Why the study?
Evidence supporting routine beta-blocker prescription after ACS and PCI comes mostly from historical trials in patients with reduced systolic function. In contemporary practice, most patients have preserved LVEF, leaving the survival benefit of routine beta-blocker therapy across the full LVEF spectrum uncertain.
Does beta-blocker prescription at discharge reduce all-cause mortality in adults discharged alive after a coronary event managed with PCI across different LVEF strata?
Does beta-blocker prescription at discharge reduce all-cause mortality in adults discharged alive after a coronary event managed with PCI across different LVEF strata?
In a large contemporary cohort of post-PCI patients, routine discharge beta-blocker therapy was associated with increased all-cause mortality in those with preserved or mildly reduced LVEF and showed no survival benefit in those with more severe systolic dysfunction, challenging routine post-PCI beta-blocker prescription.
Beta-blocker use was associated with higher mortality in preserved LVEF; challenges consensus but leaves open randomized confirmation.
Background Beta-blockers are routinely prescribed after acute coronary syndromes and percutaneous coronary intervention (PCI), yet much of the supporting evidence comes from historical trials in patients with reduced systolic function. In contemporary practice, most patients have preserved left ventricular ejection fraction (LVEF), and the survival benefit of routine beta-blocker therapy across the full LVEF spectrum remains uncertain. Purpose To assess the association between discharge beta-blocker therapy and all-cause mortality following a coronary event and PCI, stratified by LVEF. Methods We conducted a state-wide nested case-control study within a cohort of adults (≥18 years) discharged alive after a coronary event managed with PCI, using data from the Victorian Cardiac Outcomes Registry linked to the Australian National Death Index (2014–2022). Patients were stratified by LVEF (preserved ≥50%, mildly reduced 41–49%, moderately reduced 35–40%, severely reduced <35%). Within each stratum, decedents (cases) were matched 1:1 to survivors (controls) on index discharge date. The exposure was beta-blocker prescription at discharge versus no prescription. Propensity scores incorporating 15 clinical and procedural covariates were used for 1:1 matching within time-matched sets. The primary outcome was all-cause mortality. Associations were estimated using conditional logistic regression with cluster-robust standard errors. Missing LVEF (10.7%) was addressed using multiple imputation. Sensitivity analyses included complete-case models and 30-day cardiovascular mortality. Results Among 71,053 eligible patients, 67.3% received beta-blockers at discharge. After propensity score matching, beta-blocker therapy was associated with higher odds of all-cause mortality in patients with preserved LVEF (odds ratio [OR] 1.46, 95% confidence interval [CI] 1.29–1.65) and mildly reduced LVEF (OR 1.48, 95% CI 1.15–1.91). No significant association was observed in moderately reduced (OR 1.21, 95% CI 0.92–1.58) or severely reduced LVEF (OR 0.99, 95% CI 0.73–1.34). Sensitivity analyses were consistent with the primary findings: complete-case models produced similar estimates, and beta-blockers remained associated with increased 30-day cardiovascular mortality in preserved LVEF (OR 1.38, 95% CI 1.10–1.73). Conclusions In this large contemporary state-wide cohort of adults discharged alive after PCI for coronary events, beta-blocker therapy was associated with higher all-cause mortality in patients with preserved and mildly reduced LVEF and showed no survival benefit in those with more severe systolic dysfunction. These real-world findings question the generalisability of historical evidence and support a more individualised approach to beta-blocker use after PCI based on LVEF.
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Miranda et al. (2026) studied this question.
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