‘Quick and Sustained’ Bumps in HR and BP When Beta-blockers Stopped Post-MI

PARIS, France—Patients with myocardial infarction and preserved LVEF who stop their beta-blocker have significant rises in heart rate and blood pressure that appear to increase the likelihood of adverse outcomes, particularly among those with hypertension, an analysis of the ABYSS trial shows.

At 4 years, the absolute risk of major cardiovascular events—a composite of death, MI, stroke, or cardiovascular rehospitalization—was roughly 5% higher among hypertensive patients who stopped beta-blocker therapy compared with those who continued treatment.

Niki Procopi, MD (Sorbonne Université/Hôpital Pitié-Salpêtrière, Paris, France), who presented the results during a Hot Line session at EuroPCR 2025, said the bump in heart rate and systolic blood pressure was “quick and sustained” after halting beta-blockers, adding that their results highlight the particular importance of beta blockade in patients with hypertension.

“Post-MI hypertensive patients should probably be targeted for a potential intensification of their antihypertensive treatment, and could be potential candidates for renal denervation,” she said.

ABYSS was designed to show that stopping beta-blocker therapy could be done safely in post-MI patients. While beta-blockers have been a staple of post-MI care for decades, regardless of the presence of heart failure, the main argument against their use was that the evidence was out of date. Today, most patients are revascularized with PCI and receive multiple evidence-based medications for secondary prevention, and that has driven down the proportion of post-MI complications like heart failure.

The main trial results, which were reported by TCTMD last year, showed that discontinuation several years after an MI failed to meet noninferiority criteria for the combined primary endpoint when compared with ongoing beta-blocker treatment. The new analysis, which was published simultaneously in the European Heart Journal, focused on changes in heart rate and blood pressure that occurred in patients who stopped beta-blocker therapy.

The mean resting heart rate was 63 beats per minute at baseline and it increased by approximately 10 beats per minute after stopping treatment. Blood pressure was equally well controlled at baseline but increased by 3.7- and 3.3-mm Hg systolic and diastolic by 6 months in those who stopped beta-blocker therapy.

“Interestingly, during the course of the trial, doctors were allowed to adapt medication except for beta-blockers,” said Procopi. “There was an intensification in antihypertensive therapy during the course of the trial, especially at 6 months, and this intensification was more frequent in the beta-blocker-interruption group.” As a result, she said, blood pressure declined slightly but was still significantly higher than in those who stayed on beta-blockers. 

Subgroup of Hypertensive Patients

Among the nearly 3,700 patients randomized, 43% had hypertension, with 558 taking three or more antihypertensive medications. In the group with hypertension, the rate of death, MI, stroke, or cardiovascular rehospitalization at 4 years was 21.7% in those who continued beta-blockers and 25.4% in those who stopped. In those without hypertension, the primary endpoint occurred in 17.4% of those who continued treatment and 19.5% of those who stopped. 

For hypertensive patients who stopped beta-blockers, the risk of the primary endpoint at 4 years was 23% higher when compared with hypertensive patients who stayed on therapy (adjusted HR 1.23; 95% CI 1.01-1.50).

Franz Weidinger, MD (Klinik Landstrasse/Vienna Medical University, Austria), noted that quality of life is often cited as one of the reasons doctors consider stopping beta-blockers after MI patients have stabilized. Yet, in this trial, there was no improvement in quality of life after stopping. Johanne Silvain, MD, PhD (Sorbonne Université/Hôpital Pitié-Salpêtrière), the lead investigator of ABYSS, noted that the REDUCE-AMI trial, which showed no benefit of beta-blocker therapy in patients with acute MI undergoing angiography, also revealed no difference in quality of life in those not on beta-blockers.

For Silvain, in chronic coronary syndrome patients able to tolerate beta-blockers long-term, the drugs are effective antihypertensive agents and there is no need to stop medication. As he noted when the main results were presented last year, the trial selected out people who couldn’t tolerate beta-blockers over the long haul.

Davide Capodanno, MD (University of Catania, Italy), who moderated the Hot Line session, said the secondary analysis helps explain why the ABYSS study failed to show that stopping beta-blocker therapy could be safely done in stable post-MI patients.

“We always assume that beta-blockers are given in myocardial infarction to prevent the remodeling of the ventricle,” he said. “Now we discovered that there is an increase in blood pressure, which makes perfect sense. The question now is whether you [believe] the importance of beta-blockers is due to blood pressure-lowering or are they still needed to prevent dilation of ventricles as a preventive measure for remodeling?”

For Capodanno, it’s the blood pressure-lowering effect that appears to matter most in post-MI patients.