Intracoronary Abciximab administration during primary percutaneous coronary intervention (pPCI) could offer theoretical advantages over the intravenous route. Besides antiplatelet effects, Abciximab can modulate inflammation via cross-reactivity with GPIIb/IIIa, avb3, and aMb2 receptors. The aim of our study was to assess whether the Abciximab administration route could influence its anti-inflammatory effects.
Eighty-nine consecutive ST elevation myocardial infarction patient candidates for pPCI were randomized to intracoronary (Group A-47 patients) or intravenous (Group B-42 patients) Abciximab bolus administration. The primary endpoint was the extent of inflammation, measured by C-reactive protein (CRP), vascular cell adhesion molecule 1 (VCAM-1) and inter-cellular adhesion molecule 1 (ICAM-1) levels. This study is registered with ClinicalTrials.gov, NCT01757457.
Data are expressed in medians (interquartiles). In both groups, troponin levels were similar [baseline: 0.12 (0.03–0.94) vs. 0.27 (0.07–1.24) ng/ml, P = 0.73; postprocedural: 22.00 (14.75–69.43) vs. 31.96 (8.23–7.20) ng/ml, P = 0.83]. Both groups also showed similar baseline [0.31 (0.14–0.69) vs. 0.22 (0.09–0.59) mg/ml, P = 0.80] and postprocedural CRP levels [2.28 (1.37–4.23) vs. 2.16 (1.15–3.22) mg/dl, P = 0.69], similar baseline [272.5 (224.7–340.8) vs. 262.2 (221.2–306.4) ng/ml, P = 0.33] and postprocedural soluble ICAM-1 levels [281.5 (244.6–337.4) vs. 287.2 (226.9–359.2) ng/ml P = 0.71], and similar baseline [771.6 (620.9–971.0) vs. 748.6 (592.2–838.8) ng/ml, P = 0.30] and postprocedural soluble VCAM-1 levels [785.2 (671.6–947.1) vs. 745.9 (641.1–841.9) ng/ml, P = 0.17]. In-hospital and 6-month event rates were similar in the two groups.
Our study suggests that Abciximab has similar anti-inflammatory effects irrespective of the administration route. It is unlikely that the potential clinical benefits of intracoronary Abciximab can be related to modulation of integrin receptors.
aDepartment of Clinical and Experimental Medicine, University of Eastern Piedmont, Novara
bDivision of Interventional Cardiology, ‘Ospedali Riuniti Marche Nord’, Pesaro
dClinical Chemistry, ‘Maggiore della Carità’ Hospital, Novara, Italy
eDepartment of Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands
fBiomedical Research Unit, Royal Brompton & Harefield NHS Foundation Trust, London, UK
Correspondence to Gioel Gabrio Secco, Department of Clinical and Experimental Medicine, University of Eastern Piedmont, Corso Mazzini 18, 28100 Novara, Italy Tel: +39 3934333440; fax: +39 0721362292; e-mail: firstname.lastname@example.org
Received 15 October, 2013
Revised 29 March, 2014
Accepted 31 March, 2014