BACKGROUND: Cocaine is the most common illicit drug used in patients presenting with chest pain to emergency departments. Data on beta-blockers in cocaine-related chest pain syndrome are sparse. We sought out to study the causal and detrimental effects of beta-blockers in cocaine-related chest pain in a large inner city cohort of patients. METHODS AND RESULTS: All patients presenting to a large inner city emergency department with chest pain, with positive urine drug screen for cocaine were included. The group comprised predominantly young (mean age 46.8 +/- 8.2 years), African American (90.6%) males (73.4%). Evidence of myocardial infarction in the form of elevation of troponin-I was noted in 7.3%. Evidence of myonecrosis (MN) was significantly more likely in those who were taking beta-blockers at presentation as compared with those who were not (14% versus 4.4%, P < 0.01). In the absence of prospective controlled data, our observational findings seem to suggest that routine initiation or continuation or of beta-blockers after admission increased the likelihood of developing MN (23.3% versus 10.7%, P < 0.01) during the course of hospitalization. CONCLUSIONS: MN as reflected by elevation of cardiac biomarkers is uncommon in patients presenting with cocaine-related chest pain. Preexisting use of beta-blockers seems to render a higher risk of myocardial injury in patients presenting with cocaine-related chest pain. In addition initiation or continuation of beta-blockers during hospitalization should be discouraged.
BACKGROUND:Cocaine is the most common illicit drug used in patients presenting with chest pain to emergency departments. Data on beta-blockers in cocaine-related chest pain syndrome are sparse. We sought out to study the causal and detrimental effects of beta-blockers in cocaine-related chest pain in a large inner city cohort of patients. METHODS AND RESULTS: All patients presenting to a large inner city emergency department with chest pain, with positive urine drug screen for cocaine were included. The group comprised predominantly young (mean age 46.8 +/- 8.2 years), African American (90.6%) males (73.4%). Evidence of myocardial infarction in the form of elevation of troponin-I was noted in 7.3%. Evidence of myonecrosis (MN) was significantly more likely in those who were taking beta-blockers at presentation as compared with those who were not (14% versus 4.4%, P < 0.01). In the absence of prospective controlled data, our observational findings seem to suggest that routine initiation or continuation or of beta-blockers after admission increased the likelihood of developing MN (23.3% versus 10.7%, P < 0.01) during the course of hospitalization. CONCLUSIONS: MN as reflected by elevation of cardiac biomarkers is uncommon in patients presenting with cocaine-related chest pain. Preexisting use of beta-blockers seems to render a higher risk of myocardial injury in patients presenting with cocaine-related chest pain. In addition initiation or continuation of beta-blockers during hospitalization should be discouraged.