Key result
Baseline TyG index is not associated with risk of MACE.
Why the study?
The prognostic capacity of the triglyceride–glucose (TyG) index as a surrogate for insulin resistance in younger patients with premature coronary artery disease remains poorly understood.
Does the baseline TyG index predict major adverse cardiovascular events in patients with premature coronary artery disease?
Cohort (n=382)
Does the baseline TyG index predict major adverse cardiovascular events in patients with premature coronary artery disease?
Odds Ratio: 1.1 (95% CI 0.65–1.85)
p-value: p=0.732
The admission TyG index does not predict coronary anatomical severity or long-term clinical outcomes in patients with premature CAD presenting with ACS.
TyG index should not guide prognosis in premature CAD; leaves open its value in broader or prospective cohorts.
Background: Premature coronary artery disease (PCAD) represents a growing clinical concern. Although insulin resistance is central to atherogenesis and the triglyceride–glucose (TyG) index serves as a practical surrogate for insulin resistance, its specific prognostic capacity within younger patient cohorts remains poorly understood. This study sought to evaluate the prognostic value of the TyG index regarding major adverse cardiovascular events (MACE) and its correlation with angiographic disease severity in PCAD patients. Methods: Enrolling 382 consecutive patients presenting with acute coronary syndrome (ACS) undergoing primary or early invasive coronary angiography between July 2020 and March 2023, this retrospective study evaluated subjects stratified into premature CAD (males ≤ 45, females ≤ 55 years; n = 138) and late-onset CAD (n = 244) cohorts. Lesion complexity was evaluated via the Gensini score. Primary prognosis was evaluated via cumulative MACE during a mean follow-up of 40.7 months. Results: Baseline values for the TyG index did not exhibit significant variance between early-onset and late-onset cohorts (9.09 ± 0.71 vs. 9.06 ± 0.65, p = 0.716). Stratification by median TyG index in early-onset CAD showed expected metabolic clustering but no difference in Gensini scores (41.68 ± 25.90 vs. 44.12 ± 22.75, p = 0.321). In univariable logistic regression, baseline TyG index was not associated with MACE (OR = 1.10, 95% CI: 0.65–1.85, p = 0.732), whereas older age (OR = 1.06, 95% CI: 1.01–1.11, p = 0.017) and elevated baseline CRP levels (OR = 1.04, 95% CI: 1.01–1.08, p = 0.007) showed significant univariable associations with adverse clinical outcomes. Sensitivity analysis in non-diabetic patients (n = 275) confirmed no significant association between TyG index and MACE (OR = 0.721, 95% CI: 0.327–1.591, p = 0.418). Conclusion: In this study, the admission TyG index did not show a statistically significant relationship with coronary anatomical severity or long-term clinical outcomes in premature CAD. Risk assessment in acute coronary patients should continue to prioritize established clinical, acute inflammatory, and angiographic parameters.
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Bülüç et al. (2026) conducted a cohort in Premature coronary artery disease (n=382). Triglyceride-glucose (TyG) index was evaluated on Major adverse cardiovascular events (MACE) (OR 1.10, 95% CI 0.65-1.85, p=0.732). Baseline triglyceride-glucose (TyG) index was not significantly associated with major adverse cardiovascular events (OR 1.10; 95% CI 0.65-1.85; p=0.732).
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