Abstract
Cardiac hypertrophy is an adaptive process which occurs as a result of increased stress endured by the heart and this cardiac remodeling serves as a reactive mechanism to compensate for volume overload or pressure overload. An increase in pressure, common in hypertension or resistance training, results in a concentric hypertrophic phenotype whereas an increase in volume, as seen with valvular defects or endurance training, results in an eccentric hypertrophic phenotype. Concentric hypertrophy is associated with increased left ventricular wall thickness whereas eccentric hypertrophy is characterized by dilatation of the left ventricular chamber; however, there occurs a general increase in the overall size of cardiomyocytes under both conditions. Although various hormonal systems are activated during the development of cardiac hypertrophy, differences in the type of ventricular wall stress and strain seem to determine the occurrence of eccentric or concentric remodeling in addition to changes in myocardial structure. There are variations between the eccentric and concentric hypertrophic phenotypes with respect to gene and protein expression, signaling transduction pathways, and local hormone release. Both types of cardiac hypertrophy are known to occur under physiological and pathological situations; the lack of inflammatory response and fibrosis in the heart differentiates physiological from pathological hypertrophy. It is suggested that concentric and eccentric hypertrophy are the result of differences in the effects of increased ventricular wall tension superimposed by the impact of hormones released locally in the heart in response to stress.
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