Cardiac Remodeling and Its Prevention

Abstract

Cardiac chambers have the capacity to alter (remodel) their size and configuration in response to a chronic change in their hemodynamic load. Whether across or within species, the mass and volume of the ventricular chambers maintain a close relationship with the required external work. The changes in chamber volume and mass that accompany normal growth provide the most striking example of the heart’s intrinsic capacity to remodel in response to the insidious alterations in demand that take place as a consequence of body growth. Under pathologic conditions of chronic pressure or volume overload, the chamber remodels in direct relation to the imposed hemodynamic burden. The mass increase is attributable to both myocyte hypertrophy and growth of nonmyocyte interstitial components. However, the manner of rearrangement of these additional contractile tissues can lead to either an eccentric (chamber volume > mass) or a concentric (chamber mass > volume) pattern of ventricular growth. Although remodeling in response to a pathologic condition can in one sense be considered adaptive because it permits the restoration of pump function in the face of an imposed hyperfunctional condition, the extent of ventricular remodeling is nevertheless an important marker for poor prognosis.