|| Checking for direct PDF access through Ovid
Increased accumulation of reactive oxygen species contributes to pathophysiologic states such as endothelial dysfunction, metabolic and functional impairment, inflammatory activation, and other features of cardiovascular pathophysiology. Allopurinol acts as a xanthine oxidase inhibitor that reduces the amount of free radicals after reactive oxygen species generation.In this placebo-controlled randomized clinical trial, all patients admitted with coronary artery disease who are candidates for elective percutaneous coronary intervention (PCI) were included. The 254 patients were randomly divided into 2 groups. Blood samples for cardiac biomarkers (creatine kinase [CK]-MB and troponin T [cTnT]) were collected from all patients after admission (the day before PCI), and also 8 and 16 hours after intervention. In group 1 (133 patients), 600 mg allopurinol was orally administered on the day before PCI, and another same dose on the day of PCI, and the elective PCI was performed. In group 2 (121 patients), elective PCI was performed without pretreatment with allopurinol. In an unadjusted model, the serum levels of both CK-MB and cTnT, 16 hours after PCI were higher in the placebo group as compared with the allopurinol group, although it was statistically insignificant. We compared the maximum levels of CK-MB and cTnT (8 or 16 hours after PCI) and their maximum changes in both groups. After adjustment for confounders, use of allopurinol did not have any statistically significant association with the rise of cardiac-spec–fic enzymes.Allopurinol could not be effective significantly, in patients undergoing elective PCI, to decrease cardiac-specific enzymes, and seems not to be of use before PCI.