Platelet Function Predicts Myocardial Damage in Patients with Acute Coronary Syndromes Treated with Multiple Antiplatelet Agents

Abstract number: P1095

Marcucci¹ R, Paniccia¹ R, Giusti¹ B, Gori¹ AM, Mannini¹ L, Giglioli¹ C, Valente¹ S, Gensini¹ GF, Prisco¹ D, Abbate¹ R

¹¹Department of Medical and Surgical Critical Care, Thrombosis Center, University of Florence ¹¹Department of Medical and Surgical Critical Care, Thrombosis Center, University of Florence

Platelet activation is a hallmark of acute coronary syndromes (ACSs) and platelets play a dominant pathogenic role in the development and outcome of ACS. Aim of our study was to evaluate platelet function in patients with MI undergoing percutaneous coronary revascularization (PCI), in relation to the extent of myocardial damage and to the presence of polymorphisms in genes coding for some platelet glycoproteins (GpIIb/IIa; GpIa/IIa; P-selectin). We studied 150 patients (98 m/26F; age: 64 ± 10.7 yrs) with acute coronary syndromes (98 with STEMI and 52 with NSTEMI) undergoing a PCI with stent implantation. All patients received aspirin (500 mg i.v. followed by 100 mg/die per os) and clopidogrel (300 mg followed by 75 mg/die per os); 35 patients received also antiIIb/IIa inhibitors during PCI. Venous blood withdrawal was performed after the PCI (5–36 hrs). PFA-100 closure times by collagen-epinephrine (CT/EPI) (reference values: 90 ± 24.6 sec) and collagen-ADP (CT/ADP) (reference values: 146.3 ± 56.7 sec) were used for measuring platelet function. Polymorphism PlA1/A2 of GpIIb/IIIa, polymorphisms C807T and G873A of GpIa/IIa and polymorphism Thr715Pro of P-selectin were also studied. A control group of 101 healthy subjects, comparable for age and sex, who had not taken any antiplatelet agent for 15 days before blood sampling, was also investigated. CT/ADP and CT/EPI in patients were respectively 161.5 ± 100.5 sec and 257.7 ± 68.2 sec. 29/150 (19.3%) patients had CT/EPI under the 95^th percentile of control distribution (203 sec). CT/ADP and CT/EPI were inversely correlated with peak plasma levels of creatin kinase (CK), CK-MB, and TnT (CT/ADP: -0.39, P < 0.01; -0.35; P < 0.01 and -0.40, P < 0.01, respectively/CT/EPI: -0.35, P < 0.05; -0.36; P < 0.05 and -0.41, P < 0.05, respectively). The shorter the time needed for platelet plug formation, the greater the myocardial damage. Frequencies of A2 allele of PlA1/A2 polymorphism and of allele 807T of polymorphism C807T were significantly higher in patients than in controls (0.25 vs 0.18; P < 0.05 and 0.41 vs 0.32, P < 0.05). Genotype distributions of the polymorphisms investigated were not statistically different in relation to CT/ADP, CT/EPI or CK,CK-MB and TnT levels. This study demonstrated that CT/ADP and CT/EPI, measured after the administration of multiple antiplatelet agents, were predictive of the severity of myocardial infarction in patients with ACS undergoing PCI.