Inflammation as a mechanism and therapeutic target for in-stent restenosis.
Restenosis following coronary stenting has long been attributed to neointimal proliferation, thrombosis, and negative remodeling. More recently, the important role of inflammation in vascular healing has also been increasingly well understood. From animal models and from clinical experience, we know that endothelial injury, platelet and leukocyte interactions, and subcellular chemoattractant and inflammatory mediators are pivotal in the development of the inflammatory response following stent implantation. By examining the specific mechanisms governing the inflammatory response to percutaneous coronary intervention, we may gain insight into potential therapeutic targets and strategies to prevent restenosis in clinical practice.
Drachman
Douglas E
DE
Division of Cardiology, Massachusetts General Hospital, Boston, MA 02114, USA. ddrachman@partners.org
Simon
Daniel I
DI
D015906:Angioplasty, Balloon, Coronary; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D023903:Coronary Restenosis / Q000209:etiology* / Q000517:prevention & control*; D004730:Endothelium, Vascular / Q000293:injuries; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007249:Inflammation / Q000150:complications* / Q000188:drug therapy*; D023421:Models, Animal; D015607:Stents / Q000009:adverse effects*
D000893:Anti-Inflammatory Agents; D007166:Immunosuppressive Agents