Heparin-released extracellular superoxide dismutase is reduced in patients with coronary artery atherosclerosis

Objectives We studied whether the amount of heparin-released extracellular superoxide dismutase (EC-SOD), which is an antioxidative enzyme, is associated with coronary artery disease (CAD). Methods and results EC-SOD was measured in plasma at basal and at post-heparin injection in 315 patients. Heparin-released EC-SOD was calculated as the difference between the two values. After exclusion of a mutant EC-SOD group (n = 27:8.6%), 288 patients were divided into three groups by angiographic findings; those with normal coronary (the normal group; n = 63), those with atherosclerosis without significant stenosis (the mild atherosclerosis group; n = 36), and those with significant stenosis (the atherosclerosis group; n = 189). Although the basal values were similar among the three groups, heparin-released EC-SOD levels were significantly lower in the atherosclerosis group (131.0 ± 42.8 ng/ml, p = 0.0003) than in the normal group (156.9 ± 66.2 ng/ml). Moreover, logistic analysis revealed that heparin-released EC-SOD independently contributed to CAD. The coronary score showed a significant correlation with heparin-released EC-SOD. As for factors affecting the level of heparin-released EC-SOD, the level of high-density lipoprotein cholesterol and age showed a positive correlation. Conclusions The results suggest that heparin-released EC-SOD is significantly reduced in CAD and that the tissue-bound location of this enzyme might be important for antioxidative function.