Key result
Premorbid beta-blocker exposure is linked to ~38% lower troponin I levels and preserved cardiac function.
Why the study?
Beta-blockers have shown potential benefits in sepsis, but their clinical use remains limited due to concerns regarding hemodynamic impacts.
Does premorbid use of beta-blockers improve cardiac function and mortality outcomes in patients with sepsis?
Cohort (n=1,005)
No
Does premorbid use of beta-blockers improve cardiac function and mortality outcomes in patients with sepsis?
Absolute Event Rate: 87.9% vs 142%
p-value: p=0.004
Premorbid beta-blocker use is associated with preserved cardiac function, reduced myocardial injury, and lower short-term mortality in patients admitted to the ICU with sepsis.
Should not yet change sepsis management; leaves open whether premorbid beta-blockers protect cardiac function, warranting prospective trials.
Background: Beta-blockers have been reported to exert potential beneficial effects in sepsis in recent years. However, their clinical application in sepsis remains limited due to concerns regarding hemodynamic impacts. This study aims to explore whether premorbid use of beta-blockers is associated with improvements in cardiac function and favorable clinical outcomes among patients with sepsis. Methods: This single-center, retrospective cohort study was conducted in the Intensive Care Unit (ICU) of a university-affiliated hospital. All patients diagnosed with sepsis admitted between August 2022 and March 2024 were enrolled. Exclusion criteria included age < 18 years, hospitalization duration < 48 hours, a history of severe underlying cardiac conditions, and incomplete clinical records. Primary outcomes included myocardial injury markers, echocardiographic parameters, and electrocardiographic indices to assess cardiac function. Secondary outcome was mortality. Results: Among 1005 septic patients, 228 had received premorbid beta-blockers. No significant difference in baseline disease severity was observed between the two groups. Patients with premorbid beta-blocker exposure had lower levels of cardiac troponin I (TnI, 87.9 [IQR, 23.4-306.0] vs 142.0 [IQR, 37.8-481.2]), lactic dehydrogenase (LDH, 274.0 [IQR, 175.0-496.0] vs 319.0 [IQR, 229.0-456.8]), and B-type natriuretic peptide (BNP, 267.9 [IQR, 118.1-1065.1] vs 509.3 [IQR, 184.8-1203.0]). Echocardiographic assessments revealed that premorbid beta-blockers were associated with a higher left ventricular ejection fraction (LVEF, 58% [IQR 52-60] vs 55% [IQR 50-60]). Additionally, premorbid beta-blockers were linked to lower 14-day (13.6% [IQR 9.1-18.1] vs 21.5% [IQR 18.6-24.4]), 28-day (17.5% [IQR 12.6-22.5] vs 27.4% [IQR 24.3-30.6]), and in-hospital (18.9% [IQR 13.7-24.0] vs 28.8% [IQR 25.6-32.0]) mortality rates. Conclusions: Among septic patients, premorbid beta-blockers are associated with preserved cardiac function and improved clinical outcomes. These findings highlight the need for prospective or randomized controlled trials to further explore the potential cardioprotective role of beta-blockers in sepsis.
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Yang et al. (2026) conducted a cohort in Sepsis (n=1,005). Premorbid beta-blockers vs. No premorbid beta-blocker exposure was evaluated on Cardiac troponin I (TnI) level (myocardial injury marker) (p=0.004). Premorbid beta-blocker exposure was associated with preserved cardiac function, demonstrated by lower levels of cardiac troponin I (87.9 vs 142.0 pg/ml, p=0.004) and higher left ventricular ejection fraction (58% vs 55%).
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