Abstract Objectives Coronary artery ectasia (CAE) is characterised by an increase in the diameter of a coronary artery of ≥1.5 times its diameter at the adjacent vessel. It is evident that alterations in the extracellular matrix changes contribute to the development of CAE. Lysyl oxidases (LOXs) are copper-dependent monoamine oxidase enzymes that play a crucial role in the regulation of connective tissue. Deficiencies in these enzymes have been linked to vascular changes, consequently leading to cardiovascular diseases. The objective of this study was to assess the association between the LOX -G473A (rs1800449) variation and inflammatory markers in CAE development. Methods The current cross-sectional study includes 88 patients whom CAE was confirmed in one of the coronary arteries by coronary angiography and 75 controls with positive exercise tests and angiographically normal coronary arteries without any typical ischemic symptoms and family history of cardiac diseases. Luminex technology was used to detect inflammatory markers. The fluorescence end-point PCR method was used for genotyping. Results Significantly higher plasma levels of TNF-α, sE-selectin, and hypercholesterolemia were observed in the CAE group (p<0.05). Male gender was found as risk factor for CAE. Although the genotype and allele distributions did not showed statistical significance, CAE patients with GA genotype had significantly higher levels of TNF-α and sP-selectin compared to patients with GG genotype. In addition, patients with right coronary artery (RCA) ectasia had higher TNF-α levels than patients with non-RCA ectasia. Conclusions Our findings could suggest that LOX -G473A polymorphism could be associated with the increase in inflammatory markers and CAE development.
Kılıçarslan et al. (2026) studied this question.