Key result
T2D is linked to ~72% carotid plaque prevalence compared to none in normoglycemia.
Why the study?
The extent to which carotid plaque burden and morphology differ across the full glycaemic spectrum, and which cardiometabolic factors are most strongly associated with this burden, remain incompletely characterised.
Does dysglycaemia (prediabetes and type 2 diabetes) increase carotid plaque burden and alter plaque morphology compared to normoglycaemia in adults aged 40-70 years?
Cross-Sectional (n=169)
No
Does dysglycaemia (prediabetes and type 2 diabetes) increase carotid plaque burden and alter plaque morphology compared to normoglycaemia in adults aged 40-70 years?
p-value: p=<0.001
Carotid plaque burden is substantially elevated in prediabetes compared to normoglycaemia, suggesting early subclinical vascular involvement prior to the onset of overt type 2 diabetes.
Carotid plaque evaluation may refine CV risk stratification across glycaemic states; leaves open whether dysglycaemia directly alters plaque burden or morphology.
Background Dysglycaemia accelerates atherosclerosis, but the extent to which carotid plaque burden and morphology differ across the full glycaemic spectrum, and which cardiometabolic factors are most strongly associated with this burden, remain incompletely characterised. This study aimed to evaluate carotid plaque burden and morphology across the glycaemic spectrum, from normoglycaemia to type 2 diabetes mellitus (T2D). Methods This cross-sectional study included 169 participants: 24 normoglycaemic controls, 28 with prediabetes, and 117 with T2D stratified by glycaemic control. All underwent clinical, laboratory, and carotid ultrasonographic assessment. Plaque presence, morphology, and stenosis severity were evaluated. Multivariable logistic regression and receiver operating characteristic analyses were performed. Results Carotid plaque was present in 50.9% of participants (0% in normoglycaemia, with 8.3% showing isolated intima–media thickness [IMT] increase); a combined outcome of carotid plaque or isolated IMT increase was present in 60.4% overall. Carotid plaque prevalence increased markedly from normoglycaemia (0%) to prediabetes (42.9%) and ranged from 58.6% to 72.4% across the HbA1c-defined T2D subgroups, without a consistent further increase within this range ( p < 0.001). Plaque morphology also differed across glycaemic categories, with echolucent plaques proportionally more frequent in prediabetes and echogenic plaques predominating in T2D. In the multivariable model, age, urinary albumin-to-creatinine ratio (UACR), and total cholesterol were independent predictors of carotid plaque, whereas diabetes duration, HOMA-IR, and glycated haemoglobin (HbA1c) were not (AUC 0.821). Conclusions Carotid plaque burden is markedly higher across the dysglycaemic spectrum than in normoglycaemia, and is already substantial in prediabetes, suggesting early subclinical vascular involvement. Age, UACR, and total cholesterol, rather than HbA1c alone, showed the strongest associations with carotid atherosclerosis. Carotid ultrasonography, including assessment of plaque morphology, may provide additional information for cardiovascular risk stratification beyond glycaemic status alone. This potential role merits evaluation in future prospective studies.
No takes yet. Share an insight, caveat, or question.
İhsan Boyacı (2026) conducted a cross-sectional in Dysglycaemia and Type 2 Diabetes (n=169). Dysglycaemia (Prediabetes and Type 2 Diabetes) vs. Normoglycaemia was evaluated on Carotid plaque presence (p=<0.001). Carotid plaque prevalence increased significantly from 0% in normoglycaemia to 42.9% in prediabetes and up to 72.4% in type 2 diabetes, with age, UACR, and total cholesterol acting as independent predictors.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: