The imbalance between coronary reserve and wall stress explains the severity of ventricular dysfunction in hypertension

Background: 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 (103·dyn·cm−2) were determined using echocardiography, and coronary reserve was calculated using trans‐esophageal Doppler echocardiography. Coronary reserve/ stress (cm2·dyn−1) 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