Intracoronary abciximab and local anti-inflammatory effects

Abstract

To the Editor:We have read with great interest the article by De Rosa et al., in re-lation to a meta-analysis of clinical trials on the use of intracoronaryabciximab [1]. In our opinion, the author's state in the discussiononly one possible potential mechanism by which the intracoronaryabciximab obtains better results compared to intravenously, a higherdegree of GP IIb/IIIa receptor occupancy and a more pronounced plate-let inhibition. We would like to point out another possible mechanismthat can account for the potential clinical benefits observed in pa-tients receiving intracoronary abciximab, the local anti-inflammatoryproperties.Platelets are a central cellular component in both thrombotic andinflammatory processes characteristic of coronary atherosclerosis.Platelets modulate inflammatory processes by binding to and alteringleukocyte function [2]. In addition to forming circulating aggregateswith leukocytes, platelets regulate inflammation by secreting a va-riety of inflammatory modulators, including CD40 ligand (CD40L).CD40L is an essential component in the pathophysiology of athero-sclerosis and platelets are the predominant source of circulating solu-ble CD40L (sCD40L) [3].Glycoprotein IIb/IIIa antagonists (abciximab, eptifibatide, tirofiban)have been reported to inhibit the release of sCD40L and plateletaggregation initially in vitro and, afterward, in clinical studies [4].Morespecifically, abciximab reduced circulating sCD40L and leukocyte–platelet aggregation in patients with acute coronary syndrome under-going percutaneous coronary intervention [5]. Moreover, in patientswith ST-elevation myocardial infarction undergoing primary percuta-neous coronary intervention, results from our group have shown thatintracoronary bolus administration of abciximab was associated withalargerdecreaseinsCD40Llevelscomparedwithstandardintravenousbolus [6]. Therefore, we believe that the rationale of intracoronaryabciximab use is based not only on its dose-dependent antiplatelet,antithromboticeffectbutalsoonitslocalanti-inflammatoryproperties.AcknowledgmentsThe authors of this manuscript have certified that they complywith the Principles of Ethical Publishing in the International Journalof Cardiology.References