Cocaine-associated Myocardial Infarction Research Articles

Acute Cardiovascular Toxicity of Cocaine.

Cocaine is one of the most commonly abused drugs and represents a major public health concern. Cocaine users frequently present to the emergency department, with chest pain being the most common presenting complaint. The incidence of acute myocardial infarction in patients with cocaine-associated chest pain is often quoted as 6%, but it is highly variable depending on the included population. Risk assessment can be challenging in these patients; serial assessment of electrocardiograms and troponins is often required. This review focuses on the assessment and management of patients presenting with cocaine-associated chest pain and cardiotoxicity. Specific treatments are discussed, including benzodiazepines, nitroglycerin, calcium channel blockers, and phentolamine, and how treatment priorities differ from patients with noncocaine presentations. The use of beta-blockers in this population remains controversial, and the literature around its use is reviewed. The most recent literature and recommendations for the use of percutaneous coronary intervention and fibrinolytics in cocaine-associated myocardial infarction is discussed as well. Cocaine-associated dysrhythmias are suggested to be the cause of sudden cardiac death in some users. The pathophysiology and evidence-based treatments for dysrhythmias are reviewed. This review provides evidence-based recommendations for the assessment and management of patients presenting with cocaine-associated cardiovascular toxicity.

Cocaine-associated myocardial infarction: Features of diagnosis and treatment

Temporal relation of myocardial infarction with cocaine use was first reported in 1982, coronary spasm being the presumed aetiology since most patients presented with normal coronary arteries. However, severe and diffused coronary atherosclerosis is also common in cocaine users with myocardial infarction. The management of these patients presenting with chest pain includes therapy directed to antagonize sympathetic activation and mechanical reperfusion or thrombolytic therapy if ischaemia continues.

Heightened risk of cardiac events following percutaneous coronary intervention for cocaine-associated myocardial infarction.

IntroductionSeveral works have suggested heightened risk for cardiac events in cocaine users following percutaneous coronary intervention (PCI). Such studies have generally been performed in small, poorly defined samples and have not utilised optimal control groups. We aimed to define the short-term risk for death or recurrent myocardial infarction (MI) when PCI was performed for myocardial infarction in subjects presenting with urine toxicology positive for cocaine in relation to subjects testing negative for cocaine use.Material and methodsOur institutional electronic health record (EHR) was queried for all subjects with urine toxicology performed for cocaine exposure within 5 days before or after having elevated troponin-T assay between 1/1/08 and 12/31/13. Query results were cross-referenced with our institutional cardiology database to identify the sample who had PCI on the same admission as the cocaine test. Subsequent readmission for MI was assessed from the EHR, and deaths were identified from the National Death Index.ResultsPCI had been performed in 380 subjects who tested negative for cocaine and 44 subjects who tested positive. In the cocaine-positive group, incidences of death or MI at 30 days and 1 year were 18% and 23%, respectively. Those who tested positive for cocaine had increased odds (odds ratio (OR) = 2.3, 95% confidence interval (CI): 1.0–5.1, p = 0.04) for death or MI at 30 days post PCI, after adjustment for age, sex, prior MI, and comorbidity index. Although the odds for events 1-year post PCI were not increased (OR = 2.0, 95% CI: 0.9–4.3), the p-value approached significance in this small sample (p = 0.09).ConclusionsThis retrospective study suggests that PCI performed in cocaine-associated myocardial infarction comes with a high 30-day and one-year risk. Further prospective studies are needed to better define this risk and to lend insight into better management strategies.

