Mohri M, Koyanagi M, Egashira K, Tagawa H, Ichiki T, Shimokawa H, Takeshita A
Research Institute of Angiocardiology and Cardiovascular Clinic, Kyushu University, Faculty of Medicine, Fukuoka, Japan.
Lancet. 1998 Apr 18;351(9110):1165-9. doi: 10.1016/S0140-6736(97)07329-7.
Microvascular angina can occur during exercise and at rest. Reduced vasodilator capacity of the coronary microvessels is implicated as a cause of angina during exercise, but the mechanism of angina at rest is not known. Our aim was to test the hypothesis that primary hyperconstriction (spasm) of coronary microvessels causes myocardial ischaemia at rest.
Acetylcholine induces coronary artery spasm in patients with variant angina. We tested the effects of intracoronary acetylcholine at graded doses in 117 consecutive patients with chest pain (at rest, during exertion, or both) and no flow-limiting (>50%) organic stenosis in the large epicardial coronary arteries. We also assessed the metabolism of myocardial lactate during acetylcholine administration in 36 of the patients by measurement of lactate in paired blood samples from the coronary artery and coronary sinus vein.
Of the 117 patients, 63 (54%) had large-artery spasm, 29 (25%) had microvascular spasm, and 25 (21%) had atypical chest pain. The 29 patients with microvascular spasm developed angina-like chest pain, ischaemic electrocardiogram (ECG) changes, or both spontaneously (two patients) or after administration of acetylcholine (27 patients) without spasm of the large epicardial coronary arteries. Testing of paired samples of arterial and coronary sinus venous blood showed that lactate was produced during angina attack in nine of 11 patients with microvascular spasm. There was more women (p<0.01) and fewer coronary risk factors (p<0.01) in patients with microvascular spasm than in those with large-artery spasm.
Coronary microvascular spasm and resultant myocardial ischaemia may be the cause of chest pain in a subgroup of patients with microvascular angina.
微血管性心绞痛可在运动时和静息时发作。冠状动脉微血管舒张能力降低被认为是运动时心绞痛的一个原因，但静息时心绞痛的机制尚不清楚。我们的目的是检验冠状动脉微血管原发性过度收缩（痉挛）导致静息时心肌缺血这一假说。
乙酰胆碱可诱发变异型心绞痛患者的冠状动脉痉挛。我们对117例连续的胸痛患者（静息时、运动时或两者皆有）进行了冠状动脉内不同剂量乙酰胆碱的试验，这些患者的心外膜大冠状动脉无血流限制性（>50%）器质性狭窄。我们还通过测量36例患者冠状动脉和冠状静脉窦成对血样中的乳酸，评估了乙酰胆碱给药期间心肌乳酸的代谢情况。
117例患者中，63例（54%）有大动脉痉挛，29例（25%）有微血管痉挛，25例（21%）有非典型胸痛。29例微血管痉挛患者自发（2例）或在未发生心外膜大冠状动脉痉挛的情况下给予乙酰胆碱后（27例）出现心绞痛样胸痛、缺血性心电图（ECG）改变或两者皆有。对动脉血和冠状静脉窦血的成对样本检测显示，11例微血管痉挛患者中有9例在心绞痛发作时产生了乳酸。微血管痉挛患者中的女性多于大动脉痉挛患者（p<0.01），冠状动脉危险因素少于大动脉痉挛患者（p<0.01）。
冠状动脉微血管痉挛及由此导致的心机缺血可能是微血管性心绞痛亚组患者胸痛的原因。
