheav and F. Callens-El Amrani

U 127 INSERM, Hospital Lariboisiére, 41 Bd de la Chapelle 75010, Paris, France

Address for correspondence: B. Swynghedauw, U127-INSERM, Hopital Lariboisiére, 41 Bd de la Chapelle, 75010, Paris, France

To study the diastolic properties of the heart includes examining active relaxation, passive ventricular stiffness and atrial contraction, (i) The main determinant of active relaxation is the adenosine triphosphate (ATP) concentration. Relaxation needs to occur so that the ATP content of the cell can be decreased by activation of the myosin ATPase, which in turn depends upon an intracellular messenger, elevation of the calcium transient. In a model of cardiac hypertrophy active relaxation is always slower. This slowing accompanies a slowing of the calcium transient, a diminution in the activity of the Na+/Ca2+ exchanger, a change in the properties of Na+, K+ ATPase and a decreased concentration of Ca2+ ATPase in the sarcoplasmic reticulum. (ii) Chamber stiffness is likely to be increased only in relation to the degree of ventricular hypertrophy. The main, if not unique, determinant of ventricular diastolic tissue stiffness is the structure and concentration of the collagen. Consequently tissue stiffness is augmented in cardiac hypertrophy in which the ventricular collagen concentration is elevated. It is important that both clinically and experimentally cases of cardiac hypertrophy, even those resulting from pressure overload in which myocardial stiffness and cardiac collagen concentration remain unchanged, have been documented. A good example of this is the DOCA-salt model of arterial hypertension. (iii) Atrial contraction is normally more rapid than ventricular contraction, the biological basis for which is the difference in isomyosin content. The enhanced atrial contribution to ventricular filling overloads the atria and induces an adaptational modification in the expression of the genes coding for the atrial β myosin heavy chain. (iv) On an isolated heart, global anoxia induces contracture. This phenomenon is exaggerated in cardiac hypertrophy because the hypertrophied myocyte is in a fragile equilibrium in terms of calcium homeostasis.

Key Words: Diastole • relaxation • ventricular compliance • collagen • troponin • heart failure • cardiac hypertrophy • hypertensive heat


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