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Evaluating the Effect of Intracoronary N-Acetylcysteine on Platelet Activation Markers After Primary Percutaneous Coronary Intervention in Patients With St-Elevation Myocardial Infarction Publisher Pubmed



Eshraghi A1 ; Talasaz AH2, 3 ; Salamzadeh J4 ; Salarifar M5 ; Pourhosseini H5 ; Nozari Y5 ; Bahremand M6 ; Jalali A7 ; Boroumand MA8
Authors
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Authors Affiliations
  1. 1. Department of Pharmacology and Toxicology, Faculty of Pharmacy-International Campus, Iran University of Medical Sciences, Tehran, Iran
  2. 2. Department of Clinical Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Department of Pharmaceutical Care, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, 1411713138, Iran
  4. 4. Department of Clinical Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  5. 5. Cardiology Department, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran
  6. 6. Cardiology Department, Kermanshah University of Medical Sciences, Kermanshah, Iran
  7. 7. Research Department, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran
  8. 8. Department of Molecular Pathology, Tehran Heart Center, Tehran, Iran

Source: American Journal of Therapeutics Published:2016


Abstract

During percutaneous coronary intervention (PCI), trauma occurs in the arterial endothelium, resulting in platelet activation and aggregation. As platelet aggregation may lead to coronary thrombosis, antiplatelet agents are essential adjunctive therapies in patients undergoing PCI. The aim of this study was to determine the effect of the intracoronary administration of high-dose N-acetylcysteine (NAC) for the evaluation of its antiplatelet effects in human subjects. In this triple-blind trial, 147 patients undergoing primary PCI were enrolled. Finally, 100 patients were randomized to receive high-dose intracoronary NAC (100 mg/kg bolus, followed by 10 mgkg21h21 intracoronary continued intravenously for 12 hours) (n 5 50) or dextrose solution (n 5 50). Platelet activation biomarkers were measured before and 24 hours after the procedure. Secondary end points, comprising all-cause death, reinfarction, and target-vessel revascularization, were assessed at 30 days and 2 years. In comparison with the placebo, NAC could not reduce the level of platelet activation biomarkers within a 24-hour period after its prescription. Major adverse clinical events at 30 days and 2 years were infrequent and not statistically different between the 2 groups. Our results revealed that NAC, compared with the placebo, did not provide an additional clinical benefit as an effective antiplatelet agent after PCI. Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.