To study the cardiac determinants of regression of left ventricular hypertrophy in hypertension, left ventricular mass, fractional shortening and end-systolic wall stress were measured echocardiographically in 36 patients with essential hypertension and left ventricular hypertrophy. The patients were classified into two groups. Group I consisted of 15 patients with subnormal end-systolic wall stress, and Group II consisted of 21 patients with normal end-systolic wall stress. There were no significant differences between groups in systolic or diastolic blood pressure. After treatment for 4.4±1.7 years, echocardiographic studies were repeated. There were no significant differences between groups in the duration of the follow-up period and the kinds of antihypertensive drugs. After treatment, blood pressure decreased significantly in both groups (p < 0.001 for both), with no significant difference between groups. Left ventricular mass increased significantly in Group I (from 331 ± 7 to 363 ± 24 g, mean ± SEM, p < 0.05), whereas it decreased significantly in Group II (from 318 ± 16 to 268 ± 17 g, p < 0.001). Myocardial contractility (the relation between end-systolic wall stress and fractional shortening) remained almost the same as before treatment. In conclusion, in patients with hypertensive ventricular hypertrophy with subnormal end-systolic wall stress (inappropriate hypertrophy, probably induced by a neurohumoral factor), a decrease in blood pressure with antihypertensive treatment does not lead to regression of left ventricular hypertrophy, but rather to an increase in left ventricular mass. In patients with normal end-systolic wall stress (appropriate hypertrophy, probably induced by high arterial pressure) antihypertensive treatment decreases left ventricular mass if it has the potency to cause regression of hypertrophy. © 1990.