Prevention of restenosis after stenting: the emerging role of inflammation

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.