chapter  43
Vascular endothelial growth factor (VEGF) eluting stents Neil Swanson and Anthony Gershlick
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At angioplasty or stent implantation, significant damage is unavoidably done to the endothelial lining of the vessel. It is thought that the loss of the protective endothelial lining of the artery is one of the key stimuli to the smooth muscle cell proliferation that is the hallmark of the restenotic lesion. This is probably due to the loss of the endothelial cell products, such as nitric oxide (NO) and prostacycline, which normally inhibit smooth muscle cell growth. An intact endothelium also acts as a physical barrier to platelets that will otherwise adhere to the subendothelial layers of the vessel wall. As well as potentially causing vessel thrombosis, these platelets produce factors that stimulate smooth muscle cells, leading to restenosis. For a delayed period, endothelial function around a stent is impaired compared to the recovery seen after angioplasty alone.1 The lack of endothelial recovery is exacerbated in patients receiving vascular brachytherapy,2 and this may be the cause of the ‘late thrombosis’ seen in up to 11% of these patients.3