Kurnik P B, Courtois M R, Ludbrook P A
Circulation. 1986 Jul;74(1):126-34. doi: 10.1161/01.cir.74.1.126.
To determine whether alteration of intrinsic myocardial stiffness is responsible for the reduction of left ventricular filling pressure and volume by nifedipine in patients with impaired baseline ventricular function, we evaluated the hemodynamic responses in 32 patients undergoing diagnostic cardiac catheterization. Micromanometric pressure and ventriculographic dimensional data were acquired before and 30 min after randomly assigned administration of nifedipine (20 mg sublingual) or placebo. A mathematical model requiring no assumptions about the stress-radius relationship or direct measurement of strain was used. No hemodynamic variables were changed after placebo. Left ventricular end-diastolic volume and pressure declined and cardiac output increased after nifedipine, particularly in subjects with impaired ventricular performance. Despite these salutary effects, intrinsic myocardial stiffness, elastic stiffness at a common level of stress, chamber stiffness, and rate of isovolumic relaxation were unchanged after nifedipine, even in patients with abnormal baseline ventricular function. The potent peripheral arteriodilator effect of nifedipine, rather than any direct myocardial or ventricular effects, appears to be responsible for the improved systolic and diastolic performance.
为了确定在基线心室功能受损的患者中,心肌固有僵硬度的改变是否是硝苯地平降低左心室充盈压和容积的原因,我们评估了32例接受诊断性心导管检查患者的血流动力学反应。在随机给予硝苯地平(20mg舌下含服)或安慰剂之前和之后30分钟,获取微测压压力和心室造影尺寸数据。使用了一个无需假设应力-半径关系或直接测量应变的数学模型。安慰剂治疗后,血流动力学变量未发生变化。硝苯地平治疗后,左心室舒张末期容积和压力下降,心输出量增加,尤其是在心室功能受损的受试者中。尽管有这些有益作用,但硝苯地平治疗后,心肌固有僵硬度、共同应力水平下的弹性僵硬度、腔室僵硬度和等容舒张速率均未改变,即使在基线心室功能异常的患者中也是如此。硝苯地平强大的外周动脉扩张作用,而非任何直接的心肌或心室效应,似乎是其改善收缩和舒张功能的原因。