Abstract 17208: Trends in Hospitalizations Due to Cocaine-Induced Acute Myocardial Infarction: Results From National Inpatient Sample, 2005-2014

Introduction: According to the National Institute on Drug Abuse, lifetime cocaine use has remained stable since 2009. An estimated 1.5 million individuals aged ≥12 years reported cocaine use in 2014. Cocaine use is a significant risk factor for acute myocardial infarction (AMI), especially in the age group 18-45 years. Hence, we examined trends in hospitalizations due to cocaine-induced AMI in the United States. Methods: The current study was a retrospective analysis of the National Inpatient Sample, collected during the period 2005-2014. Participants between 18 and 45 years were included in the analysis. Cocaine-induced AMI hospitalizations were identified using ICD-9-CM codes 304.2X and 305.6X for cocaine dependence or abuse, and 410.XX for AMI diagnosis. We used Cochran Armitage test for categorical variables and Cuzick nonparametric test for trends for continuous variables. Results: A total of 49,715 weighted cocaine-induced AMI hospitalizations were reported during the study period. Cocaine-induced AMI hospitalizations increased from 4,619 in 2005 to 5,065 in 2014 (relative increase, 9.7%, P trend =0.124). Majority of the patients were non-White (55.3%), men (79.3%), in the age group 41-45 years (83.1%), and with Medicare/Medicaid coverage (51.2%). Highest change in trend was observed for non-White population and Medicare/Medicaid payers. Conclusion: Our study showed that cocaine-induced AMI hospitalizations remained stable during the years 2005-2014. Initial results point towards structural and racial disparities in such hospitalizations, especially among non-White men and population with Medicare/Medicaid coverage. Effective interventions to reduce cocaine use are needed, and treatment must be based on 2008 AHA guidelines for cocaine-associated chest pain and myocardial infarction.

Characteristics, Management, and Outcomes of Cocaine-Positive Patients With Acute Coronary Syndrome (from the National Cardiovascular Data Registry)

Although cocaine ingestion may cause or contribute to myocardial infarction (MI), few contemporary data are available describing cocaine-associated MI. We describe the characteristics, management, and outcomes of patients with MI and recent cocaine use from the Acute Coronary Treatment and Intervention Outcomes Network Registry-Get With The Guidelines (ACTION Registry-GWTG) program. The study population was 102,952 patients enrolled in the American College of Cardiology ACTION Registry-GWTG from July 2008 to March 31, 2010 from 460 sites across the United States. Cocaine exposure was defined as self-reported cocaine use within the last 72 hours or a positive urine test for cocaine. Demographics and medical history, presenting characteristics, treatments, and in-hospital outcomes were reported on a standard case record form. A total of 924 patients (0.9%) were cocaine positive. Compared with cocaine-negative patients, cocaine-positive patients were younger and predominantly men with fewer cardiovascular risk factors. There was a higher percentage of ST elevation myocardial infarction (STEMI) (46.3% vs 39.7%) and cardiogenic shock at presentation in the cocaine-positive group, but the percentage of multivessel coronary artery disease was lower (53.3% vs 64.5%). Beta blockers within 24 hours (85.8% vs 90.1%, p <0.0001) and drug-eluting stents (40.1% vs 68.8%, p <0.0001 in patients with non-STEMI; 27.6% vs 54.6%, p <0.0001 in patients with STEMI) were used less commonly in cocaine-positive patients. Multivariable-adjusted in-hospital mortality was similar between cocaine-positive and cocaine-negative patients (adjusted odds ratio 1.00, 95% confidence interval 0.69 to 1.44, p value = 0.98). In conclusion cocaine-positive patients with acute coronary syndrome are younger with fewer risk factors, multivessel coronary artery disease and lower drug-eluting stent and β-blocker usage. Cocaine use was not associated with in-hospital mortality.

Relationship Between Cocaine Use and Coronary Artery Disease in Patients With Symptoms Consistent With an Acute Coronary Syndrome

