REMODELING OF INTRAMYOCARDIAL ARTERIOLES AND EXTRACELLULAR-MATRIX IN PATIENTS WITH ARTERIAL-HYPERTENSION AND IMPAIRED CORONARY RESERVE

The heart in pressure overload is threatened by the development of dia stolic and systolic dysfunction even in the absence of coronary artery disease. In pressure overload, systolic wall stress leads to an incre ase in left ventricular mass through hypertrophy of myocytes. An activ ation of myocytic as well as non-myocytic cells is present. An increas e in interstitial collagen accompanies hypertrophy of the myocytes. Th us, myocytic hypertrophy and fibrosis cause diastolic dysfunction earl y on, even when systolic function is still well preserved. In hyperten sive heart disease, the coronary microcirculation is remodelled by thi ckening of the walls of intramyocardial arterioles in relation to thei r lumen and by an increase in periarteriolar fibrosis. This remodellin g of the intramyocardial vasculature is combined with a reduction in c oronary vasodilator reserve that may lead to malnutrition and malperfu sion of the hypertrophied myocytes. The combined processes of myocytic hypertrophy, vascular remodelling and increased fibrosis may be impor tant in the process of ventricular dilatation and failure in hypertens ive heart disease.