[Cardiac structure-function relationship and the renin-angiotensin-aldosterone system in hypertensive heart disease].

Based on the epidemiologic data of the Framingham heart study, arterial hypertension and coronary artery disease are the most frequent etiologic factors for the development of heart failure. In the pressure overloaded heart, hypertrophic growth of the myocardium includes the enlargement of cardiac myocytes stimulated by ventricular loading. Non-myocyte cell growth involving cardiac fibroblasts may also occur but is not primarily regulated by the hemodynamic load. Cardiac fibroblast activation is responsible for the accumulation of fibrillar type I and type III collagens within the interstitium while vascular smooth muscle cell growth accounts for the medial thickening of resistance vessels. This remodeling of the cardiac interstitium represents a major determinant of pathological hypertrophy in that it accounts for abnormal myocardial stiffness and impaired coronary vasodilator reserve, leading to ventricular diastolic and systolic dysfunction and ultimately to the appearance of symptomatic heart failure. Several lines of evidence suggest that the renin-angiotensin-aldosterone system is involved in regulating the structural remodeling of the nonmyocyte compartment, including the cardioprotective effects of angiotensin converting enzyme (ACE) inhibition that was found to prevent myocardial fibrosis in the rat with renovascular hypertension. In rats with genetic hypertension, established left ventricular hypertrophy, abnormal diastolic stiffness due to interstitial fibrosis, and reduced coronary vasodilator reserve associated with medial wall thickening of intramyocardial resistance vessels, the ACE inhibitor lisinopril was able to restore myocardial structure and function to normal. These cardioreparative properties of ACE inhibition may be valuable in reversing left ventricular dysfunction in hypertensive heart disease.