INTERRUPTION of beta-blocker treatment after an uncomplicated myocardial infarction (MI) leads to sustained increases in blood pressure and heart rate, with potentially harmful effects on clinical outcomes, particularly in patients with a history of hypertension, according to the AβYSS trial.
Beta-blockers have been a mainstay of secondary prevention following MI, helping to reduce the risk of further cardiovascular events by lowering heart rate and blood pressure. Despite their established role, the consequences of stopping beta-blockers in stable patients after MI have not been fully understood. The AβYSS trial was designed to clarify the impact of beta-blocker interruption on blood pressure, heart rate, and clinical outcomes in a large cohort of post-MI patients, with a median follow-up of three years.
In this study, 3,698 patients were randomised to either continue or interrupt beta-blocker therapy. Changes in systolic and diastolic blood pressure, as well as resting heart rate, were assessed using linear mixed repeated models. Subgroup analyses focused on patients with and without a history of hypertension, and the primary composite endpoint included death, MI, stroke, or hospitalisation for cardiovascular reasons, analysed using adjusted Cox proportional hazards models. At six months, beta-blocker interruption was associated with significant increases in systolic blood pressure by 3.7 mmHg (95% CI 2.6 to 4.8, P < .001), diastolic blood pressure by 3.3 mmHg (95% CI 2.6 to 4.0, P < .001), and resting heart rate by 10 beats per minute (95% CI 9 to 11, P < .001). These increases persisted throughout the follow-up period, despite greater use of other antihypertensive medications in the interruption group. The effects were observed in both hypertensive (43% of participants) and non-hypertensive patients. Hypertensive patients had a higher risk of adverse events (25.8% vs 19.2%), with an adjusted hazard ratio of 1.18 (95% CI 1.01 to 1.36, P = .03). Notably, hypertensive patients randomised to beta-blocker interruption experienced a significantly greater increase in the primary endpoint risk, with a risk difference of 5.02% (95% CI 0.72% to 9.32%, P = .014).
These results highlight that stopping beta-blocker therapy after MI leads to sustained rises in blood pressure and heart rate, which may adversely affect cardiovascular outcomes, especially in patients with a history of hypertension. Clinicians should carefully consider the risks of beta-blocker interruption in post-MI management, particularly for hypertensive patients who appear more vulnerable to adverse events. Future research should explore strategies to safely manage beta-blocker therapy in this population and investigate whether tailored approaches based on individual risk profiles can improve long-term outcomes.
Reference
Procopi N et al. Beta-blocker interruption effects on blood pressure and heart rate after myocardial infarction: the AβYSS trial. European Heart Journal. 2025;ehaf170.
