Mittleman M A, Mintzer D, Maclure M, Tofler G H, Sherwood J B, Muller J E
Institute for Prevention of Cardiovascular Disease, Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Circulation. 1999 Jun 1;99(21):2737-41. doi: 10.1161/01.cir.99.21.2737.
Cocaine has been implicated as a trigger of acute myocardial infarction in patients with and those without underlying coronary atherosclerosis. However, the magnitude of the increase in risk of acute myocardial infarction immediately after cocaine use remains unknown.
In the Determinants of Myocardial Infarction Onset Study, we interviewed 3946 patients (1282 women) with acute myocardial infarction an average of 4 days after infarction onset. Data were collected on the use of cocaine and other potential triggers of myocardial infarction. We compared the reported use of cocaine in the hour preceding the onset of myocardial infarction symptoms with its expected frequency by using self-matched control data based on the case-crossover study design. Of the 3946 patients interviewed, 38 (1%) reported cocaine use in the prior year and 9 reported use within the 60 minutes preceding the onset of infarction symptoms. Compared with nonusers, cocaine users were more likely to be male (87% vs 67%, P=0.01), current cigarette smokers (84% vs 32%, P<0.001), younger (44+/-8 vs 61+/-13 years, P<0.001), and minority group members (63% vs 11%, P<0.001). The risk of myocardial infarction onset was elevated 23.7 times over baseline (95% CI 8.5 to 66.3) in the 60 minutes after cocaine use. The elevated risk rapidly decreased thereafter.
Cocaine use is associated with a large abrupt and transient increase in the risk of acute myocardial infarction in patients who are otherwise at relatively low risk. This finding suggests that studying the pathophysiological changes produced by cocaine may provide insights into the mechanisms by which myocardial infarction is triggered by other stressors.
可卡因被认为是有或无潜在冠状动脉粥样硬化患者急性心肌梗死的诱因。然而,使用可卡因后急性心肌梗死风险立即增加的幅度尚不清楚。
在心肌梗死发病决定因素研究中,我们在心肌梗死发病后平均4天对3946例急性心肌梗死患者(1282名女性)进行了访谈。收集了关于可卡因使用及其他潜在心肌梗死诱因的数据。我们采用基于病例交叉研究设计的自身匹配对照数据,将心肌梗死症状发作前1小时内报告的可卡因使用情况与其预期频率进行了比较。在接受访谈的3946例患者中,38例(1%)报告在前一年使用过可卡因,9例报告在梗死症状发作前60分钟内使用过。与未使用者相比,可卡因使用者更可能为男性(87%对67%,P=0.01)、当前吸烟者(84%对32%,P<0.001)、更年轻(44±8岁对61±13岁,P<0.001)且为少数群体成员(63%对11%,P<0.001)。使用可卡因后60分钟内心肌梗死发病风险比基线升高了23.7倍(95%可信区间8.5至66.3)。此后升高的风险迅速下降。
在其他方面风险相对较低的患者中,使用可卡因与急性心肌梗死风险的大幅突然且短暂增加相关。这一发现表明,研究可卡因产生的病理生理变化可能有助于深入了解其他应激源引发心肌梗死的机制。