title: Time course of prothrombotic and proinflammatory substance release after intracoronary stent implantation.
abstract: We hypothesized that restenosis after coronary stenting is predicted by elevated levels of markers of thrombus formation and inflammation. Plasma levels of representative markers of inflammation, the thrombin and plasmin activation systems and adhesion molecules were measured in 59 patients with stable angina pectoris before, immediately after and 6 hours (h), 12 h, 24 h, one month and six months after elective stent implantation (radioactive phosphorus-32 stents/RSs/ n = 16, bare-metal stents/BMSs/ n = 43). All patients underwent clinical and angiographic follow-up (FUP) six months after stenting. RSs had significantly higher angiographic severity of restenosis than BMSs (47.1 +/- 20.1% vs. 27.6 +/- 22.0%, p = 0.003). Repeated measures ANOVA revealed significant differences between the BMS and RS groups as regards the increases in plasma levels of vascular cell adhesion molecule-1 (VCAM-1, p = 0.022), plasminogen activator inhibitor-1 (PAI-1, p = 0.047), tissue-type plasminogen activator (tPA, p = 0.047) and CD40 ligand (CD40L, p = 0.038). tPA levels tended to increase immediately after stenting in both groups, whereas the PAI-1 level one month after stenting was elevated significantly only in the RS group. In the RS group, the plasma levels of CD40L were increased at 24 h and six months after stenting, and the VCAM-1 level rose immediately after stenting and remained high during the FUP. Multivariate analysis on pooled laboratory data of both groups revealed elevated levels of VCAM-1 at 12 h and at six months as significant predictors of the severity of stent restenosis. In conclusion, the process of inflammation and thrombosis occurring after coronary interventions seems to be prolonged and enhanced in patients with high-grade restenosis at the follow up.
authors.affiliation: Department of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria. paul.wexberg@meduniwien.ac.at
authors.forename: Paul
authors.initials: P
authors.lastname: Wexberg
authors.forename: Nelli
authors.initials: N
authors.lastname: Jordanova
authors.forename: Christoph
authors.initials: C
authors.lastname: Strehblow
authors.forename: Bonni
authors.initials: B
authors.lastname: Syeda
authors.forename: Brigitte
authors.initials: B
authors.lastname: Meyer
authors.forename: Silvia
authors.initials: S
authors.lastname: Charvat
authors.forename: Gerlinde
authors.initials: G
authors.lastname: Zorn
authors.forename: Daniela
authors.initials: D
authors.lastname: Scheinig
authors.forename: Johann
authors.initials: J
authors.lastname: Wojta
authors.forename: Kurt
authors.initials: K
authors.lastname: Huber
authors.forename: Dietmar
authors.initials: D
authors.lastname: Glogar
authors.forename: Mariann
authors.initials: M
authors.lastname: Gyöngyösi
mesh_terms: D000368:Aged; D023201:CD40 Ligand / Q000097:blood; D018925:Chemokines / Q000097:blood; D019743:Chemokines, CXC; D023903:Coronary Restenosis / Q000097:blood / Q000209:etiology*; D023921:Coronary Stenosis / Q000628:therapy*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008875:Middle Aged; D010761:Phosphorus Radioisotopes / Q000627:therapeutic use; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011379:Prognosis; D011446:Prospective Studies; D015607:Stents / Q000009:adverse effects*; D013927:Thrombosis / Q000097:blood / Q000209:etiology; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000097:blood
chemical_list: C508524:CXCL17 protein, human; D018925:Chemokines; D019743:Chemokines, CXC; D018836:Inflammation Mediators; D010761:Phosphorus Radioisotopes; D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; D023201:CD40 Ligand; D010959:Tissue Plasminogen Activator