Paulus W J, Sys S U, Nellens P, Heyndrickx G R, Andries E
Cardiovascular Center, O.L.V. Ziekenhuis, Aalst, Belgium.
Circulation. 1988 Oct;78(4):928-40. doi: 10.1161/01.cir.78.4.928.
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 increases of LV dP/dtmax after PESP in all three study groups, PESP affected LV hemodynamic relaxation indexes differently. The time constant of LV pressure decay (TPB) 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 less than 0.02) in patients with AS, and rose from 74 +/- 18 to 84 +/- 19 msec (p less than 0.02) in patients with HCM. Early diastolic LV pressure decay was measured by phi (phase of the first harmonic of a Fourier transform applied to the diastolic LV pressure waves) and by t (time interval from LV dP/dtmin to LV minimum diastolic pressure). After PESP, phi remained unaltered in normal controls but decreased in AS from 42.8 +/- 19.1 degrees to 24.0 +/- 28.8 degrees (p less than 0.001) and in HCM from 39.7 +/- 15.4 degrees to 26.9 +/- 15.7 degrees (p less than 0.001). Similarly, t was unchanged after PESP in normal controls but prolonged in AS from 146 +/- 48 to 205 +/- 86 msec (p less than 0.001) and in HCM from 168 +/- 40 to 208 +/- 53 msec (p less than 0.02).(ABSTRACT TRUNCATED AT 400 WORDS)
主动脉瓣狭窄(AS)和肥厚型心肌病(HCM)患者左心室(LV)充盈受损是由左心室压力缓慢衰减所致,这可能是由于肥厚心肌失活受抑制引起的。早搏后增强(PESP)可增加激活钙,可能导致左心室舒张功能进一步恶化。因此,研究人员在正常对照组以及由AS或HCM引起的左心室肥厚患者中,探究了PESP对左心室充盈动力学的影响。在正常窦性心律(NSR)期间以及PESP后,测定左心室血流动力学和左心室血流动力学舒张指标。通过微测压导管记录左心室压力(对照组,n = 10;AS组,n = 17;HCM组,n = 11)。对左心室肥厚患者(AS组,n = 8;HCM组,n = 5)进行同步二尖瓣血流多普勒超声心动图检查。尽管在所有三个研究组中,PESP后左心室dP/dtmax显著增加,但PESP对左心室血流动力学舒张指标的影响各不相同。在正常对照组中,PESP后从非零渐近线压力的指数曲线拟合得出的左心室压力衰减时间常数(TPB)保持不变;在AS患者中,TPB从62±17毫秒升至74±21毫秒(p<0.02);在HCM患者中,TPB从74±18毫秒升至84±19毫秒(p<0.02)。通过phi(应用于舒张期左心室压力波的傅里叶变换的一次谐波相位)和t(从左心室dP/dtmin到左心室最小舒张期压力的时间间隔)测量舒张早期左心室压力衰减。PESP后,正常对照组中的phi保持不变,但在AS患者中从42.8±19.1度降至24.0±28.8度(p<0.001),在HCM患者中从39.7±15.4度降至26.9±15.7度(p<0.001)。同样,正常对照组中PESP后t不变,但在AS患者中从146±48毫秒延长至205±86毫秒(p<0.001),在HCM患者中从168±40毫秒延长至208±53毫秒(p<0.02)。(摘要截断于400字)