Postextrasystolic potentiation worsens fast filling of the hypertrophied left ventricle in aortic stenosis and hypertrophic cardiomyopathy

Abstract

Impaired left ventricular (LV) filling in aortic stenosis (AS) and in hypertrophic cardiomyopathy (HCM) is caused by slow LV pressure decay, which could be explained by depressed inactivation of hypertrophied myocardium. Postextrasystolic potentiation (PESP), which increases activator calcium, could lead to further deterioration of LV relaxation. The influence of PESP on LV filling dynamics was, therefore, investigated in normal controls and in patients with LV hypertrophy caused by AS or by HCM. LV hemodynamics and LV hemodynamic relaxation indexes were determined during normal sinus rhythm (NSR) and after PESP. LV pressures were recorded by micromanometer tip catheters (controls, n = 10; AS, n = 17; HCM, n = 11). Simultaneous mitral flow Doppler echocardiograms were obtained in patients with LV hypertrophy (AS, n = 8, HCM, n = 5). Despite significant increased LV/dP/dt(max) after PESP in all three study groups, PESP affected LV hemodynamic relaxation indexes differently. The time constant of LV pressure decay (T(PB)) derived from exponential curve fits with nonzero asymptote pressure remained unaltered after PESP in normal controls, rose from 62 ± 17 to 74 ± 21 msec (p < 0.02) in patients with AS, and rose from 74 ± 18 to 84 ± 19 msec (p < 0.02) in patients with HCM. Eearly diastolic LV pressure decay was measured by ∅ (phase of the first harmonic of a Fourier transform applied to the diastolic LV pressure waves) and by t (time interval from LV dP/dt(min) to LV minimum diastolic pressure). After PESP, ∅ remained unaltered in normal controls but decreased in AS from 42.8 ± 19.1° to 24.0 ± 28.8° (p < 0.001) and in HCM from 39.7 ± 15.4° to 26.9 ± 15.7° (p < 0.001). Similarly, t was unchanged after PESP in normal controls but prolonged in AS from 146 ± 48 to 205 ± 86 msec (p < 0.001) and in HCM from 168 ± 40 to 208 ± 53 msec (p < 0.02). The slower early diastolic LV pressure decay after PESP reduced peak flow velocity in early diastole (AS-NSR, 0.57 ± 0.57 2+ 0.19 m/sec vs. AS-PESP, 0.51 ± 0.17 m/sec; p < 0.05) (HCM-NSR, 0.67 ± 0.22 m/sec vs. HCM-PESP, 0.57 ± 0.23 m/sec; p < 0.01) and deceleration of early diastolic flow (AS-NSR, 4.6 ± 1.9 m/sec2 vs. AS-PESP, 2.9 ± 2.3 m/sec2; p < 0.05) (HCM-NSR, 5.8 ± 1.8 m/sec2 vs. HCM-PESP, 4.3 ± 2.1 m/sec2; p < 0.01). In conclusion, PESP slows isovolumic and early diastolic LV pressure decay in patients with AS and HCM but not in normal controls. This slower LV pressure decay after PESP impedes early diastolic inflow into the hypertrophied LV and could be explained by a worsening of the imbalance between activator calcium and depressed inactivation of hypertrophied myocardium.