Concentric versus eccentric remodeling.

Abstract

Cardiac hypertrophy has long been recognized as one of the heart's mechanisms for compensating a pressure or volume overload. This compensation has often been viewed as a feedback loop in which the concentric hypertrophy, which develops in pressure overload, normalizes wall stress while the eccentric hypertrophy, which develops in volume overload, allows for an increase in total stroke volume to compensate that which is lost from regulation. While the concentric hypertrophy of pressure overload often is compensatory, many examples are noted where either too little hypertrophy occurs to normalize stress or in other cases, in which hypertrophy exceeds the amount needed for normalization. These observations invoke nonmechanical mechanisms which modulate the degree to which the mechanical signal of pressure overload is translated into an increase in myocardial mass. Hypertrophy develops when the rate of myocardial protein synthesis exceeds that of protein degradation. It now appears that in pressure overload this imbalance is created as synthesis rate increases while in volume overload hypertrophy appears to accrue because degradation rate decreases.