The cardiac hypertrophy process. Analyses of factors determining pathological vs. physiological development.

Abstract

COMPLICATED and even contradictory concepts concerning the biochemical and physiological aspects of cardiac hypertrophy are less enigmatic if we first discern whether the type of hypertrophy analyzed is physiological or pathological; i.e., whether factors secondary to the process of hypertrophy have induced the heart to augment or depress its mechanical function. In this review physiological hypertrophy is defined as hypertrophy accompanied by a normal or augmented contractile state in which the maximum rate at which myosin hydrolyzes ATP and the maximum velocity of muscle shortening are either normal or elevated. Pathological hypertrophy, on the other hand, is associated with depressed contractility without necessarily concordant heart failure, in which case the rate of myosin ATPase activity and the velocity of muscle shortening are decreased. Both types of hypertrophy may be considered compensatory in that the heart biochemically and physiologically adjusts to cellular alterations that occur according to the severity of the workload. Thus, our definition is not the same as that provided by Meerson (1976), since he did not distinguish between the two types of hypertrophy described here.To understand better the evolution of the cardiac hypertrophy process into physiological or pathological hypertrophy, this review is concerned with the immediate inciting stimuli of cardiac hypertrophy, the mechanism of its development, the various stages in its development, and its regional localization. We also are concerned with the dependency of

Physiologic or pathologic hypertrophy

“…Conversely in muscle mass is associated with normal or enhanced pathological hypertrophy there is no or only myocardial function, hypertrophy is termed physio-incomplete reversibility of morphological alterations. logical" 1 1 ". The prototype of physiological hypertrophy is the These definitions do not take into account the hypertrophy consequent to exercise conditioning.…”

Sanguineous normothermic, intermittent cardioplegia, effects on hypertrophic myocardium. Morphometric, metabolic and ultrastructural studies in rabbits hearts

“…Morphometric, metabolic and ultrastructural studies in rabbits hearts and 3.9 for obvious failure. In this initial understanding of myocardial hypertrophy, it is reasonable to distinguish two types of cardiac hypertrophy: a physiological normal or increased contractility, and, a pathologically reduced contractile function [22].…”

Beta-adrenergic pathway in healthy and hypertrophied hearts

“…When this balance is broken due to abnormal overload, the heart responds with the development of hypertrophy. Depending on the characteristics of the overload imposed (type, intensity and installation mode) and the animal undergoing the overload (age, gender and species), the hypertrophied tissue may show normal or altered biologic properties (in RNA, protein and myosin synthesis, in energetic metabolism and mainly in the intracellular Ca 2+ cycle) [42][43][44][45] . …”

“…Cardiac hypertrophy should not be understood only as an expansion of the contractile complex, because the hypertrophy process is characterized by an increase in the synthesis of ribonucleic acid (RNA), proteins and myosins, and induction of new genetic expressions of protein synthesis 42 . Therefore, as proteins, the components of the β− adrenergic pathway may undergo changes during the development of cardiac hypertrophy.…”