Prevention of restenosis after stenting: the emerging role of inflammation.
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.
Versaci
Francesco
F
Cattedra di Cardiochirurgia, Università di Roma Tor Vergata, Rome; Divisione di Cardiologia, Ospedale S. Eugenio, Rome, Italy. francescoversaci@yahoo.it
Gaspardone
Achille
A
D000209:Acute-Phase Proteins / Q000032:analysis; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D023903:Coronary Restenosis / Q000097:blood / Q000209:etiology* / Q000276:immunology / Q000517:prevention & control*; D016207:Cytokines / Q000097:blood; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000276:immunology; D015607:Stents / Q000009:adverse effects*; D017539:Tunica Intima / Q000276:immunology; D014652:Vascular Diseases / Q000150:complications / Q000276:immunology
D000209:Acute-Phase Proteins; D000893:Anti-Inflammatory Agents; D016207:Cytokines