Beta-Blockers and CAD?
Abstract & Commentary
By Andrew J. Boyle, MBBS, PhD. Assistant Professor of Medicine, Interventional Cardiology, University of California, San Francisco. Dr. Boyle reports no financial relationships relevant to this field of study.
Source: Bangalore S, et al. Beta-blocker use and clinical outcomes in stable outpatients with and without coronary artery disease. JAMA 2012;308: 1340-1349.
Beta-blockers have long been a cornerstone of therapy for patients who have suffered myocardial infarction (MI). However, most studies of beta blockade following MI were performed before the current era of reperfusion therapy, statins, and antiplatelet agents. Whether beta-blockers have a clinical benefit over more modern therapies is not known. Accordingly, Bangalore and colleagues studied patients from a large international registry to determine whether beta-blocker use is associated with lower rates of cardiovascular events in the modern era. They grouped the patients into three cohorts: those with prior MI, those with known coronary artery disease (CAD) but without prior MI, and those with CAD risk factors only. Within each of these cohorts, they compared the rate of cardiovascular events in patients who were taking beta-blockers to those who were not. Because of significant baseline differences between those who were and those who were not taking beta-blockers, the authors performed propensity matching to account for 27 baseline clinical variables. The primary endpoint of the study was a composite of cardiovascular death, nonfatal MI, or nonfatal stroke. The secondary outcome was the primary outcome plus hospitalization for atherothrombotic events or a revascularization procedure (coronary, cerebral, or peripheral). Tertiary outcomes were all-cause mortality, cardiovascular mortality, nonfatal MI, nonfatal stroke, and hospitalization, which were considered as separate outcomes. The median duration of follow-up was 44 months.
In each cohort, there were more than 3000 matched pairs of patients. In the prior MI cohort comparing patients taking beta-blockers to those who were not, there was no difference in the rate of the primary endpoint (16.9% vs 18.6%; P = 0.14), the secondary endpoint (31.0% vs 33.1%; P = NS), or any tertiary endpoints. In the CAD without MI cohort, comparing patients taking beta-blockers to those who were not, there was no difference in the rate of the primary endpoint (12.9% vs 13.6%; P = 0.31). The rate of the secondary endpoint was higher in those taking beta-blockers (30.6% vs 27.8%; P = 0.01). There was no difference in the tertiary endpoints. In the risk factors alone cohort, the event rates were higher in those taking beta-blockers compared to those who weren't for the primary endpoint (14.2% vs 12.1%; P = 0.02) and the secondary endpoint (22.0% vs 20.2%; P = 0.04), but there was no difference in the tertiary endpoints. To confirm these findings, the authors performed secondary statistical analyses and found that these agreed with their initial results. The authors conclude that in this observational study of patients with either CAD risk factors only, known prior MI, or known CAD without MI, the use of beta-blockers was not associated with a lower risk of composite cardiovascular events.
Commentary
This is a very important and interesting study. The current ACC/AHA guidelines give a class 1 recommendation for beta-blocker use after MI for up to 3 years, but a class 2a recommendation for longer use. Beta-blockers receive a class 2b recommendation in other patients with coronary or peripheral arterial disease. The salubrious effects of beta-blockers in patients following MI are often extrapolated to patients in other clinical situations, such as those with multiple risk factors. This study casts doubt on this practice, and suggests that the effects of beta-blockers in the modern era are not as profound as they were in times past. There are potentially patient subgroups that benefit from beta-blockade. This study suggests that the higher the patient's risk, the more potential there is to receive benefit from beta-blockers. Beta-blockade was associated with a trend toward improvement in the prior MI cohort, no improvement in the CAD without MI cohort, and worse outcomes in the risk-factor only cohort, suggesting that there may be more benefit from beta-blockers in patients at the higher end of the spectrum of risk. However, many questions remain. First, this study did not separate the different agents within the beta-blocker family, and there may be distinct differences between them. Along the same lines, we are not told what doses were used, nor how they were titrated. Second, the region of MI (i.e., anterior, inferior, or lateral) and the left ventricular function are not mentioned, and these factors may change the patient's risk profile and likelihood of deriving benefit from beta-blockers. Third, the time from MI to study inclusion is not stated. Fourth, this was a registry study, not a randomized study, and thus there may be unmeasured confounders. What should we do with these data? Should we abandon beta-blockers altogether? The answer is no. We should continue to treat post-MI patients with beta-blockers if they can tolerate them. Despite the limitations of this study, it raises important questions about the need for beta-blockers in these patient populations in the current era. Future randomized controlled trials are needed to address these questions.
Beta-blockers have long been a cornerstone of therapy for patients who have suffered myocardial infarction (MI). However, most studies of beta blockade following MI were performed before the current era of reperfusion therapy, statins, and antiplatelet agents.You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
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