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Overview on Pathogenesis of Cardiac Hypertrophy

Some of the factors that may be involved in the pathogenesis of cardiac hypertrophy have been reviewed. The hypotheses that transient ATP depletion secondary to increased work load or, alternatively, that increased muscle stretch itself may be the stimuli leading to cardiac hypertrophy have been discussed. The possibility that the myofibrillar and mitochondrial elements are under separate control was considered. In the earliest stages of the development of cardiac hypertrophy, mitochondrial mass and enzyme activation increase, but after longer periods of pressure-induced hypertrophy, mitochondrial mass relative to other cardiac muscle proteins decreases. Data showing the rapid turnover of myocardial components were presented, and the participation of alterations in degradation rate, as well as synthetic rate, in the accumulation of cardiac components was emphasized. For example, the degradation of mitochondrial cytochrome c is decreased during the earliest stages of cardiac hypertrophy following aortic constriction. Experiments showing that cardiac protein and RNA quickly decline after removal of a restricting aortic band indicate that regression of cardiac hypertrophy is a rapid process.