Matrix metalloproteinase-2 and inflammatory indices as discriminatory biomarkers for coronary artery ectasia versus stenosis: A cross-sectional study
DOI:
https://doi.org/10.38029/babcockuniv.med.j..v9iS1.1583Keywords:
Coronary Artery Disease, Coronary Aneurysm, Matrix Metalloproteinase 2, Inflammation, DyslipidaemiasAbstract
Objective: To evaluate serum matrix metalloproteinase-2 (MMP-2), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), red cell distribution width (RDW), and lipid profiles for discriminating coronary artery ectasia (CAE) from coronary artery stenosis (CAS) and healthy controls.
Methods: This cross-sectional study enrolled 120 participants (40 with angiographically confirmed CAE, 40 with CAS, and 40 healthy controls) between November 2024 and March 2025. Serum MMP-2 was measured using an enzyme-linked immunosorbent assay. Lipid profiles and complete blood counts were determined using automated analysers. Group comparisons employed Kruskal–Wallis H tests with Bonferroni correction. Receiver operating characteristic (ROC) curve analysis assessed diagnostic performance.
Results: MMP-2 levels were significantly elevated in CAE (73.48 ± 7.65 ng/mL) compared to CAS (38.49 ± 4.40 ng/mL) and controls (15.01 ± 4.70 ng/mL) (p < 0.001 for all pairwise comparisons). ROC analysis demonstrated excellent discrimination (area under the curve = 1.000) for distinguishing CAE from both CAS and controls, though this finding requires validation in larger cohorts. The CAE group exhibited the most severe atherogenic dyslipidaemia, with the highest total cholesterol, triglycerides, and lowest high-density lipoprotein cholesterol. Inflammatory indices (NLR, PLR, RDW) were significantly higher in CAE than in CAS and controls (p < 0.001), indicating a pronounced neutrophil-dominant inflammatory milieu in ectatic disease.
Conclusion: Marked MMP-2 elevation combined with severe dyslipidaemia and amplified inflammatory indices distinguishes CAE from CAS, suggesting that excessive proteolytic and inflammatory pathways drive pathological vascular dilation in coronary artery ectasia.
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Copyright (c) 2026 Jalil NI, Al-Rubaye AS, Al-Timimi RJ

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