Cocaine-Induced Myocardial Infarction 

9/22/99 (Del Rio)

Question: How can cocaine trigger a myocardial infarction?

Link Directly to Fulltext Article at Publisher

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Unique Identifier: 99280465

Authors: Mittleman MA. Mintzer D. Maclure M. Tofler GH. Sherwood JB. Muller JE.

Institution: Institute for Prevention of Cardiovascular Disease, Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. mmittlem@hsph.harvard.edu

Abstract: BACKGROUND: 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. METHODS AND RESULTS: 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. CONCLUSIONS: 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.

Link Directly to Fulltext article in Ovid

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Unique Identifier: 98149616

Authors: Hollander JE. Levitt MA. Young GP. Briglia E. Wetli CV. Gawad Y.

Institution: Department of Emergency Medicine, Hospital of the University of Pennsylvania, Philadelphia 19104-4283, USA. Jholland@mail.med.upenn.edu

Abstract: We evaluated whether recent cocaine use alters the specificity of CK-MB, myoglobin, and cardiac troponin I for acute myocardial infarction (AMI) in patients who are seen in the emergency department for chest pain. Patients <60 years old with potential myocardial ischemia underwent a standardized history and physical examination and routine CK-MB assays every 8 to 12 hours and had study serum obtained at presentation for CK-MB, myoglobin, and cardiac troponin I immunoassays, as well as benzoylecgonine, cocaine's main metabolite. We enrolled 97 patients, 19 (20%) of whom had recent used cocaine. Patients with and without cocaine use were similar with regards to sex, race, renal and muscular disease, diabetes, family history, and hypertension and rate of AMI (12% vs 11%, p = 1.0). In patients without MI, the mean myoglobin level was higher in cocaine users than noncocaine users (179 vs 74 ng/ml; Mann-Whitney p = 0.003), but the mean values were similar for CK-MB (2.2 vs 2.1 ng/ml; Mann-Whitney p = 0.58) and for cardiac troponin-I (0.02 vs 0.02 ng/ml; Mann-Whitney p = 0.87). The specificities of the markers in patients with and without cocaine use were as follows: cardiac troponin I, 94% vs 94%, (p = 1.0); CK-MB, 75% vs 88% (p = 0.24); and myoglobin, 50% vs 82%, (p = 0.02), respectively. Our data demonstrate that the specificity of myoglobin was altered by recent cocaine use. The specificity of CK-MB was affected less and the specificity of cardiac troponin I was not affected by recent cocaine use.

Link Directly to Fulltext Article at Science Direct

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Unique Identifier: 97360601

Authors: Hollander JE. Shih RD. Hoffman RS. Harchelroad FP. Phillips S. Brent J. Kulig K. Thode HC Jr.

Institution: Department of Emergency Medicine, University Medical Center, Stony Brook, New York 11794-8350, USA.

Abstract: PURPOSE: To identify clinical criteria predictive of underlying coronary artery disease in patients with cocaine-associated myocardial infarction. PATIENTS AND METHODS: Using a retrospective cross-sectional study design at 29 acute care hospitals, we identified 70 patients with cocaine-associated myocardial infarction who had a determination of the presence or absence of coronary artery disease. Clinical characteristics of patients with coronary artery disease (> 50% stenosis on cardiac catheterization or reversible ischemia on stress test) were compared with patients without coronary artery disease (< 50% stenosis on cardiac catheterization). RESULTS: Compared with patients without coronary artery disease (n = 21), patients with coronary artery disease (n = 49) were older (42 versus 31 years; P < 0.001), had more traditional cardiac risk factors (2.3 versus 1.5; P < 0.001), more frequent history of hypertension (odds ratio [OR], 5.3; 95% confidence interval [CI], 1.4 to 20.4); more frequent family history of myocardial infarction (OR, 4.4; 95% CI, 1.3 to 15.1), more bradydysrhythmias (OR, 8.0; 95% CI, 1.0 to 65.5), and more likely to have an inferior infarct location (P = 0.04). CONCLUSION: Age, number of cardiac risk factors, location of myocardial infarction, and bradydysrhythmias predict underlying coronary artery disease in patients with cocaine-associated myocardial infarction. If validated, this knowledge may be used to develop a medically appropriate, cost-effective evaluation strategy for patients following cocaine-associated myocardial infarction.

