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Published on: January 28, 2020
Elevated oxidative stress markers as independent predictors of isolated coronary artery ectasia
Sadettin S Baysal1, Şahbender Koç2, Kerem Özbek3
1Başakşehir Çam and Sakura City Hospital, Istanbul, Türkiye.
Insights
Oxidative stress is elevated in isolated coronary artery ectasia (CAE), indicated by higher total oxidative status (TOS) and lipid hydroperoxide (LOOH) levels. This suggests oxidative imbalance contributes to CAE pathogenesis, warranting targeted therapies.
Area of Science:
- Cardiovascular Research
- Biomarker Analysis
- Oxidative Stress Studies
Background:
- Coronary artery ectasia (CAE) is a dilation anomaly, sharing traits with coronary artery disease (CAD) but with unclear independent pathophysiology.
- Endothelial dysfunction and inflammation are often linked to CAE.
- The role of oxidative stress in isolated CAE requires further investigation.
Purpose of the Study:
- To assess oxidative and antioxidant biomarker levels in patients with isolated CAE.
- To elucidate the potential role of oxidative stress in the pathogenesis of isolated CAE.
Main Methods:
- Compared 48 isolated CAE patients with 32 controls using normal coronary angiograms.
- Measured oxidative stress markers: total oxidative status (TOS), oxidative stress index (OSI), lipid hydroperoxide (LOOH).
- Assessed antioxidant markers: paraoxonase-1 (PON1), ceruloplasmin (CP), free sulfhydryl (SH) groups, total antioxidant status (TAS).
Main Results:
- CAE patients showed significantly higher TOS, OSI, and LOOH levels compared to controls.
- No significant differences in TAS, PON1, CP, or SH levels were observed between groups.
- Smoking, TOS, and hsCRP independently predicted CAE via logistic regression.
Conclusions:
- Elevated TOS, OSI, and LOOH indicate a pro-oxidant state in isolated CAE.
- Antioxidant defenses appear largely unchanged, suggesting oxidative stress is a key factor.
- Findings support oxidative stress's role in CAE pathogenesis, highlighting the need for therapies targeting oxidative imbalance.
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 H2O2 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 H2O2 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.
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