title: Changes of plasma activated Factor XII type A (XIIaA) concentrations following percutaneous coronary intervention (PCI).
abstract: BACKGROUND
  Recent research has demonstrated that in-vivo XIIa exists in a number of different types and that treatment with tenecteplase increases the plasma concentration of XIIaA. Only limited data exist on changes in activated Factor XII (XIIa) levels following mechanical revascularisation, such as percutaneous coronary intervention (PCI).
  
  
  METHODS
  Citrated blood samples were obtained from 31 PCI-treated patients admitted with ST-elevation myocardial infarction (STEMI) and 20 patients undergoing elective PCI. Samples were taken immediately before the invasive procedure, 30-90 min after PCI and (in patients undergoing primary PCI) 4-6 days following intervention. Additional samples were taken after angiography, just prior to the follow-on PCI procedure, in 16 of the patients undergoing elective PCI, to investigate possible effects of contrast fluid and heparin. XIIa measurements were performed using 2 ELISA assays designed to preferentially measure different types of XIIa; XIIaA and XIIaR.
  
  
  RESULTS
  In the group undergoing primary PCI, XIIaA showed a significant increase from 68 (48-93) pM in the pre-treatment sample to 100 (75-123) pM [median and 25- and 75% percentiles] in the 30-90-min post-treatment sample (p < 0.001), returning to pre-intervention levels by day 4-6. A similar increase in XIIaA was obtained in patients undergoing elective PCI. In contrast, no significant changes in XIIaR concentration were observed. Whilst XIIaA concentrations remained unchanged in 6 non-heparinised patients undergoing elective coronary angiography, XIIaA levels rose significantly from 56 (51-75) pM to 98 (71-125) pM [median and 25- and 75% percentiles], (p < 0.01) in 10 patients after the addition of heparin.
  
  
  CONCLUSIONS
  A significant short-lasting increase in specific types of XIIa (namely XIIaA) was observed following PCI. These increases are most likely induced by the concomitant treatment with heparin.
authors.affiliation: Department of Medicine, Stavanger University Hospital, POB 8100, 4068 Stavanger, Norway. volker.poenitz@lyse.net
authors.forename: Volker
authors.initials: V
authors.lastname: Pönitz
authors.forename: David
authors.initials: D
authors.lastname: Pritchard
authors.forename: Heidi
authors.initials: H
authors.lastname: Grundt
authors.forename: Mai-Britt
authors.initials: MB
authors.lastname: Mehus
authors.forename: Dennis Winston T
authors.initials: DW
authors.lastname: Nilsen
mesh_terms: D015906:Angioplasty, Balloon, Coronary; D003287:Contrast Media / Q000494:pharmacology; D017023:Coronary Angiography; D004797:Enzyme-Linked Immunosorbent Assay; D005174:Factor XII / Q000032:analysis* / Q000187:drug effects; D006493:Heparin / Q000494:pharmacology; D006801:Humans; D009203:Myocardial Infarction / Q000628:therapy; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D003287:Contrast Media; D005174:Factor XII; D006493:Heparin