Key result
Elevated albumin-corrected anion gap is linked to increased all-cause mortality in ICU-admitted acute heart failure.
Why the study?
The prognostic value of albumin-corrected anion gap (ACAG) in patients with acute heart failure (AHF) admitted to the ICU remains unclear.
Does elevated albumin-corrected anion gap predict increased all-cause mortality in ICU patients with acute heart failure?
Cohort (n=2,754)
Does elevated albumin-corrected anion gap predict increased all-cause mortality in ICU patients with acute heart failure?
Hazard Ratio: 1.09 (95% CI 1.07–1.11)
p-value: p=<0.001
Elevated albumin-corrected anion gap is nonlinearly associated with increased short- and long-term all-cause mortality in ICU patients with acute heart failure, suggesting its utility as a prognostic marker.
BACKGROUND: The albumin-corrected anion gap (ACAG) has been associated with adverse outcomes in critically ill patients. However, its prognostic value in patients with acute heart failure (AHF) remains unclear. This study is aimed at investigating the association between ACAG levels and all-cause mortality in AHF patients. METHODS: This retrospective study included AHF patients admitted to the intensive care unit (ICU) for the first time, utilizing data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. Patients were stratified into tertiles (T1-T3) based on ACAG levels. The primary endpoints were 30- and 365-day all-cause mortality, whereas the secondary endpoints included 90- and 180-day all-cause mortality. Kaplan-Meier (K-M) survival analyses, Cox proportional hazards models, and restricted cubic spline (RCS) analyses were employed to assess the association between ACAG and all-cause mortality. RESULTS: A total of 2754 patients were included, with a mean age of 74 years, and 56.5% of the participants were male. K-M curves demonstrated that elevated ACAG levels correlated with increased mortality at 30, 90, 180, and 365 days (all log-rank p < 0.001). Cox regression analysis indicated that T3 was associated with a higher risk of mortality compared with T1. RCS analysis revealed a nonlinear relationship between ACAG and all-cause mortality. Above certain thresholds, each 1-unit increase in ACAG was linked to a 9% increase in the risk of 30-day mortality (hazard ratio [HR] 1.09, 95% confidence interval [CI] 1.07-1.11) and an 8% increase in the risk of 365-day mortality (HR 1.08, 95% CI 1.06-1.09). CONCLUSION: ACAG levels were associated with all-cause mortality in patients with AHF. Thus, ACAG may serve as a valuable prognostic marker for this patient population.
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Pu et al. (2026) conducted a cohort in Acute Heart Failure (n=2,754). Albumin-corrected anion gap (ACAG) vs. Lower ACAG levels (Tertile 1) was evaluated on 30-day all-cause mortality (HR 1.09, 95% CI 1.07-1.11, p=<0.001). Each 1-unit increase in albumin-corrected anion gap above certain thresholds was associated with a 9% increased risk of 30-day mortality (HR 1.09; 95% CI 1.07-1.11) in ICU patients with AHF.
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