Cocaine use has been associated with both acute and chronic cardiovascular diseases. These include acute myocardial infarction, myocardial ischemia (both silent ischemia and ischemia associated with angina), acceleration of the development of atherosclerosis, myocarditis, cardiomyopathy (both dilated and hypertrophic), arrhythmias, hypertension, aortic dissection, and endocarditis. An estimated 25 million Americans have tried cocaine at least once.
Cocaine may be administered by smoking, nasal insufflation, or intravenous injection; cardiac events can follow administration by any of these routes. Cocaine is rapidly absorbed through the respiratory tract; smoking cocaine delivers the substance to the circulation within seconds to minutes. After nasal insufflation (“snorting”) of cocaine powder, peak concentrations are found in the blood within 30 to 60 minutes. Although cocaine can be taken orally, it is poorly absorbed by the gastrointestinal tract.
The literature is replete with cases of acute myocardial infarction after cocaine use, which probably involves several mechanisms
The risk of acute myocardial infarction is highest within the first hour after cocaine use and then rapidly declines. However, some reports suggest that myocardial infarction can occur as early as minutes after cocaine administration or as late as a few days afterward. Although any user is at risk, the typical patient is a man in his early 30s; cigarette smoking is a commonly associated risk factor. There is no clear relation between the dose of cocaine and the occurrence of an acute coronary event. Myocardial infarction may develop in first-time users, occasional users, and long-term users. Electrocardiographic abnormalities occur in 90 percent of patients with cocaine-induced myocardial infarction and include ST-segment elevation, T-wave inversions, and Q waves. Measurement of cardiac troponin may be superior to measurement of creatine kinase in making the diagnosis. Two-dimensional echocardiography may be used to confirm the presence of a new regional wall-motion abnormality.
Recognizing that ischemia or infarction is due to cocaine use is critical for optimal management. Although thrombolysis has been successfully performed in patients with previous cocaine use, there may be certain contraindications to thrombolysis in patients who have recently used cocaine, such as severe hypertension, seizures, intracerebral hemorrhage, or aortic dissection. Primary percutaneous coronary intervention may be a safer approach in those with definite infarction. Patients with angina but not myocardial infarction may be treated with nitroglycerin, oxygen, aspirin, benzodiazepines, or oral calcium antagonists. Coronary-artery vasospasm may respond to nitrates, calcium-channel blockers, or alpha-blockers. Beta-blockers should be administered with caution, since their use may worsen vasospasm by allowing unopposed stimulation of alpha receptors.
Not all episodes of cocaine-related chest pain constitute an acute coronary syndrome, however. Only about 6 percent of episodes of cocaine-induced chest pain are due to acute myocardial infarction. Chest pain may be due to ischemia without infarction, or it may be extracardiac (e.g., pleuritic) in nature. Since the majority of cases of cocaine-induced chest pain are not due to myocardial infarction, what is the best approach in the emergency department?
Retrospective analyses have suggested that use of a 12-hour observation period during which serial electrocardiograms and cardiac-enzyme values are obtained would be a reasonable approach for ruling out acute myocardial infarction. In this issue of the Journal, Weber and associates (pages 510–517) report on a prospective study in which they validated the hypothesis that such an approach is safe. They evaluated 344 patients with cocaine-related chest discomfort. Forty-two of these patients (12 percent) were admitted to the hospital with acute myocardial infarction, unstable angina, or another cardiac condition. Among the remaining 302 patients, those who had no new electrocardiographic changes indicative of ischemia, as well as normal levels of cardiac troponin I, a negative exercise test, and no cardiovascular complications during a 9-to-12-hour period in an observation unit, were discharged. Thirty-day follow-up in this cohort revealed that none of the patients died of a cardiovascular event. Four patients sustained a nonfatal myocardial infarction; however, these patients had continued to use cocaine.
It is clear that not all patients who come to the hospital with chest pain after cocaine use will need to be admitted. Establishing chest-pain observation units should permit the correct identification of those who do need admission and those who can be safely discharged and followed as outpatients. This approach is expected to be highly cost effective.
An otherwise healthy young person presenting with chest pain or myocardial infarction should be asked about substance abuse, including cocaine use. Many patients have little or no idea of the cardiovascular risks associated with cocaine use. It is crucial that patients be educated about the dangers of this substance and that those who use it be encouraged to stop and referred to services that can help them do so.
From the Heart Institute, Good Samaritan Hospital, and the Division of Cardiovascular Medicine, Keck School of Medicine, University of Southern California — both in Los Angeles (R.A.K.); and the Department of Cardiology, Marshfield Clinic, Marshfield, Wis. (S.H.R.).
Robert A. Kloner, M.D., Ph.D., and Shereif H. Rezkalla, M.D.