Minor R L, Scott B D, Brown D D, Winniford M D
Department of Medicine, University of Iowa Hospitals and Clinics, Iowa City 52242.
Ann Intern Med. 1991 Nov 15;115(10):797-806. doi: 10.7326/0003-4819-115-10-797.
To review the reported cases of myocardial infarction temporally related to recreational and topical anesthetic use of cocaine, with special regard for underlying etiologic factors in patients subsequently found to have normal coronary arteries.
Personal records of three cases and a comprehensive literature review using MEDLINE and supplemented by Index Medicus and the bibliographies of case reports.
A total of 114 cases of cocaine-induced myocardial infarction were identified. The coronary anatomy was defined by angiography or autopsy in 92 patients, 38% of whom had normal coronary arteries. In these 35 patients (average age, 32; range, 21 to 60 years), myocardial infarction typically involved the anterior left ventricular wall (77%). Moderate cigarette smoking with one or fewer associated coronary risk factors was prevalent (68%). Focal coronary vasospasm was shown convincingly in only two cases. Intracoronary thrombus was initially found on 9 of 11 angiograms (82%) done within 12 hours of the myocardial infarction. Experimental evidence suggests that cocaine has direct and indirect sympathomimetic effects on vascular smooth muscle, attenuates endothelium vasodilator capacity, exerts a potent depressant effect on cardiac myocytes, and promotes atherogenesis.
Cocaine-induced myocardial infarction in patients with normal coronary arteries probably involves adrenergically mediated increases in myocardial oxygen consumption, vasoconstriction of large epicardial arteries or small coronary resistance vessels, and coronary thrombosis. Accelerated atherosclerosis and impairment of endothelium vasodilator function may occur after chronic cocaine use.
回顾报告的与娱乐性使用及局部使用可卡因相关的心肌梗死病例，特别关注随后发现冠状动脉正常的患者的潜在病因。
三例病例的个人记录以及使用MEDLINE进行的全面文献综述，并辅以《医学索引》及病例报告的参考文献。
共确定了114例可卡因诱发的心肌梗死病例。92例患者通过血管造影或尸检明确了冠状动脉解剖结构，其中38%的患者冠状动脉正常。在这35例患者（平均年龄32岁；范围21至60岁）中，心肌梗死通常累及左心室前壁（77%）。普遍存在中度吸烟且伴有一项或更少相关冠状动脉危险因素的情况（68%）。仅在两例病例中令人信服地显示出局灶性冠状动脉痉挛。在心肌梗死后12小时内进行的11次血管造影中的9次（82%）最初发现冠状动脉内血栓。实验证据表明，可卡因对血管平滑肌具有直接和间接的拟交感神经作用，减弱内皮舒张血管的能力，对心肌细胞产生强大的抑制作用，并促进动脉粥样硬化的形成。
冠状动脉正常的患者中，可卡因诱发的心肌梗死可能涉及肾上腺素介导的心肌耗氧量增加、大的心外膜动脉或小的冠状动脉阻力血管收缩以及冠状动脉血栓形成。长期使用可卡因后可能会出现动脉粥样硬化加速和内皮舒张功能受损的情况。
