Background: Cocaine produces cardiovascular toxicity through intense sympathetic stimulation and direct myocardial injury, generating presentations ranging from hypertension and tachycardia to coronary vasospasm, arrhythmia, and myocardial depression. Beta blockers are foundational therapies in acute coronary syndromes, yet their use after cocaine exposure remains controversial due to concerns about unopposed alpha adrenergic stimulation. Methods: A systematic review was conducted in accordance with PRISMA guidelines. PubMed and Google Scholar (2000 to 2026) were searched for observational studies of adults (> 18 years) presenting to acute care with recent cocaine use that compared outcomes between beta blocker recipients and non recipients. Eligible studies reported in hospital mortality, myocardial infarction/troponin rise, clinically significant arrhythmia, or haemodynamic instability. Risk of bias was assessed using the Newcastle Ottawa Scale, and certainty of evidence using GRADE. Results: Four retrospective ED cohorts (n = 1,140) met inclusion criteria; 503 patients received at least one beta blocker dose. Across studies, beta blocker use was not associated with increased in hospital mortality or malignant arrhythmias. Myocardial infarction was heterogeneous and sensitive to definition and timing. Haemodynamic data showed no hypertensive surge and modest systolic blood pressure reductions. Risk of bias was moderate, and certainty of evidence very low to low. Conclusions: In typical ED presentations of recent cocaine use, beta blocker administration does not appear to increase mortality, myocardial infarction, or malignant arrhythmias, and available haemodynamic data do not support a reproducible unopposed alpha response. However, mechanistic and preclinical evidence suggests potential harm in severe intoxication or myocardial depression. A selective, phenotype guided approach is warranted, and prospective mechanistic studies are needed.
Paterson, T., Katraj, S. V. K., Van Wyk, A., Pooranachandran, V.
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