Observational studies of patients with cocaine-associated myocardial infarction have suggested more coronary disease than expected on the basis of patient age. The study objective was to determine whether cocaine use is associated with coronary disease in low- to intermediate-risk emergency department (ED) patients with potential acute coronary syndrome (ACS). The authors conducted a cross-sectional study of low- to intermediate-risk patients<60 years of age who received coronary computerized tomographic angiography (CTA) for evaluation of coronary artery disease (CAD) in the ED. Patients were classified into three groups with respect to CAD: maximal stenosis <25%, 25% to 49%, and ≥50%. Prespecified multivariate modeling (generalized estimating equations) was used to assess relationship between cocaine and CAD. Of 912 enrolled patients, 157 (17%) used cocaine. A total of 231 patients had CAD ≥25%; 111 had CAD ≥50%. In univariate analysis, cocaine use was not associated with a lesion 25% or greater (12% vs. 14%; relative risk [RR]=0.89, 95% confidence interval [CI]=0.5 to 1.4) or 50% or greater (12% vs. 11%; RR=1.15, 95% CI=0.6 to 2.3). In multivariate modeling adjusting for age, race, sex, cardiac risk factors, and Thrombosis in Myocardial Infarction (TIMI) score, cocaine use was not associated with the presence of any coronary lesion (adjusted RR=0.95, 95% CI=0.69 to 1.31) or coronary lesions 50% or greater (adjusted RR=0.78, 95% CI=0.45 to 1.38). There was also no relationship between repetitive cocaine use and coronary calcifications or between recent cocaine use and CAD. In symptomatic ED patients at low to intermediate risk of an ACS, cocaine use was not associated with an increased likelihood of coronary disease after adjustment for age, race, sex, and other risk factors for coronary disease.

Cardiovascular Effects of Cocaine

The use of cocaine has evolved from chewing the leaves of the Erythroxylon coca bush thousands of years ago, to purification of cocaine hydrochloride over 100 years ago and its use in tonics and elixirs (at one time in popular cola drinks), to insufflating and injecting the fine, white, water-soluble, powder form, to a smokable freebase form called “crack,” which became popular in the 1980s.1 In 2007, 2.1 million Americans had recent cocaine use; 1.6 million met criteria for cocaine dependence or abuse.1 Cocaine accounted for 31% of all visits to the emergency department related to drug misuse or abuse.1 From 1971 to 1987, the incidence of deaths caused by cocaine overdose increased 20-fold in Dade County, Florida.2 In a consecutive series of 233 emergency visits by cocaine-using patients, 56% presented with cardiovascular complaints, including 40% with chest pain.3 A minority of these patients have acute myocardial infarction (MI) (≈6%),4,–,7 and overall mortality is low (<1%).3,–,5,8,–,10 However, cocaine is associated with a number of cardiovascular diseases, including MI, heart failure, cardiomyopathies, arrhythmias, aortic dissection, and endocarditis. Identifying patients with acute disease is challenging. This review describes the relationship between cocaine and various cardiovascular diseases, as well as appropriate diagnostic evaluation and therapies. ### Molecular Cocaine stimulates the sympathetic nervous system by inhibiting catecholamine reuptake at sympathetic nerve terminals,11,12 stimulating central sympathetic outflow,11 and increasing the sensitivity of adrenergic nerve endings to norepinephrine (Figure 1).12 Cocaine also acts like a class I antiarrhythmic agent (local anesthetic) by blocking sodium and potassium channels, which depresses cardiovascular parameters.13 Of these 2 primary, opposing actions, enhanced sympathetic activity predominates at low cocaine doses, whereas the local anesthetic actions …

Spectrum of electrocardiographic and angiographic coronary artery disease findings in patients with cocaine-associated myocardial infarction

Cocaine is the most common abused drug in patients presenting to the emergency room with chest pain and frequently leads to cardiac catheterization procedure. The extent of severity underlying coronary artery disease (CAD) in this subgroup of patients has not been well defined. This study set out to define the coronary anatomy as well as the extent of CAD in patients with cocaine-associated myocardial infarction (MI) and correlate that to the presenting electrocardiogram (ECG). Ninety-seven consecutive patients with documented MI and positive urine drug screen for cocaine metabolites were included in the study. Demographic, clinical, ECG and coronary angiography variables were collected. ST elevation MI was encountered in 32% of the patients. Other ECG findings included ST segment depression, T-wave inversion, left ventricular hypertrophy, conduction blocks and/or old MI in more than 80% of cases. Of the total of 66 patients who underwent angiography, 82% had obstructive CAD, with single-vessel disease being the most frequent finding. None of these presenting ECG findings correlated with angiographic location or severity of obstructive CAD. In nearly one-fifth of the patients, troponin elevation suggestive of cardiac myonecrosis occurred in the absence of ECG findings or angiographic coronary disease. The majority of patients with cocaine-associated MI have obstructive CAD with predominant single-vessel disease. Although ECG abnormalities are frequently encountered, they are of limited diagnostic value in the clinical decision making.

