Increased cardiac performance in mild essential hypertension. Left ventricular mechanics.

To analyze cardiovascular dynamics in essential hypertension, 81 subjects with untreated mild essential hypertension (mean blood pressure, 112 +/- 14 mm Hg) and 87 normotensive subjects from the same working population were studied by echocardiography and simultaneous blood pressure determination. Hypertensive subjects had significantly higher pulse pressure, stroke volume index, cardiac index, left ventricular internal dimension, end-systolic pressure/volume ratio, end-systolic stress, left ventricular mass index, and relative wall thickness than normotensive subjects. Among both normotensive and hypertensive subjects, cardiac performance was closely dependent on afterload, as indicated by close inverse linear relationships between left ventricular fractional shortening and log end-systolic stress (r = -0.83 and -0.78 respectively; both, p less than 0.001). However, 19 of 81 hypertensive patients (23%) fell above the 95% confidence limits of this relationship in normotensive subjects (p less than 0.001 compared with that in normotensive subjects), with a bimodal distribution of fractional shortening as a percent of predicted in relation to end-systolic stress among patients with essential hypertension. This subgroup of hypertensive subjects, with increased resting cardiac performance independent of afterload, was similar in age to the remaining hypertensive subjects but had higher fractional shortening (41 +/- 5% vs 35 +/- 7%; p less than 0.001) and cardiac index (4.3 +/- 1.3 L/min/m2 vs 3.4 +/- 1.0 L/min/m2; p less than 0.005) and lower total peripheral resistance (1257 +/- 502 dyn sec cm-5 vs 1582 +/- 584 dyn sec cm-5 p less than 0.05) and left ventricular relative wall thickness (0.34 +/- 0.06 vs 0.42 +/- 0.10; p less than 0.005). Thus, analysis of cardiac mechanics detected a subset of patients with essential hypertension in whom increased cardiac function cannot be attributed either to relative youth or to supercompensatory left ventricular hypertrophy.