Abciximab Suppresses the Rise in Levels of Circulating Inflammatory Markers After Percutaneous Coronary Revascularization
- 10 July 2001
- journal article
- clinical trial
- Published by Wolters Kluwer Health in Circulation
- Vol. 104 (2) , 163-167
- https://doi.org/10.1161/01.cir.104.2.163
Abstract
Background— Previous investigators have shown that systemic markers of inflammation may be increased in patients with acute ischemic syndromes or after percutaneous coronary revascularization and that persistent elevation in these markers is predictive of excess risk of subsequent adverse cardiac events. By virtue of its cross-reactivity with the glycoprotein IIb/IIIa, avβ3, and αMβ2 receptors, abciximab may reduce inflammatory processes. Methods and Results— Assays for the inflammatory markers C-reactive protein, interleukin-6, and tumor necrosis factor-α were performed on serum samples obtained from 160 patients in a placebo-controlled, randomized trial of abciximab during angioplasty. Eighty patients each had received a placebo or abciximab bolus plus a 12-hour infusion. Serum samples were drawn at baseline (before revascularization), 24 to 48 hours after study drug administration, and 4 weeks after study drug administration. Between baseline and 24 to 48 hours, the increase in C-reactive protein was 32% less in patients receiving abciximab than placebo (P=0.025); the rise in interleukin-6 levels was 76% less in the abciximab group (PP=0.112). By 4 weeks, most marker levels had returned to baseline, with no significant differences between placebo and abciximab groups. Conclusions— Systemic markers of inflammation increase in the first 24 to 48 hours after angioplasty, but the magnitude of that rise is diminished by periprocedural abciximab. Some of the long-term clinical benefit derived from this agent may be related to an anti-inflammatory effect.Keywords
This publication has 27 references indexed in Scilit:
- Plasma levels of C-reactive protein after coronary stent implantationEuropean Heart Journal, 2000
- Atherosclerosis — An Inflammatory DiseaseNew England Journal of Medicine, 1999
- Predictive value of C-reactive protein after successful coronary-artery stenting in patients with stable anginaThe American Journal of Cardiology, 1998
- Neutrophil accumulation on activated, surface-adherent platelets in flow is mediated by interaction of Mac-1 with fibrinogen bound to alphaIIbbeta3 and stimulated by platelet-activating factor.Journal of Clinical Investigation, 1997
- Evidence for Prevention of Death and Myocardial Infarction With Platelet Membrane Glycoprotein IIb/IIIa Receptor Blockade by Abciximab (c7E3 Fab) Among Patients With Unstable Angina Undergoing Percutaneous Coronary RevascularizationJournal of the American College of Cardiology, 1997
- 7E3 Monoclonal Antibody Directed Against the Platelet Glycoprotein IIb/IIIa Cross-reacts With the Leukocyte Integrin Mac-1 and Blocks Adhesion to Fibrinogen and ICAM-1Arteriosclerosis, Thrombosis, and Vascular Biology, 1997
- Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques.Journal of Clinical Investigation, 1994
- Fibrinogen mediates leukocyte adhesion to vascular endothelium through an ICAM-1-dependent pathwayCell, 1993
- The I domain is a major recognition site on the leukocyte integrin Mac-1 (CD11b/CD18) for four distinct adhesion ligands.The Journal of cell biology, 1993
- Leukocyte adhesion to endothelium in inflammationCell, 1990