# Impact of TyG index on coronary plaques in patients with coronary artery disease under aggressive lipid-lowering therapy

**Authors:** Tatsuya Fukase, Tomotaka Dohi, Norihito Takahashi, Shinichiro Doi, Iwao Okai, Hiroshi Iwata, Shinya Okazaki, Katsumi Miyauchi, Hiroyuki Daida, Tohru Minamino

PMC · DOI: 10.3389/fendo.2026.1766778 · Frontiers in Endocrinology · 2026-02-12

## TL;DR

This study found that a high TyG index is linked to more coronary plaque progression in patients with heart disease even when they are on strong cholesterol-lowering therapy.

## Contribution

The study identifies the TyG index as a residual risk factor for coronary plaque progression under aggressive lipid-lowering therapy.

## Key findings

- Patients with a high TyG index showed greater plaque progression compared to those with a low TyG index under aggressive lipid-lowering therapy.
- Baseline TyG index, male gender, and changes in LDL-C were significantly associated with plaque progression.
- There was no difference in LDL-C levels between the two groups, indicating TyG index is an independent risk factor.

## Abstract

One of residual risks of coronary artery disease (CAD) occurrence and coronary plaque progression might be a triglyceride-glucose index (TyG index). Thus, this study aimed to investigate the impact of TyG index on coronary artery plaques detected by serial intravascular ultrasound (IVUS) in patients with CAD under low-density lipoprotein cholesterol (LDL-C) lowering therapy represented by statins.

This observational cohort study included three clinical prospective trials (the ENTERPRISE trial, ESPECIAL-ACS study, and ZEUS trial) in which coronary plaques were assessed using serial grayscale IVUS at baseline and at 6–12 months follow-up. The patients were divided into two groups according to the cutoff value of baseline TyG index (dichotomized to ≥ or <8.5) based on a previous report. The primary endpoint was defined as an absolute change in percentage atheroma volume (PAV) from baseline to follow-up.

A total of 131 patients (mean age: 63 years; 92% men) completed the study and were analyzed. Compared to the low TyG index group, the high TyG index group had higher body mass index, triglyceride, and proportion of male, diabetes mellitus, and smoking history, as well as lower high-density lipoprotein cholesterol; whereas, there was no difference in LDL-C between both groups. The absolute change in PAV between the low TyG index group and high TyG index group only in patients who received aggressive lipid-lowering therapy (LLT) was −3.5±1.4% by analysis of covariance (p=0.017). In addition, the baseline TyG index, male, and %change in LDL-C were significantly associated with the absolute change in PAV under aggressive LLT by multiple linear regression analysis.

An elevated TyG index could be a residual risk of coronary plaque progression under aggressive LLT.

## Linked entities

- **Diseases:** coronary artery disease (MONDO:0005010), diabetes mellitus (MONDO:0005015)

## Full-text entities

- **Genes:** CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, SLC5A2 (solute carrier family 5 member 2) [NCBI Gene 6524] {aka SGLT2}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, GLP1R (glucagon like peptide 1 receptor) [NCBI Gene 2740] {aka GLP-1, GLP-1-R, GLP-1R}
- **Diseases:** Renal Disease (MESH:D007674), TD (MESH:D004409), CAD (MESH:D003324), LLT (MESH:D011017), smooth muscle cell dysfunction (MESH:D018235), sleep-disordered breathing (MESH:D012891), coronary plaques (MESH:D003323), atheroma (MESH:D058226), hypertriglyceridemia (MESH:D015228), thrombosis (MESH:D013927), Atherosclerosis (MESH:D050197), HbA1c (MESH:D006445), hypertension (MESH:D006973), stiffness (MESH:C566112), cardiovascular disease (MESH:D002318), coagulation disorders (MESH:D001778), insulin resistance (MESH:D007333), obesity (MESH:D009765), metabolic disorders (MESH:D008659), hyperglycemia (MESH:D006943), platelet hyperactivity (MESH:D001791), cardiac fibrosis (MESH:D005355), inflammation (MESH:D007249), ACS (MESH:D054058), dyslipidemia (MESH:D050171), DM (MESH:D003920), endothelial dysfunction (MESH:D014652), Chronic kidney disease (MESH:D051436)
- **Chemicals:** Lipid (MESH:D008055), alcohol (MESH:D000438), glucose (MESH:D005947), creatinine (MESH:D003404), LLT (-), nitroglycerin (MESH:D005996), carbohydrates (MESH:D002241), ezetimibe (MESH:D000069438), sugars (MESH:D000073893), Triglyceride (MESH:D014280)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** A1C

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## References

48 references — full list in the complete paper: https://tomesphere.com/paper/PMC12935650/full.md

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Source: https://tomesphere.com/paper/PMC12935650