Clinical Medicine & Research

Volume 5, Number 3: 172-176
©2007 Marshfield Clinic

Cocaine-Induced Acute Myocardial Infarction

Shereif H. Rezkalla, MD and Robert A. Kloner, MD, PhD

Acute myocardial infarction may occur following cocaine use. Cocaine-induced infarction is
particularly common in younger patients aged 18 to 45 years old. Patients may or may not have
angiographic evidence of coronary artery disease at the time of their acute event. Previous
studies have shown that coronary artery spasm occurs with cocaine use, and perhaps platelet
activation, both contributing to a process that may culminate in coronary artery occlusion.
Primary coronary intervention should be the preferred revascularization modality by an
experienced team.Thrombolytic therapy needs to be instituted if this intervention is unavailable.
Beta blockers should be utilized with caution since they may increase coronary spasm or cause
a paradoxical rise in blood pressure.They should be avoided in the early hours of the infarction,
but be instituted prior to patient discharge. Interruption of cocaine abuse is the cornerstone of
secondary prevention in cocaine-related myocardial infarction.
Keywords: Acute myocardial infarction; Cocaine; Heart disease; Coronary artery disease;
Coronary spasm; Platelet aggregation; Platelet function; Thrombosis

M ore than two decades ago, experimental studies
demonstrated that cocaine administered to laboratory
also has been associated with other cardiac-related disorders,
such as cardiomyopathy, hypertension, aortic aneurysm and
non-cardiac chest pain.
animals resulted in atrial and ventricular arrhythmias,
myocardial ischemia with coronary vasoconstriction, as well Incidence
as a direct depression in myocyte function.1,2 Would similar Establishing the incidence of myocardial infarction
effects occur in humans? In the mid-1980s, Isner et al3 associated with cocaine use is clearly a very difficult task;
reported high grade ventricular arrhythmias, myocardial however, in selected case reports, it appeared to be relatively
infarction, even sudden death was temporarily related to high.11 Mittleman et al12 reported a rate of 1% in a
cocaine use. A striking observation in Isner’s work was that retrospective study of 3,946 patients presenting with acute
cocaine use did not need to be chronic in order to precipitate myocardial infarction. The study suggested that the incidence
a cardiac event. In some cases, recreational use was of occurrence was highest during the first hour after
associated with myocardial infarction. Myocardial infarction administration and fell quickly in subsequent hours. Others
was described as both transmural or non-Q wave infarction.4 have shown a much higher incidence which is apparently
Years later, it became well established that adverse cardiac dependent on the city where a particular study is conducted
effects of cocaine use are a tragic reality.5,6 More disturbing and the socioeconomic status of the cohort. The incidence is
is the occurrence of adverse cardiac events even when likely to be underestimated, since the psychological state and
cocaine is used in medicine, i.e., when intranasal and euphoria that accompany cocaine use reduce the number of
intratracheal applications are utilized as a local anesthetic.7-9 those who seek help, particularly in patients with smaller
A survey conducted 3 years ago revealed that approximately and/or non-complicated myocardial infarctions. The
50% of otolaryngologists still use the solution of cocaine as incidence is much higher (25%) in younger patients aged 18
a local anesthetic.10 This report will focus on the to 45 years old13 and particularly in those with other cardiac
development of myocardial infarction in cocaine users. It is risk factors.14 However, any incidence is clearly
important for the reader to appreciate that the use of cocaine unacceptable, since it is a preventable condition. Therefore,

Reprint Requests: Shereif H. Rezkalla, MD, Department of Cardiology, Received: February 22, 2007 doi:10.3121/cmr.2007.759
Marshfield Clinic, 1000 North Oak Avenue, Marshfield, WI 54449, Revised: May 7, 2007
Tel: 715-387-5845, Fax: 715389-3808, Accepted: June 6, 2007


