Volume 139, Issue 2 , Pages 187-192, 4 March 2010
Myeloperoxidase may contribute to the no-reflow phenomenon in patients with acute myocardial infarction
Abstract
Background
The no-reflow phenomenon is a deteriorating factor for prognosis of acute myocardial infarction (AMI). Leukocyte enzymes may be involved in developing the no-reflow phenomenon. The aim of this study was to clarify the association of myeloperoxidase, a leukocyte enzyme, with the no-reflow phenomenon in patients with AMI after percutaneous coronary inetervention (PCI).
Methods
We enrolled 50 patients with AMI whose infarct-related coronary arteries were rescued by thrombectomy devices. Blood samples were collected from peripheral vein (PV), ostium and culprit lesion of infarct-related coronary artery. Myeloperoxidase, elastase and interleukin (IL)-8 were measured by ELISA. Antegrade blood flow in the infarct-related coronary artery and myocardial perfusion were evaluated according to the corrected TIMI frame counts (cTFC) and the myocardial blush grade (MBG).
Results
Plasma myeloperoxidase and IL-8 levels at the ostium and the culprit lesion of infarct-related coronary artery were significantly greater than those in PV. No-reflow was found in 10 patients (20%). Plasma levels of myeloperoxidase at the culprit lesion of infarct-related coronary artery were significantly greater in the patients with no-reflow than those without no-reflow. Plasma myeloperoxidase levels at the culprit lesion of infarct-related coronary artery positively correlated with the cTFC. Also, plasma myeloperoxidase levels were significantly higher in the patients with MBG 0–1 than those with MBG 2–3.
Conclusions
The present findings indicate that local myeloperoxidase levels in the culprit coronary artery may contribute to the no-reflow phenomenon in the patients with AMI.
Keywords: Acute myocardial infarction, Myeloperoxidase, No-reflow phenomenon
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PII: S0167-5273(08)01093-0
doi:10.1016/j.ijcard.2008.10.018
© 2008 Elsevier Ireland Ltd. All rights reserved.
Volume 139, Issue 2 , Pages 187-192, 4 March 2010
