• The introduction of stents has greatly reduced the risk of restenosis of the index coronary lesion. However, in-stent restenosis remains an important problem, particularly within the first year.

• It is currently understood that loss of lumen follows a different natural history following stent placement than after balloon angioplasty.¹

• Balloon inflation results in endothelial denudation, with resultant exposure of the thrombogenic subendothelium, release of adhesion molecules, and formation of a monolayer of platelets. Stents can cause further focal vascular trauma, with deposition of platelets and fibrinogen and subsequent formation of platelet-rich thrombi over the stent struts.

• Under the influence of cytokines, leukocytes are recruited to the growing thrombi.

• Growth factors released from platelets, leukocytes, and smooth muscle cells accompany smooth muscle cell migration and proliferation.

• The resulting neointima consists of smooth muscle cells, extracellular matrix, and macrophages. With time, the proportion of extracellular matrix increases and the lumen narrows further, accompanied by re-endothelialization of at least part of the injured area.

¹ Welt FGP, Rogers C. Inflammation and restenosis in the stent era. Arterioscler Thromb Vasc Biol. 2002;22:1769-1776.