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

**Authors:** Yashasvi Agarwal, Anjali Metgudmath, Vijayanand Metgudmath

PMC · DOI: 10.7759/cureus.102326 · Cureus · 2026-01-26

## TL;DR

This study finds that higher mean platelet volume is linked to more severe coronary artery disease in diabetic patients, suggesting it could be a useful marker for assessing disease severity.

## Contribution

The study identifies MPV as an independent predictor of coronary disease severity in diabetic patients, suggesting a potential mechanistic link between poor glycemic control and platelet activation.

## Key findings

- MPV increased with the severity of coronary artery disease and was an independent predictor after adjusting for multiple factors.
- HbA1C showed a positive association with MPV, suggesting a possible link between poor glycemic control and platelet activation.
- Structural equation modeling indicated a borderline indirect effect of HbA1C on CAD severity through MPV.

## Abstract

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.

## Linked entities

- **Diseases:** coronary artery disease (MONDO:0005010)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, ATHS (atherosclerosis susceptibility (lipoprotein associated)) [NCBI Gene 470] {aka ALP}, VWF (von Willebrand factor) [NCBI Gene 7450] {aka F8VWF, VWD}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, THPO (thrombopoietin) [NCBI Gene 7066] {aka CAMT2, MGDF, MKCSF, ML, MPLLG, THC9}, SELP (selectin P) [NCBI Gene 6403] {aka CD62, CD62P, GMP140, GRMP, LECAM3, PADGEM}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}
- **Diseases:** -vessel disease (MESH:C536223), DM (MESH:D003920), endothelial dysfunction (MESH:D014652), edema (MESH:D004487), Inflammatory (MESH:D007249), disease (MESH:D004194), MPV (MESH:D001791), angiopathy (MESH:D001018), atherogenic dyslipidemia (MESH:D050171), coronary disease (MESH:D003327), alcoholism (MESH:D000437), SVD (MESH:D012640), luminal stenosis (MESH:D003251), TVD (MESH:C536008), chest pain (MESH:D002637), stroke (MESH:D020521), coagulation (MESH:D001778), CVD (MESH:D002318), myocardial infarction (MESH:D009203), oedema (MESH:C536897), ischemic heart disease (MESH:D017202), IPF (MESH:D013724), Insulin resistance (MESH:D007333), hepatobiliary disease (MESH:D004066), ocular damage (MESH:D015817), thrombosis (MESH:D013927), hypertension (MESH:D006973), arterial occlusion (MESH:D001157), atherosclerosis (MESH:D050197), pallor (MESH:D010167), neuropathy (MESH:D009422), Inadequate (MESH:D012892), renal dysfunction (MESH:D007674), multi-vessel disease (MESH:C564969), CAD (MESH:D003324)
- **Chemicals:** bilirubin (MESH:D001663), triglycerides (MESH:D014280), sugars (MESH:D000073893), cholesterol (MESH:D002784), nitric oxide (MESH:D009569), chloride (MESH:D002712), blood glucose (MESH:D001786), urea (MESH:D014508), anti (-), potassium (MESH:D011188), Sodium (MESH:D012964), glucose (MESH:D005947), creatinine (MESH:D003404), Lipid (MESH:D008055)
- **Species:** Nicotiana tabacum (American tobacco, species) [taxon 4097], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

32 references — full list in the complete paper: https://tomesphere.com/paper/PMC12935080/full.md

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Source: https://tomesphere.com/paper/PMC12935080