The heart in pressure overload is threatened by the development of diastolic and systolic dysfunction even in the absence of coronary heart disease. In pressure overload, systolic wall stress leads to an increase in left ventricular mass through hypertrophy of myocytes. An activation of myocytic as well as non-myocytic cells is present. An increase in interstitial collagen accompanies hypertrophy of the myocytes. Thus, myocytic hypertrophy and fibrosis cause diastolic dysfunction early on, even when systolic function is still well preserved. In hypertensive heart disease, the coronary microcirculation is remodelled by thickening of the walls of intramyocardial arterioles in relation to their lumen and by an increase in periarteriolar fibrosis. This remodelling of the intramyocardial vasculature is combined with a reduction in coronary vasodilator reserve that may lead to malnutrition and malperfusion of the hypertrophied myocytes. The combined processes of myocytic hypertrophy, vascular remodelling and increased fibrosis may be important in the process of ventricular dilatation and failure in hypertensive heart disease.