Proposes the concept of 'cardiomyopathy of overload' to explain the progressive deterioration of the failing heart and provides a pathophysiological rationale for the protective role of ACE inhibitors.
Progressive deterioration of the failing heart is now recognized to be a major cause of disability and death in patients with congestive heart failure. It appears that although the normal human heart functions for at least 90-100 years, overload-induced hypertrophy shortens the heart's life span to about 5 years. This accelerated deterioration of the failing heart can be viewed as a cardiomyopathy of overload in which chronic overloading causes changes in the myocardial cells that, while increasing cell mass, reduce their long-term viability. Although the pathogenesis of this putative cardiomyopathy remains poorly understood, chronic energy starvation and altered myocardial cell growth and composition appear to be contributing factors. Preferential expression of fetal isoforms of key muscle proteins, which accompanies accelerated growth of the overloaded heart, may contribute to this cardiomyopathy. The hypothesis that the cardiomyopathy of overload is due in part to a growth abnormality is supported by evidence that deterioration of the failing heart is slowed by the converting enzyme inhibitors, which may attenuate important effects of angiotensin II to stimulate cellular growth.
Arnold M. Katz (Tue,) studied this question.