Stopping Beta-Blockers After MI Raises BP, HR, and Risks in Hypertensives, suggests study
Researchers have established that the withdrawal of Beta-blocker therapy following a myocardial infarction (MI) results in prolonged elevations in blood pressure (BP) and heart rate (HR), and much more severe outcomes in patients with prior hypertension. Results are reported from the AβYSS trial, which sought to determine the long-term consequences of β-blocker withdrawal on cardiovascular status in post-MI patients. While β-blockers are well used post-MI to control cardiac workload and decrease complications, their continued use in patients with uncomplicated recovery is controversial. This research provides insight into what happens if β-blockers are discontinued, particularly in high-risk subgroups such as those with hypertension. The study was published in the European Heart Journal by Niki P. and colleagues.
The AβYSS trial involved 3,698 patients with uncomplicated myocardial infarction and a median follow-up period of 3.0 years. Patients were randomly allocated to either continue or stop β-blocker treatment. Changes in systolic and diastolic blood pressure and resting heart rate were determined by researchers by applying a linear mixed repeated model. The researchers also evaluated the effect of these changes on a composite primary outcome including death, recurrent MI, stroke, or hospitalization for cardiovascular causes. Subgroup analysis was also aimed at identifying differences in patients with versus without a previous history of hypertension, utilizing an adjusted Cox proportional hazards model to compare outcome risks.
Results
• Patients who stopped β-blocker treatment had an increased cardiovascular parameter at six months after randomization.
• The least square mean difference (95% CI) of systolic BP was +3.7 mmHg (2.6, 4.8; P < .001), whereas diastolic BP increased by +3.3 mmHg (2.6, 4.0; P < .001).
• Moreover, there was a significant increase in resting HR by +10 beats per minute [9, 11); P < .001]. T
• these changes continued during follow-up, even with increased use of other antihypertensive medications in the β-blocker interruption group.
• Effects were observed in both hypertensive and non-hypertensive subjects.
• Yet, 43% of the trial group had a history of hypertension, and these patients reflected a very high susceptibility.
• In hypertensive patients, the event rate was 25.8% versus 19.2% in non-hypertensives.
• The hazard ratio for poor outcomes in patients with hypertension was 1.18 (95% CI 1.01–1.36; P = .03) after adjustment.
• Among hypertensive patients who were randomized to β-blocker withdrawal, the risk of reaching the primary endpoint was 5.02% higher (95% CI 0.72%–9.32%; P = .014), which represents a clinically significant increase in cardiovascular risk.
The AβYSS trial concludes that discontinuation of β-blocker therapy after an uncomplicated myocardial infarction creates a sustained increase in blood pressure and heart rate, with particularly deleterious effects in hypertensive patients. These observations underscore the importance of individualized cardiovascular treatment and raise the possibility that ongoing β-blocker therapy might be advantageous for selected high-risk subgroups even after clinical stabilization. Discontinuation decisions should consider both hemodynamic alterations and long-term cardiovascular risk patterns.
Reference:
Niki Procopi, Michel Zeitouni, Mathieu Kerneis, Guillaume Cayla, Emile Ferrari, Grégoire Range, Etienne Puymirat, Nicolas Delarche, Paul Guedeney, Farzin Beygui, Laurent Desprets, Jean-Louis Georges, Thomas Bochaton, François Schiele, Grégory Ducrocq, Marie Hauguel-Moreau, Raphaelle Dumaine, Michel S Slama, Laurent Payot, Mohamad El Kasty, Karim Aacha, Abdourahmane Diallo, Xavier Girerd, Eric Vicaut, Johanne Silvain, Gilles Montalescot, on behalf of the AβYSS Investigators of the ACTION Study Group, Beta-blocker interruption effects on blood pressure and heart rate after myocardial infarction: the AβYSS trial, European Heart Journal, 2025;, ehaf170, https://doi.org/10.1093/eurheartj/ehaf170
