SummaryBackground: The pathophysiologic role of coronary reserve impairment in hypertensive cardiac dysfunction is still debated. Previously, we demonstrated that satisfactory coronary vasodilatation may coexist with ventricular systolic dysfunction. It is conceivable that coronary reserve might otherwise be inappropriate for enhanced myocardial oxygen demand and may thus affect cardiac performance negatively.Hypothesis: Myocardial supply-demand imbalance contributes to the severity of ventricular dysfunction in hypertension (HTN).Methods: Fractional shortening (%) and end-systolic stress (10 3 ·dyn·cm Ϫ2 ) were determined using echocardiography, and coronary reserve was calculated using transesophageal Doppler echocardiography. Coronary reserve/ stress (cm 2 ·dyn Ϫ1 ) was utilized as a measure of supply-demand. Groups NL (20 healthy subjects), HTN1 (15 patients, fractional shortening ≥ 30), HTN2 (19 patients, 20 ≤ fractional shortening < 30), and HTN3 (21 patients, fractional shortening < 20) were constituted.Results: Compared with NL and HTN1, groups HTN2 and HTN3 had significantly (p < 0.05) greater end-systolic stress (NL = 72 ± 16, HTN1 = 72 ± 23, HTN2 = 143 ± 32, HTN3 = 186 ± 70). Coronary reserve was impaired in HTN3 alone (NL = 3.5 ± 0.6, HTN1 = 3.4 ± 1.0, HTN2 = 3.1 ± 1.0, HTN3 = 2.6 ± 1.1), but coronary reserve/stress was reduced in both