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Abstract & Commentary
Synopsis: Cocaine is the most commonly used illicit drug among subjects seeking care in hospital emergency departments or drug-treatment centers. In addition, it is the most frequent cause of drug-related deaths reported by medical examiners.1 In 1999, an estimated 25 million Americans admitted that they had used cocaine at least once; 3.7 million had used it within the previous year; and 1.5 million were current users. During the same year, cocaine was mentioned in 30% of all drug-related visits to emergency departments.1 As cocaine abuse has become widespread, the number of cocaine-related cardiovascular events, including angina pectoris, myocardial infarction, cardiomyopathy, and sudden death from cardiac causes, has increased dramatically.
Source: Lange R, Hillis D. N Engl J Med. 2001;345:351-358.
Lange and Hillis have written an excellent review article regarding the epidemiology of cocaine use, the pharmacology and mechanisms of action, and the varied deleterious effects of cocaine on different systems of the body.
Mechanism of Action
Cocaine blocks the presynaptic reuptake of norepinephrine and dopamine, producing an excess of these neurotransmitters at the site of the postsynaptic receptor. In short, cocaine acts as a powerful sympathomimetic agent.
Cocaine-Related Myocardial Ischemia and Infarction
Of patients who come to the emergency department with nontraumatic chest pain, 14-25% in urban hospitals and 7% in suburban hospitals have detectable levels of cocaine or cocaine metabolites in their urine.2
Most patients with cocaine-related myocardial infarction (MI) are young, nonwhite, male cigarette smokers without other risk factors for atherosclerosis who have a history of repeated use of cocaine. About half the patients with cocaine-related MI have no evidence of atherosclerotic coronary artery disease on subsequent angiography.3
The accurate identification of patients with cocaine-related MI may be difficult for at least 2 reasons. First, the electrocardiogram may be abnormal in many patients with chest pain after cocaine use, even in the absence of MI. The second reason is that serum creatine kinase concentrations are elevated in about half of cocaine users, who do not have MI, due to rhabdomyolysis.4 Accordingly, serum troponin concentrations are used.
The recently revised guidelines of the American Heart Association for emergency cardiovascular care5 recommend nitroglycerin and benzodiazepines as first-line agents for patients with cocaine-related MI or infarction and phentolamine as a second-line agent; propranolol is contraindicated. Thrombolysis is not recommended unless evidence of evolving MI persists despite medical therapy and an occluded coronary artery is shown to be present on angiography. Thrombolysis is contraindicated if uncontrolled, severe systemic arterial hypertension is present.
Cocaine, Cigarette Smoking, and Alcohol Use
The deleterious effects of cocaine on myocardial oxygen supply and demand are exacerbated substantially by concomitant cigarette smoking. This combination markedly increased the product of the heart rate and systemic arterial pressure, a value that determines myocardial oxygen demand, while simultaneously decreasing the diameter of diseased segments of the coronary arteries.
Among those with abuse of multiple substances who are seen in emergency departments, the combination of cocaine and ethanol is the most common.1 It is the second most common combination in patients who die of substance abuse, accounting for more than 1000 deaths per year.
Cocaine-Induced Myocardial Dysfunction
Long-term cocaine abuse has been reported to cause left ventricular hypertrophy6 and systolic dysfunction. Several reports have described dilated cardiomyopathy in long-term cocaine abusers, as well as reversible, profound myocardial depression after binge cocaine use.
The cardiac dysrhythmias ascribed to cocaine have occurred in the context of profound hemodynamic or metabolic derangements, such as hypotension, hypoxemia, seizures, or MI. Nonetheless, because of cocaine’s sodium-channel-blocking properties and its ability to induce an enhanced sympathetic state, it is considered likely to produce or exacerbate cardiac arrhythmias, particularly under certain pathologic conditions. The development of lethal arrhythmias with cocaine use may require a substrate of abnormal myocardium.
Lidocaine has been used safely in patients with cocaine-induced ventricular tachycardia or fibrillation. Class IA antiarrhythmic drugs, such as quinidine, procainamide, and disopyramide, should be avoided, since they may exacerbate prolongation of the QRS and QT intervals and slow the metabolism of cocaine and its metabolites.
The elevation of the heart rate and systemic arterial pressure that accompanies cocaine use may induce valvular and vascular injury that predisposes users to bacterial invasion. The immunosuppressive effects of cocaine may increase the risk of infection. Alternatively, the manner in which cocaine is manufactured, as well as the adulterants that are often present in cocaine, may increase the risk of endocarditis. In contradistinction to endocarditis associated with other drugs, the endocarditis associated with cocaine abuse more often involves the left-sided cardiac valves.7
Aortic dissection or rupture has been temporally related to cocaine use and should, therefore, be considered as a possible cause of chest pain in cocaine users. Dissection probably results from the substantial increase in systemic arterial pressure induced by cocaine. In addition to aortic rupture, cocaine-related rupture of mycotic and intracerebral aneurysms has been reported.
Comment by David Ost, MD, FACP, & Najma Usmani, MD
Cocaine use continues to increase. As a result, the number of cocaine-related visits to emergency departments, hospitalizations, cardiovascular complications, and deaths has risen dramatically. The understanding and early recognition of cocaine-related cardiovascular complications are essential to their proper management. The possibility of cocaine use should be considered in young patients with myocardial ischemia or infarction, arrhythmias, myocarditis, or dilated cardiomyopathy.
1. Office of applied studies. Substance abuse and mental Health Services Administration, August 2000. DHHS publication no.(SMA)00-3462.
2. Hollander JE, et al. Ann Emerg Med. 1995;26:671-6
3. Minor RL Jr, et al. Ann Intern Med. 1991;115:797-806.
4. Gitter MJ, et al. Ann Intern Med. 1991;1115:277-82
5. Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2000; 102:Suppl I:I-223-I-228.
6. Brickner ME, et al. Circulation. 1991;84:1130-1135.
7. Chambers HF, et al. Ann Intern Med. 1987;106:833-836.
Dr. Ost, Assistant Professor of Medicine, NYU School of Medicine, Director of Interventional Pulmonology, Division of Pulmonary and Critical Care Medicine, Northshore University Hospital, Manhasset, NY, is Associate Editor of Internal Medicine Alert. Dr. Usmani is Assistant Clinical Instructor, University of Stony Brook, Stony Brook, NY.