LEFT-VENTRICULAR CONTRACTILE PERFORMANCE, VENTRICULOARTERIAL COUPLING, AND LEFT-VENTRICULAR EFFICIENCY IN HYPERTENSIVE PATIENTS WITH LEFT-VENTRICULAR HYPERTROPHY

Contractile performance of hypertrophied left ventricle may be depress ed in arterial hypertension. Ventriculoarterial coupling is impaired w hen myocardial contractile performance is reduced and when afterload i s increased. The left ventricular contractile performance and the vent riculoarterial coupling were evaluated in 30 hypertensive patients wit h moderate left ventricular hypertrophy and 20 control subjects. Left ventricular angiography coupled with the simultaneous recording of pre ssures with a micromanometer were used to determine end-systolic stres s/volume index, the slope of end-systolic pressure-volume relationship , ie, end-systolic elastance, effective arterial elastance, external w ork, and pressure-volume area. In hypertensive patients, left ventricu lar contractile performance, as assessed by end-systolic elastance/100 g myocardial mass, was depressed (4.35 +/- 1.13 v 5.21 +/- 1.89 mm Hg /mL/100 g in control subjects P <.02), when end-systolic stress-to-vol ume ratio was comparable in the two groups (3.85 +/- 0.99 g/cm(2)/mL i n hypertensive patients versus 3.51 +/- 0.77 g/cm(2)/ml in control sub jects). Ventriculoarterial coupling, evaluated through effective arter ial elastance/end-systolic elastance ratio, was slightly higher in hyp ertensive patients (0.53 +/- 0.08 v 0.48 +/- 0.09 mm Hg/mL in control subjects, P <.05), and work efficiency (external work/pressure-volume area) was similar in the two groups (0.78 +/- 0.04 mm Hg/mL in hyperte nsive patients versus 0.80 +/- 0.03 mm Hg/mL in control subjects). Thi s study shows that despite a slight depression of left ventricular con tractile performance, work efficiency is preserved and ventriculoarter ial coupling is almost normal in hypertensive patients with left ventr icular hypertrophy. Thus, it appears that left ventricular hypertrophy might be a useful means of preserving the match between left ventricl e and arterial receptor with minimal energy cost. Am J Hypertens 1998; 11:1188-1198 (C) 1998 American Journal of Hypertension, Ltd.