Epidemiology
- There are more than 400,000 ED visits in the United States annually related to cocaine use.
- 40% of patients presenting to the ED after cocaine use report chest pain.
- 6% of patients presenting to the ED with cocaine-associated chest pain have evidence of myocardial infarction.
- The most frequent age group for these visits is 35-44 years of age.
Pathophysiology
- Cocaine prevents norepinephrine and dopamine reuptake, which leads to alpha-1 and beta-1 activation. This increases myocardial demand (increased heart rate, BP, and contractility), decreases oxygen supply by constricting coronary and peripheral arteries (decreased endothelin-1 and nitric oxide), promotes thrombus formation (increased CRP, vWF, and fibrinogen), and accelerates atherosclerosis (increased platelet activation).
- Alcohol and tobacco use appear to act synergistically.
Differential Diagnosis
- Consider cocaine-associated aortic dissection, myocarditis, arrhythmia, pulmonary HTN, and hemorrhagic alveolitis (hypoxemia, hemoptysis, respiratory failure, CXR infiltrates).
Evaluation
- Chest pain usually develops within 60 minutes, but can occur hours or days after cocaine use.
- Other symptoms accompanying acute cocaine intoxication may include dyspnea, diaphoresis, anxiety, palpitations, dizziness, and nausea.
- Obtain 12-lead ECG, troponin, u-tox, CXR, and consider the need for CTA chest.
Management
- Patients with chest pain after cocaine use with a non-diagnostic ECG and negative troponin observed over a 9-to-12-hour period have a very low risk of MI or death during the 30 days post-discharge. Pre-discharge stress testing can be considered based on signs, symptoms and risk factors for obstructive coronary artery disease.
- Patients with cocaine-associated chest pain, myocardial infarction, and ACS or possible ACS should be managed similarly to patients without cocaine use.
- Specific considerations for cocaine-associated chest pain and myocardial infarction are listed below:
- Benzodiazepines are first-line treatment; they have beneficial hemodynamic and neuropsychiatric effects.
- Nitrates are often helpful for treating coronary vasospasm/constriction.
- There is controversy regarding the use of beta-blockers in the acute setting due to the theoretical potential for increased blood pressure and coronary vasoconstriction from unopposed alpha-adrenergic stimulation. If beta-blockers are used, some suggest the use of non-selective alpha- and beta-blockers such as labetalol or carvedilol rather than beta-selective blockers such as metoprolol due to reduction in this theoretical risk. While the 2008 AHA guidelines on management of cocaine-associated chest pain and myocardial infarction recommend against the use of beta-blockers, others have suggested that the administration of beta-blockers (including metoprolol) are safe and potentially beneficial in cocaine-associated chest pain and myocardial infarction based on a more recent retrospective study of patients who received beta-blocker administration in the emergency department. We do not recommend withholding beta blockers for patients with cocaine-associated chest pain if clinically indicated.
- Consider the use of calcium channel blockers for chest pain unresponsive to benzodiazepines and nitrates if there are specific patient-level concerns about the use of beta blockers.
References
Finkel JB, Marhefka GD. Rethinking Cocaine-Associated Chest Pain and Acute Coronary Syndromes. Mayo Clin Proc. 2011 Dec;86(12):1198-1207.
Lange RA, Hillis LD. Cardiovascular complications of cocaine use. N Engl J Med 2001;345:351-358.
McCord J, Jneid H, Hollander JE, et al. Management of cocaine-associated chest pain and myocardial infarction: a scientific statement from the American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology. Circulation. 2008:1897-907.
Rangel C, Shu RG, Lazar LD, et al. Beta-blockers for Chest Pain Associated with Recent Cocaine Use. Arch Int Med 2010; 170: 874-879.
Weber JE, Shofer FS, Larkin GL, et al. Validation of a brief observation period for patients with cocaine-associated chest pain. N Engl J Med 2003;348:510-517.