Progress in Hypertensive Heart Disease. Remodeling Mechanisms Involved in the Transition from Hypertrophy to Heart Failure

Abstract

At the molecular level, hypertensive heart disease is characterized by a combination of changes in myocardial gene and protein expression that induce a series of alterations in the structure of the myocardium, thereby giving rise to structural and geometric remodeling as well as to changes in myocardial function, perfusion and electrical activity. Remodeling results from the effects both hypertension-induced mechanical overload and local activation of various humoral factors have on cardiomyocytes (inducing cell death by apoptosis) and on the extracellular matrix (resulting in changes in the density and deposition of collagen fibers). The clinical significance of these lesions stems from their contribution to the transition from left ventricular hypertrophy to heart failure in patients with hypertensive heart disease. Recent findings indicate that ventricular hypertension may be associated with novel apoptotic and fibrotic mechanisms (e.g., alterations in peroxisome proliferator-activated receptor-) that may lead to new approaches to the prevention of heart failure in patients with hypertensive heart disease.