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Thromb Haemost 2008; 99(04): 739-748
DOI: 10.1160/TH07-05-0365
Cardiovascular Biology and Cell Signalling
Schattauer GmbH

Time course of prothrombotic and proinflammatory substance release after intracoronary stent implantation

Paul Wexberg
1   Department of Cardiology, Medical University of Vienna, Vienna, Austria
,
Nelli Jordanova
2   Department of Cardiology and Emergency Medicine, Wilhelminen Hospital, Vienna, Austria
,
Christoph Strehblow
1   Department of Cardiology, Medical University of Vienna, Vienna, Austria
,
Bonni Syeda
1   Department of Cardiology, Medical University of Vienna, Vienna, Austria
,
Brigitte Meyer
1   Department of Cardiology, Medical University of Vienna, Vienna, Austria
,
Silvia Charvat
1   Department of Cardiology, Medical University of Vienna, Vienna, Austria
,
Gerlinde Zorn
1   Department of Cardiology, Medical University of Vienna, Vienna, Austria
,
Daniela Scheinig
1   Department of Cardiology, Medical University of Vienna, Vienna, Austria
,
Johann Wojta
1   Department of Cardiology, Medical University of Vienna, Vienna, Austria
,
Kurt Huber
2   Department of Cardiology and Emergency Medicine, Wilhelminen Hospital, Vienna, Austria
,
Dietmar Glogar
1   Department of Cardiology, Medical University of Vienna, Vienna, Austria
,
Mariann Gyöngyösi
1   Department of Cardiology, Medical University of Vienna, Vienna, Austria
› Author Affiliations
Further Information

Publication History

Received: 22 May 2007

Accepted after major revision: 28 January 2008

Publication Date:
25 November 2017 (online)

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Summary

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 highgrade restenosis at the follow up.

Keywords

Coronary artery disease - stent - restenosis - inflammation - thrombosis
 

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