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

Jenny A. Van Amburgh, PharmD


November 29, 2016


While there is a consensus that cocaine causes cardiotoxicity that is multifactorial in nature, is the role of beta-blockers in mitigating its effects any more clear?

Jenny Van Amburgh, PharmD
Assistant Dean of Academic Affairs; Clinical Professor, School of Pharmacy, Northeastern University; Director, Clinical Pharmacy Services & Residency Program, Harbor Health Services, Inc., Boston, Massachusetts

Background and Pathophysiology

Cocaine is one of the most commonly abused substances, with a 2014 National Survey on Drug Use and Health reporting that approximately 1.5 million people in the United States use cocaine.[1] Extracted from leaves of the plant Erythroxylum coca, cocaine was originally used to treat various illnesses; however, because of its addictive nature, it is now a Schedule II drug with limited medical use as a local anesthetic.[2]

Chest pain induced by illicit cocaine use is one of the leading causes of drug-related visits to hospital emergency departments ; myocardial infarction (MI) occurs in up to 6% of patients with cocaine-associated chest pain.[3,4,5] Cocaine-related ischemia and chest discomfort may be of atherosclerotic or nonatherosclerotic origin and may present identically to acute coronary syndrome (ACS). Treatment of cocaine-related chest pain is often treated similarly to ACS,[5] but the use of beta-blockers in the setting of cocaine use is debated because of the cardiac effects of each substance.

Cocaine toxicity can affect nearly every organ system, including the cardiovascular, hematologic, and neurologic systems.[6] Some of the most concerning toxicities are cardiopulmonary symptoms, which occur in up to 56% of cocaine users.[4]

Cocaine acts by blocking norepinephrine and dopamine within the synapse, resulting in accumulation of catecholamine and amplification of sympathetic neuronal signaling.[2] The sympathetic mechanisms lead to increases in heart rate, ventricular contractility, blood pressure, and myocardial oxygen demand.[4,7,8] Vasoconstriction can occur via alpha-adrenergic stimulation, as well as by increased levels of endothelin-1 (a vasoconstrictor) and reduced production of nitric oxide (a vasodilator), causing decreased oxygen supply, myocardial ischemia, and chest pain. Cocaine induces prothrombotic changes by stimulating platelet activation and upsetting the balance between procoagulant and anticoagulant factors.[4] Additionally, cocaine can cause oxidative stress on cardiomyocytes and injury to vasculature by increasing platelet coagulation and inducing the release of von Willebrand factor,[8] which increase the risk for cardiovascular events.


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