Traditional Risk Factors and Acute Myocardial Infarction in Patients Hospitalized with Cocaine‐Associated Chest Pain

Cocaine causes coronary artery constriction and may cause acute myocardial infarction (AMI). The role of traditional coronary risk factors in cocaine-associated myocardial infarction is unclear. We hypothesized that traditional risk factors play a major role in predicting AMI in patients admitted with cocaine-associated chest pain After reviewing 165 admissions for chest pain in patients with a history of recent cocaine use and/or a positive drug screen from January 2001 to December 2004, we identified 151 patients with information available on at least 6 of the following 7 risk factors: gender, hypertension, hyperlipidemia, diabetes, smoking, family history of coronary artery disease (CAD) and known CAD. AMI was diagnosed using WHO criteria. A risk score was calculated on the basis of the number of risk factors, gender and age. Association of AMI was evaluated with the individual risk factors and with the risk score. AMI was identified in 21 patients (14%). All patients diagnosed with AMI were smokers. Continuous risk score (p < 0.0001), highest vs. lowest quartile of risk score (p = 0.007), known CAD, age, hyperlipidemia and family history of CAD were individually associated with the diagnosis of AMI (p>or=0.05). Each quartile of risk score was associated with increased odds of the diagnosis of AMI and score of 8 or higher was statistically significant. Several traditional risk factors are associated with the diagnosis of AMI among patients hospitalized with cocaine-associated chest pain and increasing risk factor score was associated with increasing odds of AMI diagnosis.

Cocaine and coronary calcification in young adults: The Coronary Artery Risk Development in Young Adults (CARDIA) Study

Cocaine use is associated with myocardial ischemia and infarction, but it is unclear whether this is only because of the acute effects of cocaine on heart rate, blood pressure, and vasomotor tone or whether accelerated atherosclerosis from long-term exposure to cocaine also contributes. We sought to measure the association between cocaine exposure and coronary calcification, a marker for atherosclerosis, among participants in the CARDIA Study who received computed tomography scanning and answered questions about illicit drug use at the year 15 examination in 2000-2001. Among 3038 CARDIA participants (age 33-45 years, 55% women and 45% black), past cocaine exposure was reported by 35% and was more common among men, smokers, drinkers, and participants with less education. Powdered cocaine exposure was more common among whites, crack cocaine among blacks. Before adjustment, cocaine exposure was strongly associated with coronary calcification. After adjusting for age, sex, ethnicity, socioeconomic status, family history, and habits, however, these associations disappeared: adjusted odds ratios for coronary calcification were 0.9 (95% CI 0.6-1.3) for 1 to 10, 1.2 (95% CI 0.8-1.7) for 11 to 99, and 1.0 (95% CI 0.6-1.6) for > or =100 lifetime episodes of cocaine use, in comparison with none. Sex, tobacco, and alcohol use appeared to be primarily responsible for the confounding we observed in unadjusted models. We found no evidence of a causal relationship between long-term exposure to cocaine and coronary calcification and conclude that acute nonatherogenic mechanisms probably explain most cocaine-associated myocardial infarction.

