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

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<0·01), peak LV systolic pressure from 211±8 to 169±4 mmHg (P<0·01) and LV enddiastolic pressure from 22±3 to 13±2 mmHg (P<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<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 increasedfrom 43±4 to 54±4 ms (P<0·01). Early diastolic LV pressure decay was assessed by θ (phase of the first harmonic of a Fourier transform applied to the diastolic LV pressure waves). After PESP, θ decreased from 41±4° to 26±5° (P <0·01). This slower early diastolic LV pressure decay impedes LV inflow by reducing early mitral valve flow velocity from 0·58±0·06 to 0·52±0·05 ms−1 (P<0·01) and by slowing deceleration of early diastolic flow from 4·9±0·7 to 3·1±0·7 ms−2 (P<0·01). In conclusion, the small decrease of T and the constancy of LV filling rate after PTAV, implies reduced load dependence of LV relaxation in AS. PESP markedly slows isovolumic and early diastolic LV pressure decay and impedes LV inflow. A transient imbalance between the increased amount of activator calcium induced by PESP and the slow inactivation of hypertrophied myocardium explains these findings. Both the effects of PTAV and of PESP suggest myocardial inactivation to be the predominant control mechanism of LV relaxation in AS.