The cardiac hypertrophy process. Analyses of factors determining pathological vs. physiological development.
Author(s) -
Joan WikmanCoffelt,
W.W. Parmley,
D. T. Mason
Publication year - 1979
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/01.res.45.6.697
Subject(s) - pathological , muscle hypertrophy , cardiac hypertrophy , medicine , heart failure , cardiology
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.
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