Why the study?
Growing evidence highlights the influence of glycemic abnormalities on CAD extent, progression, and phenotype, warranting a review of pathophysiological mechanisms, coronary imaging findings, and therapeutic strategies.
Coronary imaging studies demonstrate that both diabetes and prediabetes drive accelerated atherosclerosis and vulnerable plaque phenotypes, explaining the elevated cardiovascular risk in these populations.
Supports SGLT2i preference in T2DM-CAD; extends prior CVOTs with plaque imaging data.
Type 2 diabetes mellitus (T2DM) is a complex metabolic disorder that is associated with a markedly increased risk of coronary artery disease (CAD) and cardiovascular (CV) mortality compared with the general population. Prediabetes, a heterogeneous intermediate glycemic state defined by impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT), and/or glycated hemoglobin (HbA1c) levels between 5.7% and 6.4%, is likewise associated with a significantly higher CV risk than normoglycemia. Over the past decade, both overall CAD burden and specific plaque morphologic features have been established as robust predictors of future adverse CV events using invasive and non-invasive coronary imaging modalities. More recently, growing evidence has highlighted the influence of glycemic abnormalities on the extent, progression, and phenotype of CAD, underscoring the interplay between metabolic dysfunction and atherosclerotic vulnerability. Therefore, this review aims to (i) elucidate the pathophysiological mechanisms linking T2DM and prediabetes with atherogenesis, (ii) summarize findings from coronary imaging studies in these populations, and (iii) evaluate therapeutic strategies designed to promote plaque stabilization and regression.
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Gurgoglione et al. (2026) conducted a review in Adults with type 2 diabetes mellitus (T2DM) or prediabetes and coronary artery disease (CAD), including asymptomatic and symptomatic patients with subclinical or established CAD. Various anti-diabetic therapies including Metformin, Pioglitazone, Sodium-Glucose Cotransporter-2 inhibitors (SGLT2i), and Glucagon-like peptide-1 receptor agonists (GLP-1RA); in observational and RCT settings vs. Placebo or standard care or matched controls without therapy was evaluated on Major adverse cardiovascular events (MACE) or coronary plaque progression or regression assessed by imaging (plaque volume, vulnerable plaque features such as thin cap fibroatheroma, lipid core burden).
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