Restenosis after stent implantation is mainly caused by neointimal proliferation through the stent struts. Experimental studies indicate a marked activation of inflammatory cells at the site of stent struts, which are likely to play a key role in the process of neointimal proliferation and restenosis. Coronary stenting is a strong inflammatory stimulus and the acute systemic inflammatory response to local inflammation produced by coronary stenting is highly individual and predicts restenosis and event-free survival. The benefit of anti-inflammatory therapy during the periprocedural period and long-term follow-up is dependent on the inflammatory status. Measurement of cytokine and acute phase proteins, such as C-reactive protein, may be important to identify high-risk subjects and develop specific treatment tailored to the individual patient. (C) 2004 Lippincott Williams Wilkins.
Versaci, F., Gaspardone, A. (2004). Prevention of restenosis after stenting: the emerging role of inflammation. CORONARY ARTERY DISEASE, 15(6), 307-311 [10.1097/00019501-200409000-00002].
Prevention of restenosis after stenting: the emerging role of inflammation
Versaci, Francesco
Writing – Review & Editing
;Gaspardone, AchilleMembro del Collaboration Group
2004-09-01
Abstract
Restenosis after stent implantation is mainly caused by neointimal proliferation through the stent struts. Experimental studies indicate a marked activation of inflammatory cells at the site of stent struts, which are likely to play a key role in the process of neointimal proliferation and restenosis. Coronary stenting is a strong inflammatory stimulus and the acute systemic inflammatory response to local inflammation produced by coronary stenting is highly individual and predicts restenosis and event-free survival. The benefit of anti-inflammatory therapy during the periprocedural period and long-term follow-up is dependent on the inflammatory status. Measurement of cytokine and acute phase proteins, such as C-reactive protein, may be important to identify high-risk subjects and develop specific treatment tailored to the individual patient. (C) 2004 Lippincott Williams Wilkins.File | Dimensione | Formato | |
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