title: Abciximab suppresses the rise in levels of circulating inflammatory markers after percutaneous coronary revascularization.
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, avbeta3, and alphaMbeta2 receptors, abciximab may reduce inflammatory processes. Methods and Results-- Assays for the inflammatory markers C-reactive protein, interleukin-6, and tumor necrosis factor-alpha 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 (P<0.001); and the rise in tumor necrosis factor-alpha levels was 100% less with abciximab therapy (P=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.
authors.affiliation: Department of Cardiology, The Cleveland Clinic Foundation, Cleveland, OH 44195, USA. lincofa@ccf.org
authors.forename: A M
authors.initials: AM
authors.lastname: Lincoff
authors.forename: D J
authors.initials: DJ
authors.lastname: Kereiakes
authors.forename: M A
authors.initials: MA
authors.lastname: Mascelli
authors.forename: L I
authors.initials: LI
authors.lastname: Deckelbaum
authors.forename: E S
authors.initials: ES
authors.lastname: Barnathan
authors.forename: K K
authors.initials: KK
authors.lastname: Patel
authors.forename: B
authors.initials: B
authors.lastname: Frederick
authors.forename: M T
authors.initials: MT
authors.lastname: Nakada
authors.forename: E J
authors.initials: EJ
authors.lastname: Topol
mesh_terms: D000077284:Abciximab; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects; D000911:Antibodies, Monoclonal / Q000008:administration & dosage*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D005260:Female; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000008:administration & dosage*; D007249:Inflammation / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D007262:Infusions, Intravenous; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014481:United States
chemical_list: D000911:Antibodies, Monoclonal; D015415:Biomarkers; D007140:Immunoglobulin Fab Fragments; D015850:Interleukin-6; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D000077284:Abciximab