Prognostic value of C-reactive protein–triglyceride–glucose index in hospitalised patients with acute decompensated heart failure

The C-reactive protein–triglyceride–glucose index (CTI) is a composite marker integrating systemic inflammation and insulin resistance. Although CTI has been associated with cardiovascular risk in general and cardiometabolic populations, its prognostic significance in patients hospitalised with acute decompensated heart failure (ADHF) remains unclear. This single-centre retrospective cohort study included 1,494 patients hospitalised with ADHF between January 2020 and June 2024. CTI was calculated as 0.412 × lnCRP (mg/L) + lnTG (mg/dL) × FPG (mg/dL)/2, and patients were stratified into tertiles. The endpoints were all-cause mortality, cardiovascular (CV) death, and major adverse cardiac and cerebrovascular events (MACCEs). Associations between CTI and outcomes were assessed using multivariable Cox regression and restricted cubic spline analyses. Incremental prognostic performance beyond a comprehensive clinical model was evaluated using optimism-corrected Harrell’s C-index, continuous net reclassification improvement (NRI), integrated discrimination improvement (IDI), time-dependent receiver operating characteristic curves, and decision curve analysis. During a median follow-up of 498 days, event rates increased progressively across CTI tertiles. In the fully adjusted model, each 1-standard deviation increase in CTI was independently associated with higher risks of all-cause mortality (hazard ratio HR 1.52, 95% confidence interval CI 1.29–1.80), CV death (HR 1.51, 95% CI 1.24–1.84), and MACCEs (HR 1.42, 95% CI 1.26–1.59). Patients in the highest CTI tertile had the greatest risk across all endpoints (all P for trend < 0.001). Restricted cubic spline analyses showed positive, approximately linear associations between CTI and all outcomes. Adding CTI to the clinical model yielded modest improvements in discrimination, with C-index increases from 0.665 to 0.672 for all-cause mortality, from 0.697 to 0.705 for CV death, and from 0.644 to 0.652 for MACCEs. Significant improvements in NRI and IDI were also observed for all outcomes. Elevated CTI was independently associated with increased risks of all-cause mortality, CV death, and MACCEs in patients hospitalised with ADHF. Addition of CTI to a comprehensive clinical model provided modest but statistically significant incremental prognostic value beyond established clinical predictors and related metabolic or inflammatory markers evaluated in this study. CTI may serve as a simple adjunctive marker for metabolic–inflammatory risk profiling and refined risk stratification in ADHF, pending external validation.