title: Late lumen loss after coronary angioplasty is associated with the activation status of circulating phagocytes before treatment.
abstract: BACKGROUND
  The purpose of this pilot study was to identify biological risk factors for restenosis after percutaneous transluminal coronary angioplasty (PTCA) to predict the long-term outcome of PTCA before treatment.
  
  
  RESULTS
  To investigate whether blood granulocytes and monocytes could determine luminal renarrowing after PTCA, several characteristics of these phagocytes were assessed before angioplasty in 32 patients who underwent PTCA of one coronary artery and who had repeat angiograms at 6-month follow-up. The plasma levels of interleukin (IL)-1 beta, tumor necrosis factor-alpha, IL-6, fibrinogen, C-reactive protein, and lipoprotein(a) before angioplasty were assessed as well. We found that the expression of the membrane antigens CD64, CD66, and CD67 by granulocytes was inversely associated with the luminal renarrowing normalized for vessel size (relative loss) at 6 months after PTCA, while the production of IL-1 beta by stimulated monocytes was positively associated with the relative loss. Next, these univariate predictors were corrected for the established clinical risk factors of dilation of the left anterior descending coronary artery and current smoking, which were statistically significant classic predictors in our patient group. Only the expression of CD67 did not predict late lumen loss independent of these established clinical risk factors. Multiple linear regression analysis showed that luminal renarrowing could be predicted reliably (R2 = .65; P < .0001) in this patient group on the basis of the vessel dilated and only two biological risk factors that reflect the activation status of blood phagocytes, ie, the expression of CD66 by granulocytes and the production of IL-1 beta by stimulated monocytes.
  
  
  CONCLUSIONS
  The results of the present study indicate that activated blood granulocytes prevent luminal renarrowing after PTCA, while activated blood monocytes promote late lumen loss. To validate this new finding, further study in an independent patient group is required.
authors.affiliation: Department of Biochemistry, Erasmus University Rotterdam, The Netherlands.
authors.forename: A
authors.initials: A
authors.lastname: Pietersma
authors.forename: M
authors.initials: M
authors.lastname: Kofflard
authors.forename: L E
authors.initials: LE
authors.lastname: de Wit
authors.forename: T
authors.initials: T
authors.lastname: Stijnen
authors.forename: J F
authors.initials: JF
authors.lastname: Koster
authors.forename: P W
authors.initials: PW
authors.lastname: Serruys
authors.forename: W
authors.initials: W
authors.lastname: Sluiter
mesh_terms: D000787:Angina Pectoris / Q000276:immunology / Q000628:therapy*; D015906:Angioplasty, Balloon, Coronary; D015703:Antigens, CD / Q000032:analysis*; D000943:Antigens, Differentiation / Q000032:analysis*; D015815:Cell Adhesion Molecules; D003327:Coronary Disease / Q000209:etiology* / Q000276:immunology; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism*; D016014:Linear Models; D008213:Lymphocyte Activation / Q000502:physiology; D008297:Male; D008875:Middle Aged; D010586:Phagocytes / Q000276:immunology* / Q000378:metabolism; D010865:Pilot Projects; D012008:Recurrence; D012307:Risk Factors; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015703:Antigens, CD; D000943:Antigens, Differentiation; C069847:CD66 antigens; D015815:Cell Adhesion Molecules; D007375:Interleukin-1