PATHOPHYSIOLOGICAL PRINCIPLES OF THE RELATION BETWEEN MYOCARDIAL HYPERTROPHY OF THE LEFT-VENTRICLE AND ITS REGRESSION

Authors
Citation
F. Simko, PATHOPHYSIOLOGICAL PRINCIPLES OF THE RELATION BETWEEN MYOCARDIAL HYPERTROPHY OF THE LEFT-VENTRICLE AND ITS REGRESSION, Physiological Research, 43(5), 1994, pp. 259-266
Citations number
61
Categorie Soggetti
Physiology
Journal title
ISSN journal
08628408
Volume
43
Issue
5
Year of publication
1994
Pages
259 - 266
Database
ISI
SICI code
0862-8408(1994)43:5<259:PPOTRB>2.0.ZU;2-Y
Abstract
Hypertrophy of the left heart ventricle as a consequence of a haemodyn amic overload is a process of ambiguous biological value. Although hyp ertrophy allows to increase the performance of the ventricle without s ubstantial elevation in wall tension, it represents a risk factor of c ardiac morbidity and mortality. The regression of hypertrophy seems to be a rational outcome of this ambivalent situation. Not every reversa l of hypertrophied muscle mass, however, can be unambiguously consider ed therapeutic success. The biological value of hypertrophy regression depends on the type of hypertrophy, on the level of deterioration of the heart by a longlasting haemodynamic overload, as well as on the wa y in which the reversal of hypertrophy is achieved. Even in the case w hen functional characteristics are preserved or even improved compared to the hypertrophied heart, hypertrophy regression need not automatic ally mean a decrease of the cardiovascular risk induced by ventricular hypertrophy. Regression of hypertrophy may be even disadvantageous in those situations when reduction of hypertrophy and reduction of the h aemodynamic overload proceed in a disproportional manner. Spontaneousl y developing regression of the hypertrophied left ventricle as demonst rated on the model of aortal insufficiency, is an explicitly pathologi cal state, resulting in heart failure. Regression of myocardial hypert rophy should not be considered the primary therapeutic aim but rather a part of the management of haemodynamic overload of the heart. The ma in aim is to achieve optimal perfusion of the periphery, yet at the sa me time to provide such conditions which would prevent the working loa d of the heart to become a limiting factor of survival.