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Abstract
Patients with type 2 diabetes mellitus (T2DM) undergoing percutaneous coronary intervention (PCI) remain at disproportionately high risk of major adverse cardiovascular events (MACE), repeat revascularization, and in-stent restenosis (ISR) compared with non-diabetic patients, despite advances in stent technology and antiplatelet therapy. Insulin resistance (IR) is a central pathophysiological driver of this excess risk, promoting endothelial dysfunction, vascular smooth muscle cell proliferation, and accelerated neointimal growth. Because direct measurement of IR is impractical in routine practice, several simple, laboratory-derived surrogate indices have been investigated for post-PCI risk stratification in T2DM. Of these, the triglyceride-glucose (TyG) index has accumulated the most consistent evidence, with multiple cohort studies and meta-analyses demonstrating an independent, graded association between elevated TyG values and MACE, mortality, ISR, and recurrent revascularization after PCI in diabetic populations. TyG also improves discrimination when added to established risk scores such as GRACE, and outperforms alternative markers such as the triglyceride-to-HDL-cholesterol ratio and METS-IR in this setting. Complementary inflammatory and metabolomic biomarkers add prognostic information that IR markers alone do not capture. This review summarizes the pathophysiological rationale linking IR to adverse PCI outcomes in T2DM, synthesizes the current evidence for IR-derived and complementary biomarkers, discusses methodological limitations, and outlines their potential role in post-PCI risk stratification, while highlighting the need for prospective, standardized, multi-ethnic validation before clinical adoption.
References
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