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. 2025 Jul 24;24(1):299.
doi: 10.1186/s12933-025-02870-x.

Association between triglyceride-glucose-body mass index and adverse prognosis in elderly patients with severe heart failure and type 2 diabetes: a retrospective study based on the MIMIC-IV database

Affiliations

Association between triglyceride-glucose-body mass index and adverse prognosis in elderly patients with severe heart failure and type 2 diabetes: a retrospective study based on the MIMIC-IV database

Jing Cheng et al. Cardiovasc Diabetol. .

Abstract

Objective: The triglyceride-glucose (TyG) index is a validated marker of insulin resistance (IR) and predictor of cardiovascular outcomes. However, the prognostic utility of integrating TyG with body mass index (BMI) as the TyG-BMI index in elderly patients with severe heart failure (HF) and type 2 diabetes mellitus (T2DM) remains unestablished. We aimed to evaluate associations between TyG-BMI and all-cause mortality at multiple time points in this high-risk cohort.

Methods: This retrospective cohort study analyzed 4,523 elderly patients (aged >65 years) with severe HF and T2DM from the MIMIC-IV database. Participants were stratified into TyG-BMI quartiles (Q1-Q4) at ICU admission. Primary outcomes were 60-, 90-, 180-, and 365-day all-cause mortality. Associations were assessed using Kaplan-Meier analysis, Cox proportional hazards models, and restricted cubic splines (RCS).

Results: The cohort (mean age 72.79 ± 7.84 years; 41.5% male) demonstrated graded mortality reductions with increasing TyG-BMI quartiles. Compared to Q4, Q1 (lowest TyG-BMI) had significantly higher mortality at 90 days (58.70% vs. 48.45%; p = 0.008) and 365 days (80.54% vs. 73.91%; p < 0.001), with similar 60-day trends (58.79% vs. 39.34%; p = 0.059). Adjusted Cox models confirmed progressively lower mortality risk in higher quartiles (365-day HR for Q4 vs. Q1: 0.74, 95% CI: 0.68-0.93). Subgroup analyses demonstrated a consistent inverse TyG-BMI-mortality association across all strata (age, cardiac function, comorbidities), with pronounced risk reduction in HFrEF (LVEF ≤40%; all-timepoint HR >1, p<0.05) and patients without prior myocardial infarction (365-day aHR 0.69 vs. 0.81 with infarction). RCS analysis identified nonlinear thresholds (TyG-BMI = 148.73 for 60-day; 163.38 for 365-day mortality), below which each unit increase conferred greater protective effects.

Conclusion: Lower TyG-BMI independently predicted increased short-, intermediate-, and long-term mortality in elderly patients with severe HF and T2DM. This composite index-integrating metabolic (TyG) and nutritional (BMI) dimensions-provides practical risk stratification, particularly within identified threshold ranges.

Keywords: All-cause mortality; Heart failure; Insulin resistance; Triglyceride-glucose body mass index.

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Conflict of interest statement

Declarations. Ethics approval and consent to participate: This study utilized data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database, a publicly available de-identified critical care database. Ethical approval for the creation and maintenance of MIMIC-IV was granted by the Institutional Review Boards (IRBs) of the Massachusetts Institute of Technology (MIT) and Beth Israel Deaconess Medical Center (BIDMC), with a waiver of informed consent due to the retrospective and anonymized nature of the data. All authors completed the required National Institutes of Health (NIH) training on human research participant protection and obtained data access authorization through the Collaborative Institutional Training Initiative (CITI Program) certification (Record ID: 66379984). No additional ethics approval was required for this secondary analysis of de-identified data. This study was conducted in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. Consent for publication: Not applicable. This study used de-identified data from the MIMIC-IV database, which contains no personally identifiable information. Therefore, individual patient consent for publication was not required. Competing interests: The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Workflow of the present study
Fig. 2
Fig. 2
(A) 60-day survival, (B) 90-day survival, (C) 180-day survival, (D) 365-day survival. Curves depict cumulative survival probabilities in elderly ICU patients with severe heart failure and type 2 diabetes (n=4,523), stratified by TyG-BMI quartiles at admission: Q1 (TyG-BMI <109.75, n=1,131), Q2 (109.75–127.80, n=1,131), Q3 (127.80–151.79, n=1,131), Q4 (>151.79, n=1,130). Log-rank tests confirm significantly reduced survival in Q1 (lowest TyG-BMI) versus Q4 (highest TyG-BMI) at 60-day (p<0.05), 90-day (p<0.001), 180-day (p<0.001) and 365-day (p<0.001), consistent with time-specific mortality differences reported in Table 1
Fig. 3
Fig. 3
Threshold effect of TyG-BMI on mortality risk revealed by restricted cubic spline models. (A) RCS curves for 60-day all-cause mortality across different clinical subgroups. Hazard ratios (HRs) and 90% confidence intervals (CIs) are shown relative to TyG-BMI reference values. (B) RCS curves for 90-day all-cause mortality across subgroups. (C) RCS curves for 180-day all-cause mortality across subgroups. (D) RCS curves for 365-day all-cause mortality across subgroups
Fig. 4
Fig. 4
Forest plots of stratified analyses of TyG-BMI index and 60-day all-cause mortality. Forest plot displaying hazard ratios (HR) and 95% confidence intervals (CI) from univariate Cox proportional hazards models. Variables include Age (stratified at 77.91 years), Gender, APSIII (cutoff: 53), SAPSII (cutoff: 44), Smoking status, Cerebrovascular disease, CK-MB (cutoff: 25 U/L), Troponin (cutoff: 0.2 ng/mL), BNP (stratified: ≤ 100, 100–500, >500 pg/mL), and LVEF (≤ 40%, 40–50%, ≥ 50%). Reference line at HR = 1
Fig. 5
Fig. 5
Forest plots of stratified analyses of TyG-BMI index and 90-day all-cause mortality. Unadjusted hazard ratios (95% CI) for 90-day all-cause mortality across clinical subgroups. Variables analyzed: Age (>77.91/ ≤ 77.91 years), Gender, APSIII (>53/ ≤ 53), SAPSII (>44/ ≤ 44), Smoking, Cerebrovascular disease, CK-MB (>25/ ≤ 25 U/L), Troponin (>0.2/ ≤ 0.2 ng/mL), BNP (three-tiered), and LVEF (three categories). Dashed vertical line indicates null effect (HR = 1). P-values reflect significance of subgroup differences
Fig. 6
Fig. 6
Forest plots of stratified analyses of TyG-BMI index and 180-day all-cause mortality. Univariate Cox regression results for 180-day mortality risk. Subgroups: Age (dichotomized at 77.91 years), Gender, APSIII (cutoff: 53), SAPSII (cutoff: 44), Smoking history, Cerebrovascular disease status, CK-MB levels (25 U/L threshold), Troponin levels (0.2 ng/mL threshold), BNP categories, and LVEF strata. Error bars represent 95% CIs; filled diamonds mark point estimates. All models are unadjusted for covariates
Fig. 7
Fig. 7
Forest plots of stratified analyses of TyG-BMI index and 365-day all-cause mortality. Long-term (365-day) all-cause mortality risk stratification by clinical parameters. Univariate hazard ratios shown for: Age groups, Gender, disease severity scores (APSIII/SAPSII), Smoking, Cerebrovascular disease, cardiac biomarkers (CK-MB, Troponin, BNP), and LVEF categories. Note the progressive risk elevation with higher BNP levels (HR = 3.09 for >500 pg/mL) and persistent mortality risk in reduced LVEF (≤ 40%). Scale extended to HR = 3.5 to accommodate effect sizes

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