Fenster M S, Feldman M D, Camarano G, Johnson W H, Ellis M, Linden J, Beller G A
Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville 22908, USA.
Am Heart J. 1997 Apr;133(4):406-12. doi: 10.1016/s0002-8703(97)70181-9.
To determine the frequency of true myocardial ischemia caused by hemodynamic, metabolic, and regional functional abnormalities after intravenous adenosine infusion in patients with coronary artery disease, 13 patients--11 with coronary artery disease--received intravenous adenosine and thallium 201 during cardiac catheterization. Intracoronary adenosine levels increased by an average of 9.4-fold over baseline. Of the 11 patients, all had > or = 70% stenoses with a mean number of redistribution defects per patient of 3.3 +/- 0.7. Only two (18%) patients had new wall motion abnormalities detected by echocardiography during adenosine infusion. Pulmonary capillary wedge pressure did not significantly rise (13 +/- 7 to 17 +/- 8 mm Hg, p= NS). Lactate production occurred in two patients. Coronary sinus oxygen saturation levels rose from 29% +/- 6% to 68% +/- 8%, consistent with less myocardial oxygen extraction. Thus, despite a high prevalence of defects detected by 201Tl, the prevalence of true myocardial ischemia in patients with coronary artery disease undergoing pharmacologic stress imaging with intravenous adenosine is low. Perfusion defects induced by vasodilator stress are predominantly caused by heterogeneity of flow reserve rather than true ischemia.
为了确定冠心病患者静脉注射腺苷后,由血流动力学、代谢及局部功能异常所导致的真正心肌缺血的发生率,13例患者(其中11例患有冠心病)在心脏导管插入术期间接受了静脉注射腺苷和铊201。冠状动脉内腺苷水平平均比基线升高了9.4倍。在这11例患者中,所有患者均有≥70%的狭窄,每位患者平均再分布缺损数为3.3±0.7。腺苷注射期间,只有2例(18%)患者经超声心动图检测发现有新的室壁运动异常。肺毛细血管楔压没有显著升高(从13±7 mmHg升至17±8 mmHg,p=无显著性差异)。2例患者出现乳酸生成。冠状窦血氧饱和度水平从29%±6%升至68%±8%,这与心肌氧摄取减少一致。因此,尽管通过铊201检测到的缺损发生率很高,但接受静脉注射腺苷进行药物负荷成像的冠心病患者中真正心肌缺血的发生率很低。血管扩张剂负荷诱导的灌注缺损主要是由血流储备的异质性而非真正的缺血引起的。