Should Beta-Blockers Be Used With Cocaine-Related Chest Pain?
January 2008
Should Beta-Blockers Be Used With Cocaine-Related Chest Pain?
Search Strategy: One of the difficulties in toxicology research is that it is very difficult to find randomized double blind prospective studies comparing treatments in poisoned/intoxicated patients because of ethical considerations. The other side of this was aptly put by Dr. Jerry (not Bob) Hoffman, who pointed out that you don’t need a controlled-double blind study to know that playing in traffic is dangerous. MEDLINE was searched using a sensitive therapeutic clinical query for “cocaine chest pain”: (cocaine chest pain) AND ((clinical[Title/Abstract] AND trial[Title/Abstract]) OR clinical trials[MeSH Terms] OR clinical trial[Publication Type] OR random*[Title/Abstract] OR random allocation[MeSH Terms] OR therapeutic use[MeSH Subheading]). Among the 117 citations identified was a Best Bets on the topic (http://pmid.us/16627850) which identified two classic articles on the topic, along with several recent reviews on cocaine-related chest pain which provide another reference. Finally, while perusing the ACEP website you note an unpublished article on the topic favoring the use of beta-blockers in this scenario.
A 51 year old gentleman presented to the ED complaining of substernal, intermittent chest pain radiating down his left arm. The pain lasted for approximately 20 minutes at a time and was associated with mild dyspnea. Interestingly, the pain came on suddenly at 7AM while the patient was snorting cocaine. He was also a smoker and had a history of hypertension.
On exam the patient was awake alert and appropriate. His blood pressure was 175/95; his heart rate was 120; his respiratory rate was 14; he was afebrile and his oxygen saturations were 96% on RA. The rest of his physical exam was normal. His EKG revealed T-wave inversions in leads V-5 and V-6. No old EKG was available and the CXR was unremarkable.
After treatment with aspirin, nitroglycerin and benzodiazepines, he experienced a complete resolution of his chest pain. Six hours later, he was noted to have persistent tachycardia (120’s) and a decision was made to rate-control him. A discussion ensued about the proper management of rate control in the setting of cocaine use. The attending physician felt that since the use of cocaine occurred 6 hours prior, it would be safe to give metoprolol as the cocaine had probably been metabolized. A dose of 2.5 mg was administered with no effect on the heart rate. Another dose of 2.5 mg was given 5 minutes later. Within 10 minutes of receiving this, the patient sat up in bed, clutched his chest and said “This is the worst chest pain I’ve ever had in my life.” The patient became unconscious, developed complete cardiovascular collapse and died.
PICO Question
Population: ED patients presenting suspected cocaine-related chest pain
Intervention: Beta-antagonist administration
Comparison: No beta-antagonist administration
Outcome: Cardiovascular mortality, all-cause mortality.
Years
Articles
Article 1: β-Blockers Are Associated With Reduced Risk of Myocardial Infarction after Cocaine Use — Annals of Emergency Medicine 2008
ANSWER KEY
Article 2: Influence of Labetalol on Cocaine-Induced Coronary Vasoconstriction in Humans — Am J Med 1993
ANSWER KEY
Article 3: Experience with Esmolol for the Treatment of Cocaine-Associated Cardiovascular Complications — Am J EM 1991
ANSWER KEY
Article 4: Potentiation of Cocaine-Induced Coronary Vasoconstriction by Beta-Adrenergic Blockade — Annals of Internal Medicine 1990
ANSWER KEY
Bottom Line
One new retrospective review suggests that β-blocker administration to admitted cocaine-positive angina patients is associated with a significant reduction in MI (adjusted OR 0.06, 95%, CI 0.01-0.61) and a strong trend towards decreased mortality (adjusted OR 0.22, 05% CI 0.02-2.41). Retrospective design limitations preclude the incorporation of β-blocker into routine clinical practice based upon this paper, but the study does present clinical equipoise sufficient to justify a future prospective RCT. More clinically representative cocaine-abusing populations ought to be evaluated using β-antagonists of variable route and receptors specificity measuring patient and clinician important outcomes before generally condemning β-antagonist in cocaine-related ACS. The available evidence against β-blockers in cocaine-chest pain used intracoronary β-antagonist within 15-minutes of cocaine administration to unequally allocated cath-lab patients (favoring the placebo arm every time). A case series fails to establish a dose-response effect since 2/3 bad outcomes hardly received any β-blocker prior to their adverse event.