Nishimura S, Kimball K T, Mahmarian J J, Verani M S
Department of Medicine, Baylor College of Medicine, Houston, Tex.
Circulation. 1993 Apr;87(4):1211-9. doi: 10.1161/01.cir.87.4.1211.
Myocardial ischemia attributed to coronary steal may occur in some patients receiving pharmacological coronary vasodilation. ECG ST-segment depression is a marker of myocardial ischemia in these patients, but the factors determining the presence or absence of ischemia are not well known.
To examine the angiographic, hemodynamic, and scintigraphic determinants of adenosine-induced ischemic ST-segment depression in patients with coronary artery disease, we studied 65 consecutive patients (45 men and 20 women; mean age, 65 +/- 12 years) who showed reversible perfusion defects during adenosine (140 micrograms.kg-1.min-1 for 6 minutes) 201Tl single-photon emission computed tomography. Patients with prior myocardial infarction were excluded. Ischemic ST depression occurred in one third of the whole cohort (22 of 65 patients). The presence of coronary collateral vessels (p = 0.001), systolic blood pressure at baseline (p = 0.006), and adenosine-induced anginal chest pain (p = 0.011) were the only significant independent predictors of ischemic ST-segment depression by stepwise logistic regression analysis. Rate-pressure product at baseline, systolic blood pressure, heart rate, rate-pressure product, increase in heart rate, and rate-pressure product during adenosine infusion and maximal percent stenosis were variables also significantly related to ischemic ST depression by univariate analysis but were not predictive after the three primary variables were included in the regression model. Perfusion defect size, number of diseased vessels, and age did not correlate with ST-segment depression.
The presence of collaterals, which may predispose to coronary collateral steal, is the most significant correlate of ischemic ST-segment depression during adenosine infusion. Systolic blood pressure at baseline, which may affect the myocardial oxygen supply/demand ratio and anginal chest pain induced by adenosine, are additional variables related to ischemic ST-segment depression during adenosine infusion.
在一些接受药物性冠状动脉扩张的患者中，可能会发生因冠状动脉窃血导致的心肌缺血。心电图ST段压低是这些患者心肌缺血的一个标志，但决定缺血是否存在的因素尚不清楚。
为了研究冠状动脉疾病患者中腺苷诱发的缺血性ST段压低的血管造影、血流动力学和闪烁显像决定因素，我们连续研究了65例患者（45例男性和20例女性；平均年龄65±12岁），这些患者在静脉注射腺苷（140μg·kg-1·min-1，持续6分钟）期间201Tl单光子发射计算机断层扫描显示有可逆性灌注缺损。排除既往有心肌梗死的患者。在整个队列中有三分之一的患者（65例中的22例）出现缺血性ST段压低。通过逐步逻辑回归分析，冠状动脉侧支血管的存在（p=0.001）、基线收缩压（p=0.006）和腺苷诱发的心绞痛（p=0.011）是缺血性ST段压低的仅有的显著独立预测因素。通过单变量分析，基线心率血压乘积、收缩压、心率、心率血压乘积、心率增加以及腺苷输注期间的心率血压乘积和最大狭窄百分比也是与缺血性ST段压低显著相关的变量，但在回归模型中纳入三个主要变量后，它们并无预测价值。灌注缺损大小、病变血管数量和年龄与ST段压低无关。
可能易发生冠状动脉侧支窃血的侧支血管的存在，是腺苷输注期间缺血性ST段压低的最显著相关因素。基线收缩压可能影响心肌氧供需比和腺苷诱发的心绞痛，是腺苷输注期间与缺血性ST段压低相关的其他变量。