Intravascular Ultrasound-Guided Percutaneous Coronary Intervention in a Human Immunodeficiency Virus-Positive Patient with Cocaine-Associated Acute Myocardial Infarction: Case Report and Review

Cocaine use is a major problem worldwide and there are numerous reports about cocaine-associated myocardial infarction. Nevertheless minimal data are available from randomised clinical trials to suggest evidence-based approaches to the management of cocaine-associated myocardial ischemia. Moreover, most reports have been limited to conservative management of cocaine-associated myocardial infarction. We report a case of a young male cocaine user with acute myocardial infarction, undergoing diagnostic coronary angiography and intravascular ultrasound revealing severe atherosclerosis, followed by successful stent implantation.

Coronary angiographic findings in patients with cocaine-associated chest pain

Patients who present to the Emergency Department (ED) with chest pain associated with cocaine use are a common problem. The incidence and predictors of underlying significant coronary disease in patients with and without myocardial infarction (MI) has not been well described. Patients who underwent coronary angiography within 5 weeks of an ED evaluation for cocaine-associated chest pain were studied. Significant disease was defined as ≥ 50% stenosis of a coronary artery or major branches or bypass graft. A total of 90 patients underwent coronary angiography. Significant disease was present in 45 (50%), with 1-vessel disease in 32%, 2-vessel disease in 10%, 3-vessel disease in 6%, with significant graft stenosis in 3%. Significant disease was present in 77% of patients with MI or troponin I elevations, compared to only 35% of patients without myonecrosis. Predictors of significant coronary disease included MI or troponin I elevations, prior MI, known coronary disease (prior MI or revascularization), and elevated cholesterol. Only 7 of the 39 patients (18%) without myonecrosis or a history of coronary disease had significant disease on angiography. In conclusion, significant disease is found in the majority of patients with cocaine-associated MI or troponin elevations. In contrast, only a minority of those without myonecrosis have significant coronary disease.

Percutaneous interventions in patients with cocaine-associated myocardial infarction: a case series and review.

Cocaine-associated myocardial infarction (CAMI) is a well-reported entity. Most previous reports on CAMI have been limited to conservative care utilizing benzodiazepines, aspirin, nitroglycerin, calcium channel blockers, and thrombolytics. Current guidelines on CAMI advocate immediate use of angiography and angioplasty if available rather than routine administration of thrombolytics. However, based on literature search from 1966 to 2001 (using keywords "cocaine," "myocardial infarction," and "angioplasty"), there have been only two case reports of percutaneous coronary intervention (PCI) in patients with cocaine-associated myocardial infarction. Both were notable for complications either during or immediately after the procedure. We report a series of 10 patients with cocaine-associated myocardial infarction who were treated with percutaneous interventions, which included angioplasty, stenting, and AngioJet mechanical extraction of thrombus. Despite the different arteriopathic process involved, our findings suggest that PCI can be performed safely and with a high degree of procedural success in patients with CAMI.

Predictors of Coronary Artery Disease in Patients With Cocaine-associated Myocardial Infarction

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.

Clinical Safety of Lidocaine in Patients With Cocaine-Associated Myocardial Infarction

Study objective: To evaluate the safety of lidocaine in the setting of cocaine-induced myocardial infarction (MI). Design: A retrospective, multicenter study. Setting: Twenty-nine university, university-affiliated, or community hospitals during a 6-year period (total of 117 cumulative hospital-years). Participants: Patients with cocaine-associated MI who received lidocaine in the emergency department. Results: Of 29 patients who received lidocaine in the setting of cocaine-associated MI, no patient died; exhibited bradydysrhythmias, ventricular tachycardia, or ventricular fibrillation; or experienced seizures after administration of lidocaine (95% confidence interval, 0% to 11%). Conclusion: Despite theoretical concerns that lidocaine may enhance cocaine toxicity, the use of lidocaine in patients with cocaine-associated MI was not associated with significant cardiovascular or central nervous system toxicity. [Shih RD, Hollander JE, Burstein JL, Nelson LS, Hoffman RS, Quick AM, and the Cocaine-Associated Myocardial Infarction Study Group: Clinical safety of lidocaine in patients with cocaine-associated myocardial infarction. Ann Emerg Med December 1995;26:702-706.]

