Coronary stenting and inflammation

Abstract

Restenosis after stent implantation is mainly caused by neointimal proliferation through the stent struts. Experimental studies performed in the last decade indicate that inflammatory mechanisms play a key role in the process of neointimal proliferation and restenosis. Coronary stenting is a strong inflammatory stimulus, and the acute local and systemic inflammatory responses to local inflammation produced by coronary stenting are highly individual and predictive of restenosis and event-free survival. The benefit of anti-inflammatory periprocedural therapy, such as with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) and steroids, and long-term follow-up is dependent on the individual's inflammatory status. Measurement of acute-phase reactants, such as C-reactive protein plasma concentration, appears to be important for the identification of subjects at high risk and the development of specific treatment tailored to individual patients.