Subsequent to administration of the microaggregates were observed in a separate in vitro study. At the time of decreased oxygen CM&R 2007 : 3 (October) Rezkalla and Kloner 173 . to address this important question. decrease in our animal data. Isolated case reports also suggested volunteers were incubated with cocaine dissolved in normal vasospasm as a cause for the infarction. that play a major role in the development of coronary thrombi. when the data were adjusted for a where heart rate and blood pressure increased requiring more. blood supply. Heesch diameter of the coronary arteries were measured at baseline.23. it was intuitive to consider the possibility that cocaine may accelerate coronary artery disease. blood flow. et al33 reported that cocaine caused platelet activation with and were also measured after intranasal administration of release of platelet alpha granules. Initial analysis showed that cocaine users had more disturbing was that the ischemic effect occurred at a time calcification. as well as diseased vascular segments.24 Lange et al25 saline or normal saline alone for 10 minutes at 37˚C. Coronary sinus blood flow and the aggregation induced with adenosine diphosphate. When due to risk factors in those patients.32 Platelets from human varied among dogs. The degree of coronary artery spasm at sites of computerized tomography scanner and compared the degree atherosclerosis is usually more pronounced. as well as activation of platelets may occur which an alpha adrenergic blocking agent. Mechanism of cocaine-induced myocardial catecholamines by the cell and the resultant effects. a finding consistent with Thus. however. Physiology The pathophysiology of myocardial infarction is usually associated with a progression of atherosclerotic coronary artery disease. These reports led us to study the effects of consistent in all animals. including infarction. Arteries with or without coronary artery disease will have spasm and increased platelet aggregation. make it more vulnerable to the effects of cocaine. there was a decrease in both coronary artery blood flow and epicardial artery diameter.16 Many case reports suggested that there is significant progression of coronary artery disease in cocaine users. however. since cocaine users who underwent coronary angiography had a 42% incidence of coronary artery disease. The same group utilizing similar it seems that cocaine users had more extensive coronary methodology showed that this decrease in blood flow occurs artery disease or rapid progression of that disease. variety of risk factors. Controlled studies. although the degree of vasospasm cocaine on human platelets. are the only way insult to the injury.understanding the possible mechanism(s) of cocaine-induced myocardial infarction is crucial in determining the best management strategy of such patients.038 patients in the Coronary Artery Risk Development in Young Adults (CARDIA) study with a multidetector these changes. this significance was lost.20 Inhibition of the uptake of Figure 1. suggesting that may result in the development of coronary thrombosis and stimulation of the alpha receptors is the likely mechanism of myocardial infarction. coronary spasm. and the occurrence of cocaine or normal saline. Thus. It is likely that factors unique to leading to increased platelet adhesiveness and aggregation cocaine use may contribute to the occurrence of infarctions. Pletcher et al21 examined 3. cocaine. it may be in both normal.18 while others have described coronary aneurysms19 or dissections. Cocaine studied 45 patients who underwent coronary angiography for exposure resulted in a significant increase in platelet evaluation of chest pain.15 Therefore. These effects were blocked by phentolamine.15 The occurrence was cocaine use. Furthermore. the effect in the tobacco abuse and hypertension. Multiple case reports described coronary thrombosis Two additional likely mechanisms for cocaine-induced in cocaine users presenting with acute myocardial infarction. Kolodgie et diseased coronary segments was more obvious. More users. myocardial infarction. which is a surrogate marker for the arterial segments do not have healthy endothelial cells which presence of coronary artery disease in cocaine users and non. An early study observed generalized Stenberg et al31 described a 38-year-old man with coronary artery vasospasm and a decrease in coronary flow simultaneous thrombosis of both right coronary artery and when cocaine was injected intravenously to healthy left descending coronary artery following intravenous phenobarbital anesthetized dogs. with or without plaque rupture. plaque rupture was less common in cocaine-related Cocaine use is also associated with an activation of platelets.26 Diseased of coronary calcification.17. including concomitant smoking was combined with cocaine. with acute use of the drug. myocardial infarction are coronary artery spasm and platelet occasionally in the presence of normal coronary arteries. The hypertension.28-30 activation (figure 1). has the potential of accelerating associated increase in blood pressure and heart rate adds atherosclerosis.27 al22 reported that despite extensive coronary atherosclerosis. Animal studies have shown that cocaine administration is associated with more extensive atherosclerotic changes. while not less.

