Coronary stenting and inflammation.
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.
Gaspardone
Achille
A
Division of Cardiology and S. Eugenio Hospital, ASL Room C, piazzale dell'Umanesimo 10, 00144 Rome, Italy. a_gaspardone@yahoo.com
Versaci
Francesco
F
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D019917:Blood Vessel Prosthesis Implantation / Q000009:adverse effects; D023903:Coronary Restenosis / Q000188:drug therapy / Q000209:etiology*; D003331:Coronary Vessels / Q000503:physiopathology*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D015607:Stents / Q000009:adverse effects; D014657:Vasculitis / Q000150:complications* / Q000209:etiology
D000305:Adrenal Cortex Hormones; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D010975:Platelet Aggregation Inhibitors