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Atherosclerosis and Lipoproteins |
From the Second Department of Internal Medicine (M.H., M.T., H.T., T.M., O.S., S.N., S.N., M.M., R.K., M.O., Y.N.) and the Department of Pharmacology (M.T., N.Y.), University of Occupational and Environmental Health, Kitakyushu, Japan, and the Laboratory of Clinical Pharmaceutics (T.A.), Gifu Pharmaceutical University, Gifu, Japan
Correspondence to Masato Tsutsui, MD, PhD, Second Department of Internal Medicine, University of Occupational and Environmental Health, School of Medicine, 1-1 Iseigaoka, Yahatanishi-ku Kitakyushu 807-8555, Japan. E-mail mt2498{at}med.uoeh-u.ac.jp
Objective We examined the vascular expression levels of extracellular superoxide dismutase (EC-SOD), a major antioxidant enzyme in the cardiovascular system, in patients with acute coronary syndromes.
Methods and Results Twenty-one consecutive patients with acute myocardial infarction (AMI), 14 patients with unstable angina, 11 patients with stable angina, and 20 control subjects were studied. The levels of vascular EC-SOD expression were assessed by the difference in plasma EC-SOD concentrations before and after intravenous heparan injection. In the patients with AMI, vascular EC-SOD expression (ng/mL) was significantly higher on day 1 after the onset of AMI (148±10) as compared with the control subjects (116±6, P<0.05). The vascular EC-SOD expression returned to the normal range on day 7 (104±8), and that level persisted thereafter. The vascular EC-SOD expression was also significantly higher in the patients with unstable angina (160±13) than in those with stable angina (122±10) or in the controls (116±6) (P<0.05 each). Moreover, in the patients with AMI, higher levels of vascular EC-SOD expression on day 1 were significantly associated with smaller myocardial infarct size (P<0.05).
Conclusions This is the first clinical demonstration showing that vascular EC-SOD may be upregulated in acute coronary syndromes in humans in vivo. EC-SOD may play an important protective role against increased oxidative stress during acute ischemic coronary events.
Key Words: superoxide dismutase acute coronary syndromes myocardial infarction angina pectoris oxidative stress
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