Antioxidant status and levels of antioxidant vitamins in coronary artery ectasia

作者：Koc Fatih^*; Kalay Nihat; Ardic Idris; Ozbek Kerem; Celik Atac; Ceyhan Koksal; Kadi Hasan; Karayakali Metin; Sahin Semsettin; Altunkas Fatih; Onalan Orhan; Kaya Mehmet G

来源：Coronary Artery Disease, 2011, 22(5): 306-310.

DOI：10.1097/MCA.0b013e328346b864

• gamma-glutamyltransferase
• coronary artery ectasia
• glutathione peroxidase
• superoxide dismutase
• vitamins A and E

Background Coronary artery ectasia (CAE) is a rare coronary artery anomaly. In this study, we investigated superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and gamma-glutamyltransferase (GGT) activities, and antioxidant vitamin levels (vitamins A and E) in patients with CAE.
Methods Forty-five patients who were diagnosed with CAE using coronary angiography were included in the study (26 men; mean age, 57 +/- 9 years). The control group consisted of 35 participants who had normal coronary arteries as shown by coronary angiography (14 men; mean age, 54 +/- 7 years). The plasma activity of SOD, GSH-Px, GGT, and levels of vitamins A and E were measured.
Results The plasma SOD activity was significantly lower in the CAE group compared with the control group (0.70 +/- 0.64 vs. 1.52 +/- 0.85 U/ml; P = 0.001). The serum GGT activity was higher in the CAE group compared with the control group (34 +/- 20 vs. 26 +/- 13 U/ml; P = 0.04). There were no significant differences in the plasma GSH-Px activity and vitamin A and E levels. There was a positive correlation between SOD activity and low-density lipoprotein cholesterol levels (r = 0.418; P = 0.01). There was also a positive correlation between vitamin E and low-density lipoprotein cholesterol (r = 0.410; P = 0.01) and triglyceride levels (r = 0.310; P = 0.04) in patients with CAE.
Conclusion In this study, patients with CAE had a decreased SOD plasma activity and an increased GGT activity compared with normal controls. These results suggest that oxidative stress and antioxidant status may have an important role in the pathogenesis of CAE.

• 出版日期2011-8