ABC | Volume 113, Nº3, September 2019

Short Editorial Sobral Filho & Monteiro Júnior High platelet activity in acute coronary syndrome Arq Bras Cardiol. 2019; 113(3):364-366 1. Fuentes E, Moore-Carrasco R, Paes AMA, Trostchansky A. Role of Platelet Activation and Oxidative Stress in the Evolution of Myocardial Infarction. J of Cardiovasc Pharmacol Ther.2019;24(6):509-20. 2. Anderson JL, MorrowDA. AcuteMyocardial Infarction. NEngl J Med. 2017; 376(21): 2053-64. 3. Fuentes E, Gibbins JM, Holbrook LM, Palomo I. NADPHoxidase 2 (NOX2): A key target of oxidative stress-mediated platelet activation and thrombosis. Trends Cardiovasc Med.2018;28(7):429-34. 4. Lewis HD Jr, Davis JW, ArchibaldDG, SteinkeWE, Smitherman TC, Doherty JE, et al. Protective effects of aspirin against acutemyocardial infarction and death in men with unstable angina. Results of a Veterans Administration Cooperative Study. N Engl J Med. 1983;309(7):396-403. 5. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. Lancet. 1988;2(8607):349-60. 6. Théroux P, Ouimet H, McCans J, Latour JG, Joly P, Lévy G, et al. Aspirin, heparin, or both to treat acute unstable angina. N Engl J Med. 1988;319(17):1105-11. 7. Antithrombotic Trialists’ Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ. 2002;324(7329):71-86. 8. Dracoulakis MDA, Gurbel P, CattaneoM, Martins HS, Nicolar JC, Kalil Filho R. High residual platelet reactivity during aspirin therapy in patients with non-St-Segmnt Elevation acute coronary syndrome: comparison between initial and late phases. Arq Bras Cardiol. 2019; 113(3):357-363. 9. Violi F, Carnevale R, Loffredo L, Pignatelli P, Gallin JI. Nox2 and atherothrombosis: insight from chronic granulomatous disease. ATVB 2017;37(2):218-25. 10. Violi F, Loffredo l , Carnevale R , Pignatelli P , Pastori D . Atherothrombosis and oxidative stress: mechanisms and management in elderly. Antioxid Redox Signal 2017; 27(14):1083-124. 11. Chatterjee M , Rath D , Schlotterbeck J , RheinlaenderJ , Walker-AllgaierB , Alnag- Gar N , et al. Regulation of oxidized platelet lipidome: implications for coronary artery disease. Eur Heart J. 2017;38(25):1993-2005. 12. Calvieri C, Tanzilli G, Bartimoccia S, Cangemi R, Arrivi A, Dominici M, et al. Interplay between Oxidative Stress and Platelet Activation in Coronary Thrombus of STEMI Patients. Antioxidants (Basel). 2018;7(7) pii:E83. 13. Carnevale R, Bartimoccia S, Nocella C, Di Santos S, Loffredo L, Illuminati G, et al. LDL oxidation by platelets propagates platelet activation via an oxidative stress mediatedmechanism. Atherosclerosis. 2014;237(1):108-116. 14. Patrono C, Morais J, Baigent C, Collet JP , Fitzgerald D, Halvorsen S, et al. Antiplatelet Agents for the Treatment and Prevention of Coronary Atherothrombosis. J Am Coll Cardiol. 2017;70(14):1760-76. 15. Monteiro Júnior JGM, de Oliveira CTD, Filho DCS. Hematological parameters as prognostic biomarkers in patients with cardiovascular diseases. Curr Cardiol Rev. 2019;15(4):274-82. 16. Uysal HB, Dagli B, Akgullu C, Ayal M, Xancir C, AyhanM, et al. Blood count parameters can predict the severity of coronary artery disease. Korean J Intern Med 2016; 31(6) 1093-100. 17. Violi F, Pignatelli P. Platelet Oxidative Stress and Thrombosis. Thromb Res. 2012;129(3):378-81. 18. Hovens MM, Snoep JD, Eikenboom JC, van der Bom JG, Mertens BJ, Huisman MV. Prevalence of persistent platelet reactivity despite use of aspirin: a systematic review. AmHeart J. 2007;153(2):175-81. 19. BuyukasikY,KarakusS,GokerH,HaznedarogluIC,OzatliD,SayinalpN,etal. RationaluseofthePFA-100device forscreeningofplateletfunctiondisorders and vonWillebrand disease. Blood Coagul Fibrinolysis. 2002;13(4):349-53. 20. Lordkipanidzé M, Pharand C, Schampaert E, Turgeon J, Palisaitis DA, Diodati JG. A comparison of six major platelet function tests to determine the prevalence of aspirin resistance in patients with stable coronary artery disease. Eur Heart J. 2007;28(14):1702-8. 21. Ivandic BT, Giannitsis E, Schlick P, Staritz P, Katus HA, Hohlfeld T. Determination of aspirin responsiveness by use of whole blood platelet aggregometry. Clin Chem. 2007;53(4):614-9. References thrombin. 13 These represent goals in therapeutic modulation such as cyclooxygenase-1 inhibitors, P2Y12 inhibitors, protease- activated receptors (PAR) 1 inhibitors and interindividual variability in drug responses. 14 Platelets are heterogeneous in volume and density, biological variables that determine platelet function, playing an important role in the development of intravascular thrombus. Large platelets are metabolically and enzymatically more active than small platelets, which is reflected in the increase in mean platelet volume (MPV). 15 In the study by Hilal Bektas et al., 16 the MPV value above 10.4 is a predictor of severe atherosclerosis with a sensitivity of 39% and specificity of 90% (ROC curve: 0.631, 95% CI: 0.549-0.708, p = 0.003), and can be used as a predictor of cardiac risk in patients with disease coronary artery. Another pathway includes impaired biosynthesis or inactivation of NO and/or enhanced the formation of isoprostanes, which may represent a future target of antiplatelet drugs. 17 Antiplatelet therapy is important in the prevention of MI, and despite its proven efficacy in both acute and chronic phases, there is still a high recurrence rate of ischemic events in patients with coronary artery disease. 1,17 Aspirin resistance may be present in 5% to 75% of patients. 1 In a systematic review, Hovens et al. 15 demonstrated the high variability in individual response to aspirin in different populations. There are laboratory methods such as VerifyNow (VFN), total blood aggregometry (TBA) and platelet function analyzer (PFA-100) that can assess this platelet variability. 19-21 Oxidative stress may be associated with increased aggregation due to diminished response to antiplatelet therapy. 1 However, the reason for this high platelet variability is still unclear despite the routine use of aspirin and the relative contribution of NOX2 as a key target of different platelet activation pathways in the treatment of acute and chronic coronary disease. Specific antioxidants may, therefore, represent a new approach to limit platelet-related vascular complications due to the presence of NOX2. 365