The Ongoing Debate of Beta-Blockers for Cocaine-Associated Chest Pain

Jenny A. Van Amburgh, PharmD


November 29, 2016


Cocaine toxicity is part of the differential diagnosis for any patient presenting with chest pain and suspected drug abuse; a cocaine etiology should be considered especially in adolescents and young adults presenting with chest pain.

For optimal management, such diagnostic strategies as urine toxicology screening or blood analysis should be used to determine the presence of cocaine.[4,7,8]

Historically, propranolol was the drug of choice for cocaine toxicity, but its use was abandoned because of its association with reduced survival in animal studies.[7,9,10] The adverse effect of propranolol on cocaine intoxication was likely due to the enhanced vasoconstrictive properties associated with unopposed alpha-adrenergic activity with a beta-antagonist. This increased mortality in animals with propranolol led to a shift away from all beta-blockers as first-line clinical agents in cocaine toxicity.[7]

Today, the use of beta-blockers for cocaine-induced symptoms is limited and highly debated. Beta-blockers, specifically selective beta-blockers, induce vasoconstriction via alpha-adrenergic effects, potentially worsening cocaine-induced vasospasm.[4] However, beta-blockers play a key role in decreasing mortality in patients with MI or systolic dysfunction,[11] and cocaine intoxication may mimic presenting symptoms of either emergency. Thus, the use of beta-blockers when the diagnosis is unclear remains controversial.

Several observational studies have examined the use of beta-blockers in the clinical setting of chest pain associated with cocaine use.

A retrospective analysis[12] of practice patterns on overall beta-blocker use, specific agent selected, and beta-blocker use for cocaine intoxication showed that less than half of patients presenting with cocaine-related chest pain received beta-blocker therapy, but patients showed no differences in the primary outcome (composite of MI, stroke, ventricular arrhythmia, or all-cause mortality) whether or not they were treated with beta-blockers.

Another retrospective study[11] associated beta-blocker therapy for cocaine-induced chest pain with a reduction in MI and death.

A surveillance study of beta-blocker use[13] within 24 hours of acute MI found that patients with reported cocaine use were less likely to receive beta-blockers in the first 24 hours of admission; nevertheless, most patients received beta-blockers regardless of cocaine status. Additionally, a significant number of patients, regardless of cocaine use, received beta-blockers at discharge even if they were not used during hospitalization.

Evidence and expert opinion for the use of beta-blockers in the presence of cocaine-induced events is briefly summarized in the Table below.

Table. Use of Beta-Blockers for Cocaine-Induced Events

Beta-blocker Selectivity* Findings
Esmolol Selective
  • No consistent hemodynamic benefit or consistent antihypertensive response[14]

  • Significant increase in blood pressure[14,15]

Labetalol Nonselective
  • Reduces arterial pressure but not vasoconstriction[16]

  • Increases heart rate and blood pressure[17]

Carvedilol Nonselective
  • Attenuates increases in heart rate, systolic and diastolic blood pressure in crack cocaine users[18]

Propranolol Selective
  • Exacerbates vasoconstriction[19]

*Selectivity is reported as beta-receptor activity, and "nonselective" refers to the agent having some level of alpha-receptor activity.


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