June 10, 2026Circulation
Heart Rate and Cardiovascular Outcomes in Post–Myocardial Infarction Patients Treated by β-Blockers: A Secondary Analysis of the ABYSS Trial
Michel ZeitouniNiki ProcopiGuillaume CaylaÉmile FerrariGrégoire RangéÉtienne PuymiratNicolas DelarchePaul GuedeneyThomas CuissetOlivier VarenneRomain CadorPascal MotreffL ChristiaensAnne Bellemain-AppaixMaxime FayardGilles BayetJean-Michel QuedillacPascal GoubeMarc GoralskiSimon ElhadadFrédéric HeliotChristophe CaussinJean-Charles AisenfarbJean LitalienG RambaudDavid AttiasRaphaelle DumaineMichel SlamaMohamad El KastyLaurent PayotK AachaAbdourahmane DialloÉric VicautGilles MontalescotJohanne Silvainon behalf of the AβYSS investigators of the ACTION Study Group
Key result
β-blocker interruption worsens outcomes, and higher baseline heart rate predicts ~55% greater major event risk.
- P=0.867
- n=3,698
Why the study?
Heart rate is a key prognostic factor after MI, but its relevance in the modern reperfusion era is uncertain.
Does β-blocker interruption worsen cardiovascular outcomes compared to continuation in stable post-MI patients with LVEF ≥40%, and is this effect modified by baseline heart rate?
Study Design
Type
RCT (n=3,698)
Randomization
randomized
Structured PICO
Does β-blocker interruption worsen cardiovascular outcomes compared to continuation in stable post-MI patients with LVEF ≥40%, and is this effect modified by baseline heart rate?
P
Population
3,698 stable post-MI patients with left ventricular ejection fraction ≥40%, median age 63.5 years, 17.1% female, randomized to continue or interrupt β-blockers.
I
Intervention
Interruption of β-blocker therapy
C
Comparator
Continuation of β-blocker therapy
O
Outcome
Composite of death, MI, stroke, or cardiovascular rehospitalizationcomposite
Main Result
Absolute Event Rate: 21.6% vs 22.4%
p-value: p=0.867
In stable post-MI patients with LVEF ≥40%, higher baseline heart rate is associated with increased mortality and cardiovascular events, and interrupting β-blockers increases heart rate and worsens outcomes regardless of baseline heart rate.
Discussion
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Key expert perspectives
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“Knowing our results now, I would probably not stop a drug that is well tolerated [and whose] cost is quite low. In people on chronic beta-blocker therapy, you've already selected [out] people who don't tolerate the drug, so there's not much benefit of stopping [in those on long-term treatment]. What we show here is that there's a safety signal to stopping.”
“The bump in heart rate and systolic blood pressure was quick and sustained after halting beta-blockers.”
MBMarc BonacaCardiologist, University of Colorado School of Medicine
“What drove the benefit was hospitalizations for cardiovascular causes and angina, but even when you look at the point estimates for heart failure and myocardial infarction, they all go above 1 and it's not a huge trial. So, I think the jury's still out, but fortunately there are more trials coming that should help clarify the role for beta-blockers in this population.”
Implication
Supports avoiding β-blocker interruption in patients with higher baseline heart rate; confirms resting heart rate as an independent prognostic marker in secondary prevention.
Abstract
BACKGROUND: Heart rate (HR) is a key prognostic factor after myocardial infarction (MI), but its relevance in the modern reperfusion era is uncertain. We aim to evaluate the association between HR and β-blocker interruption on cardiovascular outcomes. METHODS: A prespecified secondary analysis of the ABYSS trial (Assessment of Beta-Blocker Interruption 1 Year After an Uncomplicted Myocardial Infarction), including 3698 stable post-MI patients (left ventricular ejection fraction ≥40%) randomized to continue or interrupt β-blockers, was conducted. Patients were grouped by prerandomization HR tertiles: <60 bpm (T1), 60 to <68 (T2), and ≥68 (T3). We examined associations between HR, treatment strategy, and the primary endpoint (death, MI, stroke, or cardiovascular rehospitalization), major secondary endpoints, and on-treatment HR. RESULTS: Median age in the study population was 63.5 years (55.9–71.1), and there were 621 women (17.1%). Baseline HR was not associated with the primary endpoint (22.4% versus 21.8% versus 21.6%; P= 0.867). Higher HR was associated with increased risk of death, MI, or stroke (5.5% versus 6.4% versus 9.2%; P <0.001; T3 versus T1 adjusted hazard ratio, 1.55; 95% CI, 1.14–2.12) and death, MI, stroke, or heart failure (6.5% versus 7.1% versus 10.4%; P= 0.007; T3 versus T1 adjusted hazard ratio, 1.47; 95% CI, 1.11–1.97). All-cause mortality rose across tertiles (2.9% versus 3.4% versus 5.9%; P= 0.004; P trend=0.008). β-Blocker interruption produced a dose-dependent HR increase of ≈10–13 bpm during follow-up. The association between interruption and worse outcomes was consistent across HR tertiles (no significant interaction) and LVEF categories (40% to 49% and >50%). CONCLUSIONS: In stabilized post-MI patients with preserved ejection fraction, higher HR remains associated with adverse cardiovascular events and mortality in the reperfusion era. Interrupting β-blockers substantially increases HR and is consistently linked with worse outcomes irrespective of baseline HR, supporting continuation of β-blocker therapy.
Cite This Study
Zeitouni et al. (2026) conducted an RCT in stable post-myocardial infarction (n=3,698). Higher baseline heart rate (≥68 bpm) vs. Lower baseline heart rate (<60 bpm) was evaluated on death, MI, stroke, or cardiovascular rehospitalization (p=0.867). Higher baseline heart rate (≥68 vs <60 bpm) increased the risk of death, MI, or stroke (9.2% vs 5.5%; HR 1.55, 95% CI 1.14-2.12), and β-blocker interruption consistently worsened outcomes.