No Benefit of Long-Term Beta-Blockers after MI with Preserved EF: REDUCE AMI Trial

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By John Vitarello on

Key Points

-Beta blocker therapy in patients with acute MI is the current standard of care, but we lack clinical trials testing this concept in the era of PCI and potent anti-platelet agents

-Participants with acute MI and a preserved LVEF were randomized in an open-label trial to receive either no beta blocker or metoprolol succinate or bisoprolol 

– The primary composite outcome of all-cause death or MI was not significantly different between the group on beta blocker therapy and the group not on beta blocker therapy

Current guidelines recommend beta blocker therapy with acute myocardial infarction (MI) in both reduced and preserved left ventricular ejection fraction (LVEF). However, early trials investigating beta blockers after MI were performed in an era that predates PCI and potent anti-platelet agents. Observational studies have called into question the benefits for beta blocker therapy in acute MI in those with preserved LVEF, but clinical trials are lacking.

Dr. Troels Yndigegn a cardiologist at Skåne University Hospital (Lund, Sweden) sought to determine whether long-term oral beta-blocker treatments in patients with acute MI and preserved LVEF improves outcomes. He presented the findings of the REDUCE-AMI trial today at ACC 2024.

This registry based, open label, multi-national trial, randomized 5020 patients with acute STEMI or NSTEMI. Coronary angiography and echocardiography were performed during hospitalization and patients with obstructive coronary artery disease and LVEF ≥ 50% were included. Participants on beta blockers for reasons other than secondary prevention or with a contraindication to beta blockers were excluded. Participants in the beta blocker group were given either metoprolol succinate 100mg daily or bisoprolol 5mg daily.  The primary endpoint was a composite of death of any cause or new MI. 

The median age of participants was 65 years, 22% were female, and there were similar rates of prior cardiovascular disease between the beta blocker and no beta blocker groups. A majority of patients in both groups underwent PCI (95.8 vs 95.2% in no beta blocker group) and most were discharged on aspirin, P2Y12 inhibitor, and a statin. In the no-beta blocker group, 9.8% were discharged on a beta blocker at the discretion of the medical team. In the beta blocker group, 62% were treated with metoprolol succinate and 37% were treated with bisoprolol. The median follow-up time was 3.5 years (IQR 2.2 to 4.7). At 12 months, 81.9% of the beta blocker group reported taking the medication, while 14.3% of the no beta-blocker group reported being on beta blockers, reflecting some degree of crossover. 

The primary outcome of all-cause death or MI was not significantly different between the two groups (HR 0.96, 95% CI 0.79-1.16; p=0.64).  Likewise, there was no statistical difference in secondary endpoints including admission due to atrial fibrillation or heart failure, dyspnea as measured by the NYHA system or angina as measured by the Canadian Cardiovascular Society symptom scale. Safety endpoints including admission for bradycardia and syncope, were similar between treatment groups.

In summary, the Reduce AMI trial did not find clinical improvement with the use of beta blocker therapy in patients with preserved LVEF who underwent PCI after acute myocardial infarction.