Cocaine-associated myocardial infarction. Mortality and complications. Cocaine-Associated Myocardial Infarction Study Group

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. 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. 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%). The mortality of patients hospitalized with cocaine-associated myocardial infarction was low. The majority of complications occurred within 12 hours of presentation.

Cocaine-Associated Myocardial Infarction

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 inhospital 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. (Arch Intern Med. 1995;155:1081-1086)

Cocaine-Associated Myocardial Infarction: Clinical Safety of Thrombolytic Therapy

To determine the safety of thrombolytic use in patients with cocaine-associated myocardial infarction. Retrospective cross-sectional survey. Twenty-nine acute care institutions. Patients who sustained cocaine-associated myocardial infarction from 1987 to 1993 were identified through medical record review. Those who received thrombolytic therapy (n = 25) were compared with those who met electrocardiographic TIMI criteria but did not receive thrombolytic therapy (n = 41). None. Both groups of patients were similar with respect to age, gender, race, cardiac risk factors, time from last cocaine use until presentation, and duration of chest pain at the time of presentation (p > 0.20). There were no major complications or deaths in patients who received thrombolytic therapy (95% confidence interval, 0 to 12%). Minor complications occurred in only two patients. The presence or absence of clinical criteria for reperfusion was noted in the charts of 21 patients who received thrombolytic therapy: 67% were believed to reperfuse. The patients who did and did not receive thrombolytic therapy had similar median peak creatine kinase-MB (CK-MB) levels (180 vs 154 mg/dL, p = NS) and time until peak CK-MB (11.3 vs 13.6 h; p = NS). Thrombolytic therapy for cocaine-associated myocardial infarction appears to be safe. It remains unclear whether thrombolytic therapy is an important therapeutic intervention for patients with cocaine-associated myocardial infarction. Further study on efficacy is recommended prior to routine use.

Late coronary aneurysm formation after directional atherectomy

Treatment of myocardial infarction associated with amphetamine abuse is not clearly defined at present. Because the possible mechanisms leading to myocardial infarction are coronary spasm and thrombosis, a net benefit from thrombolytic therapy is possible but still uncertain. Thrombolysis has been shown to be effective in treating cocaineassociated myocardial infarction. In that situation, however, thrombosis is present in most patients.7 Calciumchannel blockers, which are effective in treating vasospastic angina, may play a special role in the treatment of amphetamine-related myocardial infarction. Antiplatelet agents may also be helpful. Beta-adrenergic-blocking agents should probably be avoided until the pathophysiology of this condition has been clarified because they may exacerbate vasospasm. Lang et al5 demonstrated decreased coronary blood flow and increased coronary resistance when propranolol was given intracoronarily to patients who were intranasal cocaine users. This case demonstrates a fatal complication of recent amphetamine use. Because of the significant number of adolescents and young adults who have exposure to amphetamines,a physicians caring for this patient population should maintain a high index of suspicion regarding coronary events in this otherwise low-risk population.

Cocaine Produces Coronary Artery Vasoconstriction Independent off an Intact Endothelium

Studies have demonstrated that cocaine causes coronary vasoconstriction, but this has been unassociated with myocardial ischemia. Therefore, cocaine seems unlikely to precipitate myocardial infarction in the absence of potentiating factors. We hypothesized that injury to coronary endothelium could potentiate cocaine-induced coronary vasoconstriction by decreasing EDRF. The effect of cocaine on LAD diameter was measured in dogs subjected to coronary endothelial denudation and compared with that in a non-denuded control group. Endothelial denudation was accomplished by abrasion with an inflated angioplasty balloon and confirmed in vivo by demonstrating a vasoconstrictive response to infused acetylcholine and by postmortem scanning electron microscopy. Cocaine produced a similar maximal reduction in LAD diameter in both groups. Thus, cocaine induces endothelium-independent coronary artery vasoconstriction. Failure of endothelial injury to potentiate the coronary vasoconstrictive effect by cocaine suggests that factors other than endothelial dysfunction may be important in pathogenesis of cocaine-associated myocardial infarction.