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β-Blockers have been a cornerstone secondary prevention therapy for patients with acute myocardial infarction (AMI) since large randomised controlled trials (RCTs) conducted in the 1970s and 1980s demonstrated large treatment effects on mortality. In a meta-analysis of these trials, the long-term use of β-blockers resulted in a 23% reduction in the risk of death, driven mostly by a 32% reduction in the risk of sudden death.1 Since then, the widespread use of reperfusion therapy and effective pharmacological treatment with antiplatelet drugs and statins has resulted in improved prognosis,2 so the benefits of β-blockers may have declined over time. Nonetheless, the use of β-blockers after an AMI hospitalisation has been identified as a measure of healthcare quality, resulting in 90% prescribing rates in the USA and Europe. β-blockers are similarly effective for the prevention of death in patients with heart failure due to left ventricular systolic dysfunction (LVSD).
The evidence supporting the use of β-blockers for the treatment of stable coronary artery disease (CAD) is less clear. While effective in providing relief from anginal symptoms, β-blockers do not prevent deaths or AMI in patients with stable angina when compared with placebo or active-control drugs in RCTs.3 Guidelines on the management of stable CAD from the American Heart Association and the European Society of Cardiology distinguish between these two rationales for the use of β-blockers.4 ,5 They make strong evidence-based recommendations about the use of β-blockers for the treatment of anginal symptoms, but extrapolate from evidence in the post-MI setting to suggest that β-blockers may prevent adverse cardiovascular events in patients with stable CAD. Whether β-blockers are useful for secondary prevention in this population is an open question. This gap in evidence …