title: The effect of percutaneous coronary intervention on inflammatory response and endothelial progenitor cell recruitment.
abstract: BACKGROUND
  Vascular interventions, such as percutaneous coronary interventions (PCI), lead to endothelial damage and cause an inflammatory response. Endothelial progenitor cells (EPC) have been shown to have a prominent role in re-endothelialization and repair following vascular injury. Studies have implicated a role for the chemokine, stromal-cell-derived factor-1 alpha (SDF1-alpha) in the recruitment of circulating EPCs to sites of vascular injury. However, the relationship between the inflammatory response, SDF1-alpha, and EPC levels after PCI is unclear.
  
  
  METHODS
  We enrolled one hundred patients (mean age 65.5 +/- 10.9 years, 32% females)--20 patients with NSTEMI, 27 patients with unstable angina, and 53 patients with stable angina who underwent PCI with stenting. EPC levels were measured by quantifying colony forming units in the 20 NSTEMI patients, whereas SDF1-alpha levels and hs-CRP levels were measured in all 100 patients by enzyme-linked immunosorbent assay. All three markers were measured in blood samples drawn before and 24 hr after PCI.
  
  
  RESULTS
  EPC colonies increased from 9.6 colonies per million cells before PCI to 13.2 colonies per million cells after PCI (37% increase, P = 0.03). Circulating SDF1-alpha levels increased mildly from 1707.1 +/- 480 pg/mL at baseline to 1758.6 +/- 501 pg/mL after PCI (3% increase, P = 0.0425). There was a 95% increase in the levels of hs-CRP (pre-PCI: 4.5 +/- 5.3 mg/L vs. post-PCI: 8.8 +/- 9.5 mg/L; P = 0.0004).
  
  
  CONCLUSIONS
  A robust rise in hs-CRP levels in our study suggests that PCI induced a potent inflammatory response. This combined with a proportional increase in the levels of EPCs and mild elevation in SDF1-alpha after PCI suggests the possibility that the potent inflammatory response induced by PCI may be associated with EPC recruitment.
authors.affiliation: Division of Cardiology, University of Missouri, Columbia, Missouri 65202, USA. gargr@health.missouri.edu
authors.forename: Rajeev
authors.initials: R
authors.lastname: Garg
authors.forename: Armando
authors.initials: A
authors.lastname: Tellez
authors.forename: Carlos
authors.initials: C
authors.lastname: Alviar
authors.forename: Juan
authors.initials: J
authors.lastname: Granada
authors.forename: Neal S
authors.initials: NS
authors.lastname: Kleiman
authors.forename: Eli I
authors.initials: EI
authors.lastname: Lev
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D000789:Angina, Unstable / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D002097:C-Reactive Protein / Q000032:analysis; D002465:Cell Movement; D054377:Chemokine CXCL12 / Q000097:blood; D003114:Colony-Forming Units Assay; D042783:Endothelial Cells / Q000502:physiology*; D005260:Female; D006801:Humans; D007249:Inflammation; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D013234:Stem Cells / Q000502:physiology*; D015607:Stents
chemical_list: D054377:Chemokine CXCL12; D018836:Inflammation Mediators; D002097:C-Reactive Protein