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Unique Identifier: 96388096

Authors: Hollander JE.

Institution: Department of Emergency Medicine, University Medical Center, Stony Brook, New York 11794-8350, USA.

Abstract: Myocardial ischaemia and infarction has become a well-recognized sequelae of cocaine use. The possibility of recent cocaine use should be assessed in patients with potential myocardial ischaemia because the treatment of patients with myocardial ischaemia related to cocaine differs from that of patients with myocardial ischaemia unrelated to cocaine. Patients with cocaine-associated myocardial ischaemia should receive initial treatment with benzodiazepines to decrease central adrenergic stimulation. Aspirin should be used to reduce thrombus formation, and nitroglycerin to reverse coronary vasoconstriction. Patients with continued ischaemia can be treated with either low doses of phentolamine, or verapamil. If ischaemia continues after treatment with these agents mechanical reperfusion or thrombolytic therapy should be considered depending upon the clinical circumstances. Patients with myocardial ischaemia secondary to cocaine should not receive treatment with beta adrenergic antagonists as these agents enhance coronary vasoconstriction thereby worsening ischaemia. [References: 69]

Link Directly to Fulltext article in Ovid

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Unique Identifier: 95266925

Authors: Hollander JE. Hoffman RS. Burstein JL. Shih RD. Thode HC Jr.

Institution: Department of Emergency Medicine, University Medical Center, Stony Brook, NY, USA.

Abstract: BACKGROUND: The frequency of complications in patients with cocaine-associated myocardial infarction is unknown. This study was performed to determine the short-term morbidity and mortality secondary to cocaine-associated myocardial infarction. METHODS: We performed a retrospective cohort study at 29 hospital centers throughout the United States. Patients with cocaine-associated myocardial infarction that occurred between 1987 and 1993 were identified through record review. The primary outcome measures were in-hospital mortality and the incidence and timing of major cardiovascular complications. RESULTS: Cocaine-associated myocardial infarction was identified 136 times in 130 patients. Patients were generally young (mean age, 38 years), nonwhite (72%), tobacco smokers (91%) with a history of cocaine use in the past 24 hours (88%). The initial electrocardiogram disclosed infarction in 44% and ischemia in an additional 18% of patients. Myocardial infarctions were evenly distributed between anterior (45%) and inferior (44%) and were most often non-Q-wave (61%). Complications occurred 64 times in 49 patients (36%; 95% confidence interval, 28% to 44%), including congestive heart failure in nine patients, ventricular tachycardia in 23 patients, supraventricular tachycardia in six patients, and brady-dysrhythmias in 26 patients. Most patients who had complications (90%) had them within 12 hours of presentation. Acute in-hospital mortality was 0% (95% confidence interval, 0% to 2%). CONCLUSIONS: The mortality of patients hospitalized with cocaine-associated myocardial infarction was low. The majority of complications occurred within 12 hours of presentation.

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Unique Identifier: 92299956

Authors: Hollander JE. Hoffman RS.

Institution: Emergency Department, Bronx Municipal Hospital Center, Albert Einstein College of Medicine, NY 10461.

Abstract: The objectives of this paper are to analyze the case reports of cocaine-induced myocardial infarction and to better define the clinical characteristics of this syndrome. An English language literature search was carried out using MEDLINE, and a bibliographic review of all identified articles and book chapters was conducted. Ninety-one cases of cocaine-induced myocardial infarction were identified. Intranasal, intravenous, and inhalational routes of abuse all resulted in myocardial infarction. Fourty-four percent of patients had previously noted chest pain. Eighty-seven percent of patients were cigarette smokers. Two-thirds of patients had their myocardial infarction within 3 hours of the use of cocaine (with a range of 1 minute to 4 days). Cardiac catheterizations were abnormal in 30 of 54 patients (55%). Of the 24 patients with reported follow-up, 14 (58%) had further ischemic events after discharge. In conclusion, cocaine-induced myocardial infarction identifies a group of young individuals who may be prone to recurrent complications after initial presentation. [References: 59]