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

High heparin cofactor 11 (HC11) 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 HC11 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. HC11 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 HC11 activity (less than or equal to100%, lower tertile, n=20) was 84% and 35% as compared to 93% and 72% in patients with high HC11 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 HC11 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 11 may exert a protective effect against instent restenosis also in the femoro-popliteal vessel area, confirming a prior observation after coronary stenting.