title: Impaired fibrinolysis determines the outcome of percutaneus transluminal coronary angioplasty (PTCA).
abstract: BACKGROUND
  Coronary artery stenosis lesions dilated by percutaneus transluminal coronary angioplasty (PTCA) show a disappointingly frequent recurrence of stenosis. We have investigated the possible role of fibrinolysis and various platelet-release factors - specifically in the locality of the affected vessel - by following 19 patients for 6 months after PTCA.
  
  
  METHODS
  PTCA was performed on 19 patients with a significant primary coronary stenosis, proven by quantitative CAAS analysis. Blood for measurement of local fibrinolysis and platelet activity was drawn from the aortic root and the coronary sinus, at three times: just before PTCA, 10 min after it, and 6 months later.
  
  
  RESULTS
  The incidence of restenosis at the 6 months follow-up was 37%. PTCA almost doubled the platelet-derived growth factor level (PDGF) in coronary sinus blood in all patients. The seven restenosis patients had a substantially higher tissue plasminogen activator inhibitor antigen (PAI-1ag) level in the aortic root before PTCA than the 12 who remained stenosis-free (mean 62.4 +/- 31.6 ng mL -1 compared with 33.1 + 25.3; P < 0.04) and a lower tissue plasminogen activator activity (t-PAac) level (mean 0.32 +/- 0.19 IU mL-1 compared with 0.68 +/- 0.34; P < 0.03). This was corroborated by the levels of tissue plasminogen activator inhibitor activity (PAI-1ac). At reassessment after 6 months, the restenosis patients had developed, in coronary sinus blood, a large rise of PAI-1ac (7.7 +/- 4.8 IU mL-1 rising to 15.7 +/- 13.9, P < 0.04) and a large rise of of PAI-1ag (48.8 +/- 31.3 ng mL-1 vs. 72.4 +/- 47.2; P < 0.03). But no such increase occurred in the patients who remained stenosis-free. Conclusion Our results indicate that the minor balloon injury, which is inseparable from PCTA, stimulates the local release of PDGF. We suggest that, in those patients whose fibrinolytic activity is inherently low, this rise of PDGF could be a major causative factor in restenosis. We also discuss the possibility that the preoperative level of PAI-1ac could provide a limited but useful prediction of the outcome of PTCA.
authors.affiliation: Gentofte Hospital, Copenhagen, Denmark.
authors.forename: G G
authors.initials: GG
authors.lastname: Fornitz
authors.forename: P
authors.initials: P
authors.lastname: Nielsen
authors.forename: O
authors.initials: O
authors.lastname: Amtorp
authors.forename: E
authors.initials: E
authors.lastname: Kassis
authors.forename: U
authors.initials: U
authors.lastname: Abildgård
authors.forename: C
authors.initials: C
authors.lastname: Sloth
authors.forename: K
authors.initials: K
authors.lastname: Winther
authors.forename: H
authors.initials: H
authors.lastname: Ørskov
authors.forename: J
authors.initials: J
authors.lastname: Dalsgård
authors.forename: S
authors.initials: S
authors.lastname: Husted
mesh_terms: D015906:Angioplasty, Balloon, Coronary; D000075202:Contraindications; D003327:Coronary Disease / Q000601:surgery*; D005342:Fibrinolysis; D005500:Follow-Up Studies; D006801:Humans; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D010982:Platelet-Derived Growth Factor / Q000032:analysis; D012307:Risk Factors; D010959:Tissue Plasminogen Activator / Q000097:blood; D001620:beta-Thromboglobulin / Q000032:analysis
chemical_list: D017395:Plasminogen Activator Inhibitor 1; D010982:Platelet-Derived Growth Factor; D001620:beta-Thromboglobulin; D010959:Tissue Plasminogen Activator