Impaired relaxation of the hypertrophied left ventricle in aortic stenosis: effects of aortic valvuloplasty and of postextrasystolic potentiation

Abstract

Impaired left ventricular (LV) filling in aortic stenosis (AS) is explained by slow LV pressure decay, which impedes LV inflow. This slow LV pressure decay could be explained by the altered myocardial wall stress pattern of AS or by a failure of inactivation of hypertrophied myocardium. To evaluate whether altered LV loading or impaired myocardial inactivation is the predominant control of LV relaxation and filling in AS, we studied the effects of aortic valvuloplasty (PTAV) and of postextrasystolic potentiation (PESP). LV micromanometer tip pressure recordings and simultaneous LV angiograms were obtained before and after PTAV in 10 patients with AS. PTAV reduced peak-to-peak aortic valve gradient from 101 +/- 7 to 40 +/- 5 mmHg (P less than 0.01), peak LV systolic pressure from 211 +/- 8 to 169 +/- 4 mmHg (P less than 0.01) and LV end-diastolic pressure from 22 +/- 3 to 13 +/- 2 mmHg (P less than 0.01). Despite these large drops of LV loading after PTAV, the time constant, T, of LV pressure decay decreased only slightly from 47 +/- 4 to 44 +/- 4 ms (P less than 0.05) and the LV peak filling rate remained unaltered. The influence of PESP on LV relaxation and filling was investigated in patients with AS using LV micromanometer tip pressures (n = 22) and simultaneous mitral valve Doppler echocardiograms (n = 9). After PESP the time constant, T, of isovolumic LV pressure decay increased from 43 +/- 4 to 54 +/- 4 ms (P less than 0.01).2+ 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)