# The association between insulin resistance indices and the occurrence of major adverse cardiovascular events in patients with premature myocardial infarction: a prospective cohort study

**Authors:** Yu Zhou, Yuhang Wang, Jingxi Chen, Lai Jiang, Ran Chu, Weiwei Tian, Jiaxin Wang, Yin Liu, Jing Gao

PMC · DOI: 10.3389/fnut.2026.1724362 · Frontiers in Nutrition · 2026-02-19

## TL;DR

This study finds that the TyG-BMI index is a strong predictor of cardiovascular risks in patients with premature heart attacks.

## Contribution

The study demonstrates that TyG-BMI outperforms other insulin resistance markers in predicting adverse cardiovascular events in PMI patients.

## Key findings

- TyG-BMI showed a stronger association with MACEs compared to TyG and TG/HDL-C.
- TyG-BMI's predictive power was higher in patients with diabetes and high hsCRP.
- TyG-BMI had better performance metrics (C-index, NRI, IDI) for MACE prediction.

## Abstract

Insulin resistance (IR) alternative markers, including the triglyceride-glucose index (TyG), TyG combined with body mass index (TyG-BMI), and the triglyceride/high-density lipoprotein cholesterol ratio (TG/HDL-C), have been shown to be significantly associated with prognosis of acute myocardial infarction (AMI). However, the prognostic value of these markers in patients with premature myocardial infarction (PMI) remains unclear. This study aims to investigate the association between IR markers and major adverse cardiovascular events (MACEs) in PMI patients.

This was a prospective cohort study that consecutively enrolled 1,688 PMI patients (male ≤ 50 years, female ≤ 55 years) from Tianjin Chest Hospital between February 2015 and December 2024. TyG, TyG-BMI and TG/HDL-C indices were calculated. The median follow-up time was 17.4 months (IQR: 11.4–31.9), with the endpoint being MACEs. IR indices were grouped by quartiles. The risk association between IR indices and MACEs was analyzed using Cox proportional hazards models and restricted cubic spline analysis. The predictive performance of IR indices was assessed using Harrell’s C-index, net reclassification improvement (NRI), integrated discrimination improvement (IDI).

Among 1,688 patients, 211 (12.5%) occurred MACEs. Restricted cubic spline analysis showed a positive nonlinear relationship between TyG-BMI and MACEs risk, while TyG and TG/HDL-C were linearly associated with MACEs risk. In the fully adjusted Cox proportional hazards model, the hazard ratios of occurring MACEs in the fourth quartile versus the first quartile were 2.88 [95% confidence interval (CI): 1.83–4.53] for TyG-BMI, 1.77 (95% CI: 1.11–2.82) for TyG, 1.44 (95% CI: 0.93–2.22) for TG/HDL-C. In the fourth quartile versus the first quartile of TyG-BMI, the hazard ratios of occurring MACEs were 3.85 (95% CI: 1.79–8.27) in patients with diabetes and 3.38 (95% CI: 1.78–6.43) in patients with high high-sensitivity C-reactive protein (hsCRP). Additionally, TyG-BMI demonstrated higher C-index, NRI and IDI for predicting MACEs risk in PMI patients.

In patients with PMI, TyG-BMI is an independent predictor of MACEs demonstrating significantly superior predictive performance compared to TyG and TG/HDL-C. The association between elevated TyG-BMI and MACEs risk was significant in patients with diabetes and high hsCRP levels. The effect was particularly stronger in patients with diabetes.

## Linked entities

- **Diseases:** diabetes (MONDO:0005015)

## Full-text entities

- **Genes:** ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}, INSR (insulin receptor) [NCBI Gene 3643] {aka CD220, HHF5}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, NOS3 (nitric oxide synthase 3) [NCBI Gene 4846] {aka EC-NOS, ECNOS, MYMY8, NOSIII, cNOS, eNOS}, IKBKB (inhibitor of nuclear factor kappa B kinase subunit beta) [NCBI Gene 3551] {aka IKK-2, IKK-beta, IKK2, IKKB, IMD15, IMD15A}, APOB (apolipoprotein B) [NCBI Gene 338] {aka FCHL2, FLDB, LDLCQ4, apoB-100, apoB-48}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, SLC2A4 (solute carrier family 2 member 4) [NCBI Gene 6517] {aka GLUT4}, VCAM1 (vascular cell adhesion molecule 1) [NCBI Gene 7412] {aka CD106, INCAM-100}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, APOA1 (apolipoprotein A1) [NCBI Gene 335] {aka AMYLD3, HPALP2, apo(a)}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, MAPK8 (mitogen-activated protein kinase 8) [NCBI Gene 5599] {aka JNK, JNK-46, JNK1, JNK1A2, JNK21B1/2, PRKM8}
- **Diseases:** hypoxia (MESH:D000860), triple-vessel disease (MESH:C536008), pulmonary embolism (MESH:D011655), metabolic dysregulation (MESH:D021081), metabolic (MESH:D008659), overweight (MESH:D050177), stroke (MESH:D020521), sudden cardiac death (MESH:D016757), myocardial loss (MESH:D009202), ST-segment elevation myocardial infarction (MESH:D000072657), lesions (MESH:D009059), Obesity (MESH:D009765), NSTEMI (MESH:D000072658), DM (MESH:D009223), impaired glucose metabolism (MESH:D044882), angina pectoris (MESH:D000787), Prediabetes (MESH:D011236), Diabetes (MESH:D003920), plaque rupture (MESH:D012421), valvular heart disease (MESH:D006349), ischemic (MESH:D002545), endothelial dysfunction (MESH:D014652), malignant tumors (MESH:D009369), mitochondrial dysfunction (MESH:D028361), coronary heart disease (MESH:D003327), CKM syndrome (MESH:D013577), dyslipidemia (MESH:D050171), hyperlipidemia (MESH:D006949), ARTerial disease (MESH:D002539), cardiometabolic diseases (MESH:D024821), multi (MESH:D015161), Inflammatory (MESH:D007249), chronic (MESH:D002908), hypertriglyceridemia (MESH:D015228), Unstable angina (MESH:D000789), segment (MESH:C537538), CAD (MESH:D003324), SMART (MESH:D010302), heart failure (MESH:D006333), adipose tissue (MESH:D018205), peripheral arterial disease (MESH:D058729), obstructive sleep apnea (MESH:D020181), type 2 diabetes (MESH:D003924), IR (MESH:D007333), myocardial ischemia (MESH:D017202), atrial fibrillation (MESH:D001281), ischemic stroke (MESH:D002544), AMI (MESH:D009203), MACE (MESH:D002318), ASCVD (MESH:D050197), Hypertension (MESH:D006973), Cardiac death (MESH:D003643), lipid metabolism abnormalities (MESH:D052439), hyperinsulinemic-euglycemic (MESH:D044903), restenosis (MESH:D023903)
- **Chemicals:** cholesterol (MESH:D002784), NO (MESH:D009569), FFAs (MESH:D005230), aspirin (MESH:D001241), TG (MESH:D014280), UA (MESH:D014527), ROS (MESH:D017382), glucose (MESH:D005947), Cr (MESH:D003404), alcohol (MESH:D000438), lipid (MESH:D008055), carbohydrate (MESH:D002241), TG (MESH:D013866), ACEI (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12960170/full.md

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12960170/full.md

## References

62 references — full list in the complete paper: https://tomesphere.com/paper/PMC12960170/full.md

---
Source: https://tomesphere.com/paper/PMC12960170