CLINICAL DETERMINANTS OF PLATELET FUNCTION IN PATIENTS WITH CAD UNDERGOING CORONARY ANGIOGRAPHY AND TREATED BY DUAL ANTIPLATELET THERAPY
Abstract number: O-T-034
Marcucci1 R., Paniccia1 R., Gori2 A., Romano1 E., Antonucci1 E., Poli1 S., Buonamici3 P., Antoniucci3 D., Abbate1 R., Gensini4 G.
11Surgical and Medical Critical Area, University of Florence, Florence 22Surgical and Medical Critical Area, University of Florence 33Cardiology Unit, AOU Careggi 44DOn Carlo Gnocchi Foundation, University of Florence, Florence, Italy
How-to-cite Marcucci R, Paniccia R, Gori A, Romano E, Antonucci E, Poli S, Buonamici P, Antoniucci D, Abbate R, Gensini G. CLINICAL DETERMINANTS OF PLATELET FUNCTION IN PATIENTS WITH CAD UNDERGOING CORONARY ANGIOGRAPHY AND TREATED BY DUAL ANTIPLATELET THERAPY. J Thromb Haemost 2007; 5 Supplement 2: O-T-034
Abstract
Introduction: We sought to evaluate the clinical determinants of platelet function in a large cohort of patients undergoing PCI on dual antiplatelet therapy.
Methods: We measured platelet function by both a point-of-care assay (PFA-100) and platelet aggregation (PA) with two agonists (arachidonic acid, AA, 0.5 mg/mL and ADP 2 and 10 microm/L) in 868 adult patients with coronary artery disease: 386 with acute coronary syndromes undergoing a primary PCI (group A) and 482 coronary artery disease patients scheduled to undergo an elective PCI (group B).
Results: PFA test detected 265/868 (30.5%) aspirin resistant patients (CT/EPI<203 sec). In a multivariate model, ACS (OR:1.5, 95% CI 1.1-2.1, p=.01) and chronic use of aspirin (OR:0.4, 95% CI 0.3-0.6, p=.0001) were significant and independent predictors of response to aspirin detected by PFA-100. Leukocytes and ESR were significantly higher in patients with aspirin resistance both in patients of group A and B. PA induced by AA detected 271/868 (31.2%) aspirin resistant patients (AA-PA;20%). In a multivariate model, ACS (OR:1.7, 95% CI 1.2-2.4, p=.001) and chronic use of aspirin (OR:0.4, 95% CI 0.3-0.6, p=.0001) were significant and independent predictors of response to aspirin detected by AA-PA. Leukocytes and ESR were significantly higher in patients with aspirin resistance both in patients of group A and B. 54/868 (6.2%) patients were clopidogrel resistant by ADP 2 mM and 192/868 (22.1%) by ADP 10 mM. In a multivariate model, previous use of clopidogrel (OR:0.6, 95% CI 0.3-0.9, p=.02) and diabetes (OR:1.5, 95% CI 1.1-2.2, p<.05) were significant and independent predictors of response to clopidogrel detected by ADP-PA.
Conclusions: Our data demonstrated that diabetes, ACS, chronic use of antiplatelet agents are independent predictor of the platelet response to both aspirin and clopidogrel. We provided the first evidence of a possible involvement of the inflammatory processes in the development of laboratory resistance to aspirin.
