Patel D J, Knight C J, Holdright D R, Mulcahy D, Clarke D, Wright C, Purcell H, Fox K M
Department of Cardiology, Royal Brompton Hospital, London, United Kingdom.
Circulation. 1997 Mar 4;95(5):1185-92. doi: 10.1161/01.cir.95.5.1185.
Transient ischemia in stable coronary disease peaks in the morning, reflecting increased myocardial oxygen demand and coronary vasomotor tone after walking. In acute coronary syndromes, however, ischemia may result from transient thrombus formation or coronary spasm at the site of a ruptured plaque. We report on the pathophysiological mechanisms underlying transient ischemia in acute coronary syndromes despite optimal therapy, on the basis of analysis of heart rate changes preceding ischemia and its circadian variation.
Two hundred fifty-six patients with unstable angina or non-Q-wave myocardial infarction underwent continuous ST-segment monitoring for 48 hours while receiving maximal medical therapy. All ischemic episodes were characterized by their timing, duration, association with pain, and heart rate changes before the onset of ischemia. During 10,629 hours of monitoring, 44 patients (17.2%) had 176 episodes of transient ischemia. The mean heart rate at onset of ischemia was 68 +/- 12.8 bpm, and > 55% of ischemic episodes were not preceded by a significant increase in heart rate. Ischemic activity had a single nocturnal peak, with 64% of all episodes occurring between 10 PM and 8 AM, this nocturnal preponderance being evident for episodes with or without a preceding increase in heart rate. The characteristics and timing of transient ischemia were similar in unstable angina and non-Q-wave myocardial infarction, but transient ischemia was more frequent (27.3% versus 15.1%; P < .05) and prolonged (median, 20 versus 13.5 minutes; P < .01) in non-Q-wave myocardial infarction.
In acute coronary syndromes, transient ischemia has a low threshold, occurs predominantly without an increase in myocardial oxygen demand, and is present mainly at night rather than in the morning. These findings in patients receiving maximal medical therapy suggest significant pathophysiological differences underlying transient ischemia compared with stable coronary disease.
稳定型冠心病中的短暂性缺血在早晨达到峰值，这反映了行走后心肌需氧量增加和冠状动脉血管运动张力增强。然而，在急性冠状动脉综合征中，缺血可能是由破裂斑块部位的短暂血栓形成或冠状动脉痉挛所致。基于对缺血前心率变化及其昼夜节律变化的分析，我们报告了尽管进行了最佳治疗，但急性冠状动脉综合征中短暂性缺血的病理生理机制。
256例不稳定型心绞痛或非Q波心肌梗死患者在接受最大程度药物治疗的同时，进行了48小时的连续ST段监测。所有缺血发作均根据其发生时间、持续时间、与疼痛的关系以及缺血发作前的心率变化进行特征描述。在10629小时的监测期间，44例患者（17.2%）发生了176次短暂性缺血发作。缺血发作时的平均心率为68±12.8次/分钟，超过55%的缺血发作之前心率无显著增加。缺血活动有一个夜间高峰，所有发作中有64%发生在晚上10点至上午8点之间，无论发作前心率是否增加，这种夜间优势都很明显。不稳定型心绞痛和非Q波心肌梗死中短暂性缺血的特征和时间相似，但非Q波心肌梗死中的短暂性缺血更频繁（27.3%对15.1%；P<0.05）且持续时间更长（中位数分别为20分钟和13.5分钟；P<0.01）。
在急性冠状动脉综合征中短暂性缺血阈值较低，主要在心肌需氧量未增加的情况下发生，且主要出现在夜间而非早晨。这些在接受最大程度药物治疗患者中的发现表明，与稳定型冠心病相比，短暂性缺血的病理生理机制存在显著差异。
