Correlation of Mean Platelet Volume With Angiographic Severity in Diabetic Coronary Artery Disease: A Cross-Sectional Study.

Aim To evaluate the association of mean platelet volume (MPV) and immature platelet fraction (IPF) with coronary angiographic severity, categorised by the number of significantly diseased epicardial vessels (single, double or triple vessel disease), in diabetic patients and to assess their relationship with glycaemic and metabolic parameters. Methods This cross-sectional study included 130 diabetic patients undergoing coronary angiography. Demographic variables, glycemic indices, serum metabolic markers, liver and renal function parameters, and haematological and coagulation profile markers were assessed. Platelet indices were compared with coronary angiographic severity categories. Ordinal logistic regression was used to evaluate independent predictors of increasing coronary disease severity. Spearman correlation and structural equation modelling (SEM) were employed to explore hypothesised pathways linking glycaemic control, platelet indices, and coronary artery disease (CAD) severity. Results MPV demonstrated a significant stepwise increase from single- to triple-vessel disease (p < 0.05) and remained an independent predictor of angiographic severity after adjustment for age, sex, glycated haemoglobin (HbA1C), low-density lipoprotein (LDL), smoking, and treatment factors (OR ≈ 1.50 per fL, 95% CI: ~1.05-2.15, p = 0.025). HbA1C showed a positive association with MPV (β = 0.158, p = 0.003) but not with IPF. SEM suggested a borderline indirect effect of HbA1C on CAD severity via MPV (Sobel z = 1.95, p = 0.051), indicating a potential mechanistic link between poor glycaemic control and platelet activation. IPF correlated weakly with fasting glucose but showed no independent association with angiographic severity. Other metabolic and hepatic parameters were largely within normal ranges, whereas mild renal stress was observed in a subset of patients. Conclusion MPV appears to be a clinically relevant marker of diabetes-related CAD severity. While mediation findings should be interpreted cautiously due to the cross-sectional design, they support a biologically plausible pathway linking hyperglycaemia, platelet activation, and coronary disease burden. The lack of association between IPF and glycaemic control warrants further evaluation in larger, prospective cohorts to clarify its clinical utility.