Factors associated with reactive and reparative fibrosis of the myocardium.

Abstract

Myocardial fibrosis can be defined as an abnormal increase in collagen concentration of either ventricle. This accumulation of collagen, represented predominantly by fibrillar type I collagen, can occur a) on a reactive basis in the interstitial space and adventitia of intramyocardial coronary arteries and does not require myocyte necrosis, or b) as a replacement for necrotic myocytes, where it is considered a scar. Both forms can be found in the same ventricle. Various factors have been found to contribute to the reactive and reparative fibrosis that appears in both ventricles in acquired hypertension. In the case of microscopic scarring, myocyte necrosis is related to catecholamine or angiotensin II- mediated toxicity, reduced potassium stores that accompany chronic mineralocorticoid excess, and coronary vascular remodeling. Reactive fibrosis is associated with elevations in plasma aldosterone concentrations that are inappropriate relative to dietary sodium intake. These findings set the stage for additional in vivo and in vitro studies that may shed more light on our understanding of the factors that regulate the accumulation of fibrous tissue in the myocardium--a major determinant of pathologic structural remodeling which enhances its susceptibility to reentrant arrhythmias and ventricular dysfunction.