Thromb Haemost 2004; 92(05): 1108-1113
DOI: 10.1160/TH04-05-0311
Cell Signalling and Vessel Remodelling
Schattauer GmbH

High plasma heparin cofactor II activity protects from restenosis after femoropopliteal stenting

Martin Schillinger
1   Departments of Angiology and Medical and Chemical Laboratory Diagnostics, Medical University Vienna
,
Markus Exner
1   Departments of Angiology and Medical and Chemical Laboratory Diagnostics, Medical University Vienna
,
Schila Sabet
1   Departments of Angiology and Medical and Chemical Laboratory Diagnostics, Medical University Vienna
,
Wolfgang Mlekusch
1   Departments of Angiology and Medical and Chemical Laboratory Diagnostics, Medical University Vienna
,
Jasmin Amighi
1   Departments of Angiology and Medical and Chemical Laboratory Diagnostics, Medical University Vienna
,
Sylvia Handler
1   Departments of Angiology and Medical and Chemical Laboratory Diagnostics, Medical University Vienna
,
Peter Quehenberger
1   Departments of Angiology and Medical and Chemical Laboratory Diagnostics, Medical University Vienna
,
Neda Kalifeh
1   Departments of Angiology and Medical and Chemical Laboratory Diagnostics, Medical University Vienna
,
Oswald Wagner
1   Departments of Angiology and Medical and Chemical Laboratory Diagnostics, Medical University Vienna
,
Erich Minar
1   Departments of Angiology and Medical and Chemical Laboratory Diagnostics, Medical University Vienna
› Author Affiliations
Further Information

Publication History

Received 17 May 2004

Accepted after revision 08 August 2004

Publication Date:
04 December 2017 (online)

Summary

High heparin cofactor II (HCII) activity has recently been described to protect from coronary instent restenosis, presumably by inactivating thrombin in injured arteries. In this study, we investigated the association of HCII activity and restenosis after femoropopliteal stenting. We studied 63 consecutive patients with peripheral artery disease who underwent femoropopliteal stent implantation after initial failure of plain balloon angioplasty due to a significant residual stenosis (>30% lumen diameter reduction) or a flow limiting dissection. HCII activity was measured before stenting and patients were followed for median 10 months (interquartile range 6 to 17) for the occurrence of a first instent restenosis, defined as a >50% lumen diameter reduction by color coded duplex sonography and confirmed by angiography. Cumulative freedom from restenosis at 6 and 12 months in patients with lower HCII activity (≤100%, lower tertile, n=20) was 84% and 35% as compared to 93% and 72% in patients with high HCII activity (>100%, middle and upper tertile, n=43; p=0.024 by Log Rank test). Adjusting for the material of the implanted stents (nitinol vs.Wallstents), patients with a high HCII activity had a 0.39-fold reduced risk for instent restenosis (95% CI 0.17 to 0.90, p=0.028), additional adjustment for diabetes mellitus, poor run-off, critical limb ischemia and cumulative length of the stented segment did not alter the observed effect. Higher activity of heparin cofactor II may exert a protective effect against instent restenosis also in the femoropopliteal vessel area, confirming a prior observation after coronary stenting.

 
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