The beta-blocker controversy: The use of beta-blockers in patients with CACP remains controversial given the theoretical risk of unopposed alpha-adrenergic activation. Coronary vasospasm, decreased myocardial oxygen delivery, and increased systemic vascular resistance can result from their use.30
Propranolol, a nonselective beta-blocker, was shown in catheterization studies to potentiate the coronary vasoconstriction of cocaine.31 Labetalol, a combined alpha/beta-blocker, reduced mean arterial pressure after cocaine administration during cardiac catheterization but did not reverse coronary vasoconstriction.32 This was attributed to the predominating beta greater than alpha blockade at doses administered. The selective beta-1 antagonists esmolol and metoprolol have shown no benefit in CACP.33 Carvedilol, a combined alpha/beta-blocker with both peripheral and central nervous system activity, has potential to attenuate both physiologic and behavioral response to cocaine, but it has not been well studied in this patient subset.34
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Table 1. Initial medical therapies for cocaine-associated chest pain18,38
The 2005 ACC/AHA STEMI guidelines recommended against beta-blockers in the setting of STEMI precipitated by cocaine use due to the potential of exacerbating coronary vasoconstriction.35 The 2007 ACC/AHA UA/NSTEMI guidelines stated that the use of a combined alpha/beta-blocker in patients with cocaine-induced ACS may be reasonable for patients with hypertension or tachycardia if pre-treated with a vasodilator.19 The 2008 ACC/AHA guidelines on the management of cocaine-related chest pain and MI recommended against the use of beta-blockers in the acute setting given the low incidence of cocaine-related MI and death.18
In a more recent study, Dattilo et al showed that beta-blockers administered to patients admitted with positive urine toxicology for cocaine significantly reduced MI and in-hospital mortality. Reduction of MI was of borderline significance in those admitted with a chief complaint of chest pain.36 Limitations of this study include unknown time of cocaine ingestion, lack of follow-up on discharge mortality, and a small sample size of 348 patients lacking statistical power.
Another retrospective cohort study examined patients admitted with chest pain and urine toxicology positive for cocaine and found that beta-blocker administration during hospitalization was not associated with increased incident mortality. Further, after a mean follow-up of 2.5 years, there was a statistically significant decrease in cardiovascular death.37 Drawbacks of this study included an older patient population, greater proportion of coronary artery disease, and higher follow-up of cardiovascular mortality rates than in previous studies, suggesting this subset might have received greater benefit from beta-blockers as a result of these characteristics.
The 2008 ACC/AHA guidelines instruct individualized consideration of the risk/benefit ratio for beta-blocker use in patients with CACP given the high rate of recidivism in cocaine abusers. The strongest indication is given to those with documented MI, left ventricular systolic dysfunction, or ventricular arrhythmias.18
It is important to note that these recommendations are based on cardiac catheterization laboratory studies, case reports, retrospective analyses, and animal experiments. No prospective controlled trials evaluating the role of beta-blockers in CACP and MI exist, and no trials regarding therapies to improve outcomes of patients sustaining a cocaine-associated MI have been reported.18
Back to the Case
This patient was experiencing cocaine-associated chest pain, which was confirmed with positive urine toxicology. Initial diagnostic workup with basic laboratory studies and cardiac biomarkers showed mild elevation in CK with troponin levels within normal limits. His ECG showed changes consistent with left ventricular hypertrophy. Chest radiograph was unremarkable.
He received aspirin, benzodiazepines, and nitroglycerin with normalization of vital signs, as well as subjective improvement in chest pain and anxiety. He was deemed to be at low risk for potential cardiac complications; thus, further cardiac testing was not pursued. Rather, he was admitted to an overnight observation unit with telemetry monitoring, where his chest pain did not recur.