Pasternac A, Noble J, Streulens Y, Elie R, Henschke C, Bourassa M G
Circulation. 1982 Apr;65(4):778-89. doi: 10.1161/01.cir.65.4.778.
To clarify the pathogenesis of chest pain in patients with cardiomyopathies, we compared coronary blood flow and other indicators of ischemia at rest and during pacing-induced tachycardia in nine patients with cardiomyopathy (four hypertrophic and five congestive) and in five control subjects. Coronary blood flow was reduced at rest and during pacing in cardiomyopathy patients compared with controls. In patients with hypertrophic cardiomyopathy, pacing induced chest pain in all, increased ST-segment depression in three patients and increased coronary venous lactate concentration. With pacing, two of five patients with congestive cardiomyopathy had chest discomfort and three had increased ST-segment depression, but coronary venous lactate concentration did not change significantly. In both groups of cardiomyopathies, the ratio of the systolic and diastolic pressure-time indexes tended to decrease more than in controls during pacing. Thus, myocardial perfusion is decreased in patients with cardiomyopathy, both at rest and during pacing. The changes detected during pacing point to subendocardial ischemia as the likely mechanism for angina in hypertrophic and possibly also in congestive cardiomyopathy.
为阐明心肌病患者胸痛的发病机制,我们比较了9例心肌病患者(4例肥厚型和5例充血型)及5例对照者静息时和起搏诱发心动过速时的冠状动脉血流及其他缺血指标。与对照组相比,心肌病患者静息时和起搏时冠状动脉血流均减少。肥厚型心肌病患者起搏时均诱发胸痛,3例患者ST段压低增加,冠状动脉静脉血乳酸浓度升高。充血型心肌病5例患者中有2例起搏时出现胸部不适,3例ST段压低增加,但冠状动脉静脉血乳酸浓度无明显变化。两组心肌病患者起搏时收缩压与舒张压时间指数比值下降幅度均大于对照组。因此,心肌病患者静息时和起搏时心肌灌注均降低。起搏时检测到的变化提示心内膜下缺血可能是肥厚型心肌病以及可能充血型心肌病心绞痛的发病机制。