Paraoxonase-1 activity and oxidative stress markers in anterior ST elevation myocardial infarction with and without no-reflow undergoing primary percutaneous coronary intervention

Abstract

Background: Reperfusion injury is one of the pathogenetic mechanisms of no-reflow. We aimed to investigate the relationship between no-reflow with paraoxonase activity and oxidative stress markers (total antioxidant status (TAS), total oxidant status (TOS), lipid hydro-peroxide (LOOH)) in patients with anterior ST elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). Methods: In this study, 215 consecutive anterior STEMI patients undergoing primary PCI were prospectively included (177 male, 38 female; mean age 54.9±12.0 years). No-reflow was defined as TIMI grade 0 and 1 flows or TIMI grade 3 with myocardial blush grade 0 and 1. The patients were divided into two groups as normal flow (n=179) and no-reflow (n=36) groups. Serum paraoxonase activity was measured spectrophotometrically. TAS and TOS levels were determined by using an automated measurement method. LOOH levels were measured by ferrous oxidation with xylenol orange assay. Results: Patients with no-reflow was older and had higher incidence of female gender, hypertension and diabetes. Patients with no-reflow was also had higher infarction time, higher thrombus score and SYNTAX score. Paraoxonase activities and TAS levels were significantly lower and TOS and LOOH levels were significantly higher in patients with no-reflow compared to normal flow group. On multivariate logistic regression analysis, paraoxonase activity (β=0.975, %CI=0.957-0.994, p=0.009) and TOS (β=1.142, %CI=1.058-1.233, p=0.001) as well as diabetes, infarction time, thrombus score and SYNTAX score were independent predictors of no-reflow (Table 1). View this table: Table 1 Conclusion: In patients with no-reflow, oxidants are increased, while serum paraoxonase-1 activity and antioxidants are decreased. This result shows that increased oxidative stress may have role in the pathogenesis of no-reflow.