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

Abstract Background Reperfusion and ischemic injuries are pathogenetic mechanisms of no-reflow. Oxidative stress plays a critical role during ischemia as well as during the reperfusion phase following ST elevation myocardial infarction (STEMI). We sought to investigate the relationship between no-re...

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Published in:Atherosclerosis 2014-06, Vol.234 (2), p.415-420
Main Authors: Gür, Mustafa, Türkoğlu, Caner, Taşkın, Abdullah, Uçar, Hakan, Börekçi, Abdurrezzak, Şeker, Taner, Gözükara, Mehmet Yavuz, Kaypaklı, Onur, Akyol, Selahattin, Selek, Şahbettin, Şahin, Durmuş Yıldıray, Elbasan, Zafer, Çaylı, Murat
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Language:English
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Summary:Abstract Background Reperfusion and ischemic injuries are pathogenetic mechanisms of no-reflow. Oxidative stress plays a critical role during ischemia as well as during the reperfusion phase following ST elevation myocardial infarction (STEMI). We sought to investigate the relationship between no-reflow with paraoxonase-1 (PON-1) activity and oxidative stress markers (total antioxidant capacity (TAC), total oxidant status (TOS), oxidative stress index (OSI), lipid hydro-peroxide (LOOH)) in patients with anterior STEMI undergoing primary percutaneous coronary intervention (PCI). Methods In this study, 319 consecutive anterior STEMI patients undergoing primary PCI were prospectively included (mean age 56.5 ± 12.5 years). The patients were divided into two groups as normal flow ( n  = 231) and no-reflow ( n  = 88) groups. Serum PON-1 activity was measured spectrophotometrically. TAC and TOS levels were determined by using an automated measurement method. LOOH levels were measured by ferrous oxidation with xylenol orange assay. Results PON-1 activity and TAC levels were significantly lower and TOS, OSI and LOOH levels were significantly higher in patients with no-reflow compared to normal flow group ( p  
ISSN:0021-9150
1879-1484
DOI:10.1016/j.atherosclerosis.2014.03.005