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Updated: May 9, 2026

A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
Inflammatory mechanisms of adverse reactions to drug-eluting stents
Rocco A Montone1, Vito Sabato, Gregory A Sgueglia
1Institute of Cardiology, Catholic University of the Sacred Heart, Rome, Italy.
In-stent restenosis and stent thrombosis represent the main adverse reactions to coronary stents and individual susceptibility appears to play an important role in their onset. In particular, inflammatory status, classically assessed by C-reactive protein levels, predicts the risk of in-stent restenosis after bare-metal stent implantation but not after drug-eluting stent (DES) implantation. On the other hand, C-reactive protein seems to predict the risk of stent thrombosis after treatment with DES but not with bare-metal stent. If DES have considerably reduced, as compared to bare-metal stent, the rate of adverse reaction in the first year after implantation, concern is emerging about late events that seem to be related to delayed healing and allergic reactions to polymers, a process in which eosinophils play an important role by enhancing restenosis and thrombosis.
In-stent restenosis and stent thrombosis represent the main adverse reactions to coronary stents and individual susceptibility appears to play an important role in their onset. In particular, inflammatory status, classically assessed by C-reactive protein levels, predicts the risk of in-stent restenosis after bare-metal stent implantation but not after drug-eluting stent (DES) implantation. On the other hand, C-reactive protein seems to predict the risk of stent thrombosis after treatment with DES but not with bare-metal stent. If DES have considerably reduced, as compared to bare-metal stent, the rate of adverse reaction in the first year after implantation, concern is emerging about late events that seem to be related to delayed healing and allergic reactions to polymers, a process in which eosinophils play an important role by enhancing restenosis and thrombosis.
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