Impact of Acute Beta-Blocker Therapy for Patients with Non–ST-Segment Elevation Myocardial Infarction
Abstract
Purpose
Early use of beta-blockers is a quality indicator for the treatment of patients with non–ST-segment elevation myocardial infarction (NSTEMI), despite limited data from randomized clinical trials in this population. We sought to determine the impact of acute beta-blocker therapy on outcomes in patients with NSTEMI.
Subjects and Methods
We examined acute (<24 hours) beta-blocker use in 72,054 patients with NSTEMI from the Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes with Early Implementation of the American College of Cardiology/American Heart Association Guidelines (CRUSADE) initiative at 509 US hospitals from 2001-2004. We analyzed patient and provider factors associated with beta-blocker use and the impact of beta-blocker therapy on unadjusted, risk-adjusted, and propensity matched outcomes in the overall sample and among selected high-risk subgroups.
Results
A total of 82.5% of patients without documented contraindications received acute beta-blocker therapy. Factors strongly associated with acute beta-blocker use included prior beta-blocker use, higher presenting systolic blood pressure, lower heart rate, lack of signs of heart failure, and cardiology care. Acute beta-blocker use was associated with lower in-hospital mortality (unadjusted 3.9% vs 6.9%, P <.001, adjusted odds ratio 0.66, 95% confidence interval 0.60-0.72), lower adjusted mortality among most of 6 subgroups determined by propensity to receive acute beta-blockers, and lower adjusted mortality in patients with and without signs of heart failure and in those <80 years and those ≥80 years old.
Conclusions
The majority of NSTEMI patients receive acute beta-blocker therapy. Certain patient subgroups remain undertreated. Because treatment with acute beta-blockers was associated with improved clinical outcomes in nearly all patient subgroups assessed, broader use in patients with NSTEMI appears warranted.
aWake Forest University Health Sciences, Winston-Salem, NC
bDuke Clinical Research Institute, Duke University Medical Center, Durham, NC
cPennsylvania Hospital, University of Pennsylvania School of Medicine, Philadelphia
dUniversity of Cincinnati College of Medicine, Cincinnati, Ohio.
Requests for reprints should be addressed to Eric Peterson, MD, MPH, Duke Clinical Research Institute, 2400 Pratt Street, Room 7009, Durham, NC 27705.
CRUSADE is funded by the Schering-Plough Corporation. Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership provides additional funding support. Millennium Pharmaceuticals, Inc. also funded this work.
ABSTRACT
