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Cocaine-Associated Chest Pain the Differential Diagnosis for Cocaine-Associated Chest Pain Is Broad and Can Involve Symptoms Commonly Seen with Other Conditions

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Cocaine-Associated Chest Pain the Differential Diagnosis for Cocaine-Associated Chest Pain Is Broad and Can Involve Symptoms Commonly Seen with Other Conditions Cocaine-Associated Chest Pain The differential diagnosis for cocaine-associated chest pain is broad and can involve symptoms commonly seen with other conditions. In this review, the author describes the complex pathophysiology of these disorders and the specific diagnostic and therapeutic approaches necessary to prevent serious consequences. James H. Jones, MD ince the first reported case of cocaine- anesthetic properties of the ester type and also has associated acute myocardial infarction a direct effect on the myocardium, where it blocks (AMI) in 1982,1 the incidence of cardio- fast sodium channels. The systemic effects of cocaine vascular disorders arising from cocaine use are produced from the inhibition of monoamine Shas steadily increased.1 According to the Drug Abuse reuptake pumps (both peripherally and centrally) in Warning Network, the number of cocaine-related the presynaptic membrane for norepinephrine, epi- emergency department (ED) visits reported in 2005 nephrine, dopamine, and serotonin. This inhibition, was higher than in 2004, reaching nearly 484,000.2,3 in turn, produces increased extracellular and plasma Not surprisingly, chest pain is the most common concentrations of these neurotransmitters, leading to symptom.4 Cocaine accounts for 25% of AMIs in the typical sympathomimetic toxidrome seen with co- patients aged 18 to 45 years.5 The incidence of AMI caine. The drug’s metabolism and elimination occur among patients who present with cocaine-associated by several mechanisms. Between 30% and 50% of the chest pain is as high as 6%, and AMI is 24 times more drug is quickly hydrolyzed by liver and plasma cho- likely than not to occur within the first hour after the linesterases. Nonenzymatic hydrolysis accounts for drug is used.6 Thus, the emergency medicine clini- another 40% of its breakdown. Several of cocaine’s cian must be vigilant when caring for patients who metabolites are thought to be biologically active, in- present with cocaine-associated chest pain. cluding benzoylecgonine, which is typically found in the urine for 48 to 72 hours after the drug is used and PHARMACOLOGY is the compound detected by most urine drug screens.7 The pharmacology of cocaine plays a significant role The combination of alcohol and cocaine produces co- in its clinical effects. Cocaine can be ingested, insuf- caethylene, which has a half-life exceeding 2 hours flated (snorted), inhaled, and intravenously injected. and prolongs the euphoric experience associated with The onset of the drug’s effects cocaine. It is also a potent sodium channel blocker and >>FAST TRACK<< is dependent upon the route directly depresses the myocardium.8,9 Cocaine possesses local of administration. With in- anesthetic properties of travenous injection and inha- PATHOPHYSIOLOGY the ester type and also lation, the effects are almost The pathophysiology of cocaine-associated myocar- has a direct effect on immediate, whereas with in- dial ischemia may be best explained in terms of the the myocardium, where sufflation, they peak within drug’s actions on the heart over time. Its immedi- it blocks fast sodium 30 minutes. When smoked, ate effects take two forms. First, the tachycardia and channels. crack cocaine gives an almost hypertension that accompany this sympathomimetic instantaneous high, an effect toxidrome lead to increased myocardial oxygen de- that contributes to the drug’s potency and increases mand, which is primarily centrally mediated.10 Sec- the likelihood of addiction. Cocaine possesses local ond, cocaine causes coronary vasoconstriction of both healthy and diseased epicardial coronary ar- Dr. Jones is a professor of clinical emergency medicine 10,11 and vice chair in the department of emergency medicine at teries. This effect seems to be greatest at sites the Indiana University School of Medicine, Indianapolis. involving atherosclerotic lesions, which, when com- 22 EMERGENCY MEDICINE | OCTOBER 2009 www.emedmag.com COCAINE-ASSOCIATED CHEST PAIN bined with the increased oxygen demand mediated by cocaine, can produce myocardial ischemia.12 TABLE 1. Differential Diagnosis of The intermediate result of cocaine’s effect on the Cocaine-Associated Chest Pain myocardium is due to enhanced thrombus forma- tion. The drug’s direct effects on platelets lead to ag- Acute coronary syndrome Pericarditis gregation.13-15 Although thrombus formation is more Pneumothorax Myocarditis common with underlying coronary artery disease, it can occur in healthy coronary arteries.11 Pneumomediastinum Pneumonia The long-term consequences of cocaine use on the Pneumopericardium