Cardioreparation in hypertensive heart disease

The normal myocardium is composed of a variety of cells. Cardiac myocytes, tethered within an extracellular matrix of fibrillar collagen, represent on e third of all cells; noncardiomyocytes account for the remaining two third s. Ventricular hypertrophy involves myocyte growth. Hypertensive heart dise ase (HHD) includes myocyte and nonmyocyte growth that leads to an adverse s tructural remodeling of the intramural coronary vasculature and matrix. In HHD, it is not the quantity of myocardium but rather its quality that accou nts for increased risk of adverse cardiovascular events. Structural homogen eity of cardiac tissue is governed by a balanced equilibrium existing betwe en stimulator and inhibitor signals that regulate cell growth, apoptosis, p henotype, and matrix turnover. Stimulators (eg, angiotensin II, aldosterone , and endothelins) are normally counterbalanced by inhibitors (eg, bradykin in, NO, and prostaglandins) in a paradigm of reciprocal regulation. To redu ce the risk of heart failure and sudden cardiac death that accompanies HHD, its adverse structural remodeling must be targeted for pharmacologic inter vention. Cardioprotective agents counteract the imbalance between stimulato rs and inhibitors. They include ACE and endopeptidase inhibitors and respec tive receptor antagonists. Cardioreparative agents reverse the growth-promo ting state and regress existing abnormalities in coronary vascular and matr ix structure. ACE inhibition has achieved this outcome with favorable impac t on vasomotor reactivity and tissue stiffness. Today's management of hyper tension should not simply focus on a reduction in blood pressure, it must a lso target the adverse structural remodeling that begets HHD.