Beta blockers are indicated for management of acute coronary syndromes, but they generally
are withheld in patients with cocaine-associated chest pain because of concerns for
adverse outcomes related to the unique physiological effects of cocaine. Because few
clinical studies have evaluated this interaction, we identified patients with toxicology
screen results positive for cocaine treated for chest pain at 2 academic hospitals.
Clinical characteristics and in-hospital outcomes were compared between patients with
and without β-blocker therapy. We then constructed propensity scores to evaluate the
independent relation between β-blocker use and the composite primary end point of
myocardial infarction, stroke, ventricular arrhythmia, or all-cause mortality after
adjusting for clinical characteristics. Of 376 consecutive patients with cocaine-related
chest pain, β blockers were used in 164 (44%). Compared with no β blockers, patients
treated with β blockers were more likely to describe anginal chest pain, to have known
cardiovascular risk factors, and to receive other antiatherosclerotic therapies. Despite
these higher risk clinical characteristics, patients treated with β blockers experienced
similar peak troponin levels, individual adverse events, and rates of the composite
primary end point (15.9% vs 12.3%, p = 0.32). The primary end point also was similar
after propensity score analysis (odds ratio 1.37, 95% confidence interval 0.64 to
2.93, p = 0.42), including specific comparisons of beta-1 selective (odds ratio 1.83,
95% confidence interval 0.79 to 4.24) and nonselective (odds ratio 0.90, 95% confidence
interval 0.33 to 2.42) β blockers, when compared with patients not receiving β blockers.
In conclusion, no differences in outcomes were observed between patients treated versus
not treated with β-blocker therapy in the setting of cocaine-related chest pain.
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Article Info
Publication History
Published online: March 17, 2014
Accepted:
March 4,
2014
Received in revised form:
March 4,
2014
Received:
November 29,
2013
Footnotes
See page 1806 for disclosure information.
Identification
Copyright
© 2014 Elsevier Inc. Published by Elsevier Inc. All rights reserved.