Coronary artery in-stent stenosis persists despite inhibition of the von Willebrand factor--collagen interaction in baboons - PubMed
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Georg Thieme Verlag Stuttgart, New York
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Thromb Haemost
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. 2007 Dec;98(6):1343-9.
doi: 10.1160/th07-05-0335.
Coronary artery in-stent stenosis persists despite inhibition of the von Willebrand factor--collagen interaction in baboons
Simon F De Meyer 
1
, Stephanie Staelens, Philip N Badenhorst, Henry Pieters, Seb Lamprecht, Jan Roodt, Stefan Janssens, Muriel Meiring, Karen Vanhoorelbeke, André Bruwer, Stephen Brown, Hans Deckmyn
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1 Laboratory for Thrombosis Research, I.R.C., KULeuven Campus Kortrijk, E. Sabbelaan 53, 8500 Kortrijk, Belgium.
PMID:
18064334
DOI:
10.1160/th07-05-0335
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Coronary artery in-stent stenosis persists despite inhibition of the von Willebrand factor--collagen interaction in baboons
Simon F De Meyer et al.
Thromb Haemost.
2007 Dec.
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. 2007 Dec;98(6):1343-9.
doi: 10.1160/th07-05-0335.
Authors
Simon F De Meyer 
1
, Stephanie Staelens, Philip N Badenhorst, Henry Pieters, Seb Lamprecht, Jan Roodt, Stefan Janssens, Muriel Meiring, Karen Vanhoorelbeke, André Bruwer, Stephen Brown, Hans Deckmyn
Affiliation
1 Laboratory for Thrombosis Research, I.R.C., KULeuven Campus Kortrijk, E. Sabbelaan 53, 8500 Kortrijk, Belgium.
PMID:
18064334
DOI:
10.1160/th07-05-0335
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Revascularization techniques, such as angioplasty and stent implantation, frequently lead to restenosis due to the formation of neointima after platelet activation and the concomitant release of various smooth muscle cell mitogenic and attractant factors. We here investigate whether inhibition of initial platelet adhesion after stent implantation can decrease neointima formation in a clinically relevant baboon model of in-stent stenosis using standard treatment with aspirin, clopidogrel and heparin. Inhibition of platelet adhesion was established by administration of the anti-von Willebrand factor (VWF) monoclonal antibody 82D6A3, which inhibits VWF binding to collagen. Administration of 82D6A3 resulted in a complete inhibition of VWF binding to collagen during the first three days after stent implantation. No thrombocytopenia or prolongation of the bleeding time was observed. Our results show that the formation of neointima was not affected in the group of baboons where primary platelet adhesion was abolished with 82D6A3 when compared to the control group. Vascular injury scores were the same in both groups. Inhibition of platelet adhesion during the first three days after stenting, on top of standard treatment with aspirin, clopidogrel and heparin, had no effect on neo-intima formation in a baboon model of in-stent stenosis. During the last decade, attempts to translate seemingly effective therapies based on smaller animal experimentation to the clinic have consistently failed. This study, using a non-human primate model that more closely resembles the clinical situation, presents a model that may be of further clinical interest for studying the prevention of restenosis.
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