title: Systemic inflammation after drug-eluting stent placement.
abstract: BACKGROUND
  Systemic inflammation after coronary intervention identifies patients at increased risk of subsequent cardiac events. Cardiac events are less frequent after use of drug eluting stents (DES) compared with bare metal stents (BMS). Thus, we sought to determine whether attenuation of the systemic inflammatory response was contributing to the improved outcomes.
  
  
  METHODS
  A prospective registry was initiated in late 2003. Peripheral venous blood samples from 75 patients undergoing percutaneous coronary intervention (PCI) were obtained before PCI, and both 1 hour and 24 hours after stenting. The concentrations of C-reactive protein (CRP), interleukin-6 (IL-6) and interleukin-1 receptor antagonist (IL1-Ra) were determined by ELISA. Eleven patients were excluded from the analysis because they had both DES and BMS.
  
  
  RESULTS
  Patients treated with BMS (n=29) compared with DES (n=34) had a higher incidence of marker-positive acute coronary syndromes (40% vs. 17%, p=0.06), vein graft PCI (p=0.02) and a larger final balloon diameter (p=0.04). Consistent with the lower baseline clinical risk, pre-PCI concentrations of cytokines were lower in the DES group (p=0.04 for IL-6 and p=0.08 for CRP). Comparable and significant increases in CRP, IL-6 and IL1-Ra were evident 24 hours after PCI in patients treated with either DES or BMS. After controlling for baseline levels of CRP, there remained a similar and robust (300%) relative increase in CRP for both DES and BMS patients.
  
  
  CONCLUSIONS
  The inflammatory response to PCI appears similar in those treated with DES and BMS. Accordingly, the reduction in restenosis after DES is likely not mediated by attenuation of the systemic markers CRP, IL-1Ra, or IL-6.
authors.affiliation: Division of Cardiology, University of Vermont College of Medicine, 111 Colchester Avenue, Burlington, Vermont 05401, USA.
authors.forename: Prospero B
authors.initials: PB
authors.lastname: Gogo
authors.forename: David J
authors.initials: DJ
authors.lastname: Schneider
authors.forename: Matthew W
authors.initials: MW
authors.lastname: Watkins
authors.forename: Edward F
authors.initials: EF
authors.lastname: Terrien
authors.forename: Burton E
authors.initials: BE
authors.lastname: Sobel
authors.forename: Harold L
authors.initials: HL
authors.lastname: Dauerman
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D020099:Coated Materials, Biocompatible; D005260:Female; D006083:Graft Occlusion, Vascular; D006801:Humans; D007249:Inflammation / Q000175:diagnosis / Q000209:etiology*; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D004364:Pharmaceutical Preparations / Q000008:administration & dosage*; D011446:Prospective Studies; D012795:Sialoglycoproteins / Q000097:blood; D015607:Stents / Q000009:adverse effects*; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D020099:Coated Materials, Biocompatible; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6; D004364:Pharmaceutical Preparations; D012795:Sialoglycoproteins; D002097:C-Reactive Protein