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(Circulation. 2001;103:2328.)
© 2001 American Heart Association, Inc.
Brief Rapid Communications |
Effects of Abciximab on the Architecture of Platelet-Rich Clots in Patients With Acute Myocardial Infarction Undergoing Primary Coronary Intervention
Presented in part at the 49th Congress of the American College of Cardiology, Atlanta, Ga, March 7–10, 1999, and published in abstract form (J Am Coll Cardiol. 1999;33:1220).
From the Department of Cardiology (J.P.C., G.M., R.C., G.D., D.T.) and the Hematology Laboratory (C.L.), Pitié-Salpêtrière Hospital, Paris; Unité Propre de Service 937 (Z.M., J.S., C.S.), Centre National de Recherche Scientifique, Paul Brousse Hospital, Villejuif; Eli Lilly Company (P.P.), Saint-Cloud; and Clinique Beauregard (P.B.), Marseille, France.
Correspondence to G. Montalescot, MD, PhD, Department of Cardiology, Centre Hospitalier Universitaire Pitié-Salpêtrière, 47 boulevard de l’Hôpital, 75013 Paris, France. E-mail gilles.montalescot{at}psl.ap-hop-paris.fr
Background—Abciximab plus aspirin improves the TIMI 3 flow rate of the infarct-related artery in patients treated with either percutaneous coronary intervention or thrombolysis. The present study investigated whether the reperfusion efficacy of abciximab relates to modifications of clot architecture in patients admitted for acute myocardial infarction (AMI).
Methods and Results—A total of 23 AMI patients in the Abciximab before Direct angioplasty and stenting in Myocardial Infarction Regarding Acute and Long term follow-up (ADMIRAL) trial received, in a double-blind fashion, either abciximab (n=13) or placebo (n=10) before primary stenting. Viscoelastic (G' in dyne/cm2) and morphological (mean platelet aggregate surface area [SAG] in µm2) indexes of ex vivo platelet-rich clots (PRC) were assessed in a double-blind fashion before and after the bolus administration of abciximab or placebo. G' and SAG reflect the mechanical and morphological impact of activated platelets on the PRC fibrin network, respectively. Abciximab administration reduced G' by 63% (P=0.0001) and SAG by 65% (P=0.0007), and no effect was seen in the placebo group. These abciximab-related changes increased fibrin exposure as a consequence of the platelet-aggregate surface reduction and may have improved endogenous fibrinolysis. These effects were identified in all patients, independent of previous heparin administration.
Conclusions—Abciximab dramatically reduces platelet aggregate size and increases the fibrin accessibility of ex vivo PRC in AMI patients. These modifications could participate in the better coronary artery patency observed with abciximab.
Key Words: myocardial infarction • fibrin • platelets • abciximab • thrombosis
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