title: Coronary collaterals remain recruitable after percutaneous intervention.
abstract: BACKGROUND
  Rapid loss of collateral support has been reported after percutaneous coronary intervention (PCI), leaving the myocardium susceptible to subsequent infarction. However, well-developed collaterals have been found in normal hearts, suggesting that collaterals exist even in the absence of an ischemic stimulus. We assessed the plasticity and determinants of collateral supply after PCI.
  
  
  RESULTS
  Collateral flow index (CFI) was calculated in 60 patients as (P(w)-P(v))/(P(a)-P(v)) by measurement of aortic (P(a)), central venous (P(v)), and coronary wedge (P(w)) pressures. CFI was reassessed during transient balloon occlusion 5 minutes and 24 hours after PCI in the first 29 patients and at 6 months in the subsequent 25 patients. We also evaluated the relationship between collateral supply, lesion characteristics, and circulating hemopoietic cells numbers before and after successful PCI. CFI at baseline was 0.23+/-0.10, with no change 5 minutes and 1 day later (0.21+/-0.12, P=0.62; and 0.22+/-0.11, P=0.96, respectively). At 6 months, CFI was 0.14+/-0.07 or 63+/-27% of the baseline value (P<0.001). CFI was proportional to severity of the coronary lesion at baseline (r=0.63, P<0.0001) but not 6 months after PCI (r=-0.04, P=0.87). The number of circulating CD133+ and CD34+ cells was associated with CFI 6 months after PCI (CD133, r=0.59, P=0.035; CD34, r=0.63, P=0.037).
  
  
  CONCLUSIONS
  Coronary collateral flow remains undiminished for at least 24 hours after successful PCI. Functional collateral support subsequently declines but does not regress completely.
authors.affiliation: Cardiovascular Division, Rayne Institute, St Thomas' Hospital Campus, King's College, London, UK.
authors.forename: Divaka
authors.initials: D
authors.lastname: Perera
authors.forename: Gajen S
authors.initials: GS
authors.lastname: Kanaganayagam
authors.forename: Mrinal
authors.initials: M
authors.lastname: Saha
authors.forename: Rizwan
authors.initials: R
authors.lastname: Rashid
authors.forename: Michael S
authors.initials: MS
authors.lastname: Marber
authors.forename: Simon R
authors.initials: SR
authors.lastname: Redwood
mesh_terms: D000071916:AC133 Antigen; D015906:Angioplasty, Balloon, Coronary; D015703:Antigens, CD / Q000096:biosynthesis; D018952:Antigens, CD34 / Q000096:biosynthesis; D001783:Blood Flow Velocity; D001794:Blood Pressure; D003097:Collateral Circulation; D003326:Coronary Circulation; D003327:Coronary Disease / Q000628:therapy*; D005260:Female; D005434:Flow Cytometry; D006023:Glycoproteins / Q000096:biosynthesis; D006412:Hematopoietic Stem Cells / Q000276:immunology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010455:Peptides; D011446:Prospective Studies
chemical_list: D000071916:AC133 Antigen; D015703:Antigens, CD; D018952:Antigens, CD34; D006023:Glycoproteins; C000606023:PROM1 protein, human; D010455:Peptides