IIB/IIIA platelet receptor inhibitors should be an induced myocardial infarction needs to be suspected in young integral part of acute intervention. serial electrocardiograms administered propranolol to 30 patients following intranasal with no significant changes. cardiac are an important part of the pathophysiology in coronary enzymes and classic electrocardiographic findings. no recurrent cardiac symptoms cocaine administration. thrombolytic therapy should be screening may be obtained if there is a high index of administered intravenously. particularly cerebral bleed. emphasizing If a cocaine user presents with ST elevation myocardial the sequence of events that may culminate in myocardial infarction within 6 hours of onset of chest pain. however. obtaining the perfusion image urgently and in the inherent time delay that is involved. Lange et al45 Those who had normal troponin I. and therefore direct inquiry When a coronary catheterization laboratory is not about drug use is important. many cocaine using patients.40 In a retrospective study of suspicion for cocaine use. nitrates and benzodiazepines should be two-dimensional echocardiogram showing a clear regional immediately administered. While cocaine does not last long in cocaine users. thrombolytic therapy or acute percutaneous coronary intervention needs to be implemented as soon as possible in Diagnosis patients with definite ST elevation myocardial infarction. While some patients will have a clear diagnosis. unopposed alpha observed in the emergency department for 9 to 12 hours. effects of cocaine results in hypertension and tachycardia. Since platelets of the patient along with appropriate laboratory tests. Blood and urine for drug immediately available. Patients who were at mild or moderate risk were demand and infarction size. Counseling be observed in the department before a final plan of patients to avoid cocaine use should be performed routinely. beta blocker use with evidence of acute transmural myocardial infarction and at should be avoided in the early phases of treatment while high risk (e. and pleuritic noncardiac chest pain. Those at low to intermediate risk may discharge when cocaine’s effects have abated. History taking can be a real challenge considered. others may decreases cardiac arrhythmias and improves mortality.44 It is recommended that all wall motion abnormality. cocaine users may have altered consciousness and sustained various injuries that may not be obvious on initial Elevated troponin may be more specific than creatinine evaluation. If there is any neurologic symptom or picture when atypical symptoms are present or the sign detected. but started prior to hospital for immediate therapy. A careful examination and with technetium-99m Sestamibi may be useful if acquired in chest x-ray should be obtained prior to initiation of a timely manner. In not. 18% of patients simply had Cocaine has a potent effect on membrane ion to the myocardium. beta blocker of the patients died and the risk for recurrent cardiac events administration resulted in a further decrease in flow and an was very low. but the patient’s blood.37 In the emergency department. causing paradoxically increased to the emergency room with cardiac symptoms following blood pressure which may increase myocardial oxygen cocaine use. In addition. aspirin. In a study by Gitter et al38 of 101 cocaine patients admitted with chest pain. and in that setting.45 Thus.36 A perfusion image may clarify the clinical thrombolytic therapy. Such patients do not voluntarily admit to cocaine use. injury. those patients increase in coronary resistance. then appropriate imaging may need to be electrocardiogram is not diagnostic. disposition is made. none decrease in coronary artery blood flow. and therefore bleeding risk should be carefully kinase in this setting. which reduces infarction size. the intense sympathomimetic electrocardiograms often showed ST or T wave abnormalities..35 Resting perfusion imaging thrombolytics should be avoided. At 30 days. cocaine metabolites such as patients must meet the accepted inclusion and exclusion benzoylecgonine and ecgonine may be detected in the urine criteria before this therapy should be initiated. Diagnosis of cocaine-induced acute myocardial infarction is Acute intervention is always preferred if a qualified made by obtaining a careful history and physical examination interventional team is readily available onsite. thrombolytic therapy was found to be safe. this has not obtained emergently to rule out carotid artery dissection or a gained a wide clinical application because of the difficulty in cerebral bleed.g. The the abnormalities were nonspecific and were mostly related to resulting increase in tissue demands adds an insult to the hypertensive heart disease or early repolarization. thrombosis. Zimmerman et al34 described a young 29-year-old man with normal coronary arteries who developed coronary spasm Management and a coronary thrombus following cocaine use. A word of for up to 8 days after intake and for a very long time in the caution about the use of thrombolytic therapy in this group of patient’s hair. While cocaine administration led to a and no cardiac arrhythmias were discharged.39. blockade can induce coronary artery vasospasm. patients presenting with infarction. patients with myocardial infarction receive beta blocker therapy at presentation. While admitting when this effect is added to tissue ischemia and left 174 Cocaine-induced acute myocardial infarction CM&R 2007 : 3 (October) . however. The most useful bedside test is the Oxygen. patients. How should emergency departments handle these cases? cocaine users. immediate infarction.41-43 Aortic dissection with the altered level of consciousness that is observed in has been reported with cocaine use. elevated cardiac enzymes) need to be admitted cocaine’s effects are still present. Cocaine. blocking beta receptors may leave the Weber et al37 prospectively studied 302 patients who presented alpha effect unopposed.

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