Abstract
INTRODUCTION: Coronary artery ectasia (CAE) is a vascular anomaly characterized by abnormal coronary artery dilation, often associated with endothelial dysfunction and inflammation. While CAE shares features with coronary artery disease (CAD), its independent pathophysiology remains unclear, particularly in cases without concurrent CAD. AIM: To evaluate oxidative and antioxidant biomarker levels in patients with isolated CAE to understand their role in its pathogenesis. MATERIAL AND METHODS: Our study was conducted involving 48 patients with isolated CAE and 32 controls with normal coronary angiograms. Oxidative stress markers, including total oxidative status (TOS), oxidative stress index (OSI), and lipid hydroperoxide (LOOH), were measured, alongside antioxidant markers such as paraoxonase-1 (PON1), ceruloplasmin (CP), free sulfhydryl (SH) groups, and total antioxidant status (TAS). RESULTS: CAE patients exhibited significantly higher levels of TOS (30.14 ±8.81 vs. 23.88 ±4.74 mmol H(2)O(2) equiv./l, p = 0.004), OSI (3.21 ±1.12 vs. 2.43 ±0.53 arbitrary units, p < 0.001), and LOOH (11.95 ±2.88 vs. 10.13 ±1.66 µmol H(2)O(2) equiv./l, p = 0.003). No significant differences were found in TAS, PON1, CP, or SH levels between groups (p > 0.05 for all). Logistic regression identified smoking, TOS, and high sensitivity C-reactive protein (hsCRP) as independent predictors of CAE. CONCLUSIONS: Elevated oxidative stress markers, particularly TOS, OSI, and LOOH, indicate a heightened pro-oxidant state in CAE, while antioxidant defenses remain largely unaltered. These findings suggest that oxidative stress may contribute to CAE pathogenesis, emphasizing the need for therapies targeting oxidative imbalance.