Early β-blocker therapy was associated with significantly lower 28-day mortality (36.1% vs 51.1%; HR 0.53; 95% CI 0.41-0.67; P<0.001) compared to alternative antiarrhythmics in sepsis-induced NOAF.
Cohort (n=560)
No
Does early beta-blocker therapy reduce all-cause mortality in critically ill patients with sepsis-induced new-onset atrial fibrillation?
Early beta-blocker therapy in critically ill patients with sepsis-induced new-onset atrial fibrillation is associated with significantly lower short- and long-term mortality and decreased organ-support burden compared to alternative antiarrhythmic drugs.
Hazard Ratio: 0.53 (95% CI 0.41–0.67)
Absolute Event Rate: 36.1% vs 51.1%
p-value: p=<.001
Abstract Sepsis-induced new-onset atrial fibrillation (NOAF) is a potentially life-threatening arrhythmogenic complication, partially driven by catecholamine-mediated atrial remodeling. While β-adrenergic receptor blockers may mitigate this pathophysiology through sympatholytic and rate-controlling mechanisms, their association with patient survival remains incompletely characterized due to heterogeneous evidence. To elucidate the association between the administration of anti-catecholaminergic antiarrhythmic drugs and all-cause mortality in critically ill patients with sepsis-induced NOAF.This retrospective cohort study utilized data from the Medical Information Mart for Intensive Care-IV database. We included adult patients admitted to a tertiary academic medical center between 2008 and 2019 who fulfilled the Sepsis-3 criteria and developed NOAF during their ICU stays.Based on the initial antiarrhythmic drug administration within 24 h following time-zero, patients were categorized into either β-blocker group or alternative antiarrhythmic drug group. The matched cohort comprised 560 patients (mean age 74.1 SD 11.5 years; 64.6% male), among whom 280 were assigned to the β-blocker group and 280 to the alternative antiarrhythmic drug group. The β-blocker group demonstrated significantly lower 28-day mortality (36.1 vs. 51.1%; adjusted HR, 0.53; 95% CI, 0.41–0.67; P < .001) and 1-year mortality (50.7 vs. 63.6%; adjusted HR, 0.68; 95% CI, 0.55–0.85; P = .001). ICU mortality was also reduced in the β-blocker group (22.1 vs. 42.5%; P < .001). Furthermore, this group had more vasopressor-free days (median IQR, 24.0 18.0–26.0 vs. 16.0 0.0–23.0) and ventilator-free days (24.0 18.0–26.0 vs. 17.0 0.0–24.0) (both P < .001). Safety outcomes included less bradycardia (12.5 vs. 20.0%; P = .016) but more hypotension (26.4 vs. 18.6%; P = .039). Subgroup and mediation analyses suggested greater benefit in high-risk patients, partially mediated (15.92%) by reduced vasopressor requirements. In critically ill patients with sepsis-induced NOAF, early β-blocker therapy was associated with markedly lower 28-day and 1-year mortality, along with decreased organ-support burden, warranting prospective trials are warranted to confirm these survival benefits.
Huang et al. (Mon,) conducted a cohort in Sepsis-induced new-onset atrial fibrillation (NOAF) (n=560). β-blocker therapy vs. Alternative antiarrhythmic drug was evaluated on 28-day mortality (adjusted HR 0.53, 95% CI 0.41-0.67, p=<.001). Early β-blocker therapy was associated with significantly lower 28-day mortality (36.1% vs 51.1%; HR 0.53; 95% CI 0.41-0.67; P<0.001) compared to alternative antiarrhythmics in sepsis-induced NOAF.