The pathophysiology of restenosis involves early elements of direct injury to smooth muscle
cells, deendothelialization, and thrombus deposition. Over time, this leads to smooth muscle …

Restenosis following coronary stenting has long been attributed to neointimal proliferation,
thrombosis, and negative remodeling. More recently, the important role of inflammation in …

Inflammatory response is triggered when tissues are ex-posed to a variety of insults. This
response consists of a cascade of events that includes release of various chemical …

The cellular and molecular processes that control vascular injury responses after
percutaneous coronary intervention involve a complex interplay among vascular cells and …

Next is a granulation or cellular proliferation phase. Growth factors are subsequently
released from platelets, leukocytes, and SMCs, which stimulate migration of SMCs from the …

Inflammation plays a critical role in the vascular response to injury. In particular, mechanical
injury using techniques such as balloon angioplasty and stenting results in complex …

Restenosis after stent implantation is mainly caused by neointimal proliferation through the
stent struts. Experimental studies performed in the last decade indicate that inflammatory …

Restenosis after endovascular treatment of atherosclerotic lesions in the peripheral,
cerebrovascular, and coronary circulation is the major drawback of this minimally invasive …

Four principal processes—vasculogenesis, angiogenesis, arteriogenesis, and collateral
growth—characterize tissue repair and remodelling in acute and chronic ischaemic vascular …

Angioplasty causes substantial injury to the coronary artery intima and media that is
unrecognizable by angiography. On the basis of a substantial body of research in oncology …