Coronary circulation and left ventricular function in hypertension

In hypertensive heart disease, coronary vasodilatory capacity can be reduced owing to vascular, myocardial, extravascular compressive and metabolic factors, all of which may predispose to myocardial ischaemia and consequently ventricular dysfunction. Vascular alterations at the level of the intramural arterioles are characterized by medial hypertrophy and perivascular fibrosis, as well as by an endothelial dysfunction leading to an inappropriate vasodilator function and an increased vasoconstrictor response. Functional and structural alterations of the intramyocardial vasculature may even precede the development of left ventricular hypertrophy, which may further reduce coronary microcirculation by scar formation and increased end-diastolic pressure. In dilated hearts, coronary reserve is further reduced by an increased metabolic demand. Anti-hypertensive therapy in acute hypertensive situations should aim to reduce afterload, lower metabolic demand and increase myocardial coronary blood flow. Long-term anti-hypertensive therapy aims to achieve reparation of the vasculature and regression of myocardial hypertrophy and fibrosis, consequently improving systolic and diastolic function.