Endocarditis heart include accelerated atherogenesis, left ventricular hypertrophy, and dilated cardiomyopathy.10,11,16 Pro- Aortic dissection “Crack lung” longed cocaine use increases the risk of premature and Pulmonary embolism Musculoskeletal pain more severe coronary atherosclerosis.17 Angiographic studies show that as many as 40% of long-time users of cocaine have significant coronary artery disease, defined as stenosis involving greater than 70% oc- initially denied using the drug.20 In addition, the clusion, often in the absence of other established risk method and amount of cocaine use are not predictive factors for ischemic heart disease.18 In addition, this of the development of myocardial ischemia, nor are disease is generally more severe than that observed the location, duration, and severity of the associated among age-matched control subjects. Left ventricular symptoms. Almost all cocaine-associated MIs occur hypertrophy that occurs with prolonged cocaine use is within 24 hours after the drug is used.6,21 similar to that seen in other hyperdynamic states such The ECG is the most important initial test, as as thyrotoxicosis and aortic stenosis. the results likely determine the appropriate ther- apy. Unfortunately, as many as 35% of patients DIFFERENTIAL DIAGNOSIS presenting with cocaine-associated chest pain may The differential diagnosis of chest pain associated demonstrate signs consistent with benign early re- with cocaine is broad (Table 1). Although the imme- polarization.22 This, along with ECG evidence of diate evaluation for myocardial ischemia and infarc- left ventricular hypertrophy in some patients, can tion is mandatory, it is important for the clinician not make interpretation of ischemia challenging, espe- to establish a specific diagnosis too quickly. In cases cially when J-point and ST-segment elevation are of cocaine use, many other causes of chest pain can considered. Research has shown that the sensitivity be seen, such as pneumothorax and pneumomedias- of the ECG for AMI is lower in cocaine users than tinum. Cocaine has been noted to be a cause for aor- in other patient populations.21 tic dissection.19 Pneumonia, pericarditis, endocardi- Clinicians also rely upon the use of cardiac mark- tis, myocarditis, and pulmonary embolism have all ers in determining the appropriate treatment for been associated with cocaine use. If not considered patients with cocaine-associated chest pain. Such and promptly recognized, all of these disorders can assessments can be complicated by false elevations have serious consequences. of creatine kinase and cre- atine kinase MB, which are >>FAST TRACK<< EVALUATION presumably caused by agi- Almost all cocaine- Patients with cocaine-associated chest pain must tation and rhabdomyoly- associated MIs occur undergo an evaluation that focuses not only on the sis.23 Troponins I and T do within 24 hours after the toxidrome that may accompany cocaine use but also not exhibit cross-reactivity drug is used. on specific end-organ disorders. As mentioned pre- with human skeletal muscle viously, chest pain is the most frequent symptom troponins and are therefore as sensitive but more among this population. Unfortunately, such patients specific than the creatine kinase and creatine kinase may not always be forthcoming about their recent MB measurements.24,25 drug use or may present hours after symptoms be- Another important diagnostic test is chest radiog- gin. In one prevalence study, 28% of cocaine users raphy, which is useful for determining any noncar- www.emedmag.com OCTOBER 2009 | EMERGENCY MEDICINE 23 COCAINE-ASSOCIATED CHEST PAIN tional series, case series and reports, and very small TABLE 2. Treatment for Cocaine- clinical trials. In general, patients who present with Associated Acute Coronary Syndromes cocaine-associated chest pain and suspected myocar- dial ischemia and injury should undergo the same Oxygen Recommended treatment as those with traditional acute coronary Aspirin Recommended syndrome (ACS); as exceptions, beta-adrenergic blockade must be avoided and calcium channel block- Benzodiazepines Recommended ers may be considered as an option (Table 2). Nitroglycerin Recommended Decades of clinical experience with intravenous benzodiazepines demonstrate that these drugs are ef- Heparin Recommended fective in attenuating the rise in heart rate and blood Beta-blockers Contraindicated pressure associated with cocaine use and lead to a decrease in myocardial oxygen demand.10,28 Calcium channel Consider if benzodiazepines Aspirin and heparin are important treatments. The blockers and nitroglycerin are pathophysiology of thrombus formation secondary to ineffective platelet aggregation suggests that the role of both of Phentolamine Consider if hypertension these agents makes theoretical sense, although little persists evidence supports this approach.27 Nevertheless, the benefits of these agents likely outweigh their risks. Ni- Percutaneous
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