Most acute and subacute stent failures are secondary to platelet aggregation and as such, post procedure heparinization is not necessary. Assuming the stent remains patent for the initial 30 days following implantation, we must consider the risks of delayed stenosis. There is inadequate literature concerning intracranial stent patency simply because of the paucity of cases. In the cardiology literature, intimal hyperplasia has been shown to be the major component of late lumen loss after stent implantation. Risk factors for restenosis include stent implantation at a site that stenosed following a previous angioplasty, use of multiple stents regardless of whether or not they overlap, extent of residual stenosis following initial stenting, stent placement in a totally occluded vessel, diabetes mellitus, and stent placement in a vessel with a normal diameter less than 3.0mm.
Intimal hyperplasia follows a fairly predictable time course.
Serial angiographic studies in humans demonstrate that the greatest smooth muscle proliferation occurs between one and three months with only a small number of stents exhibiting further narrowing between six and twelve months. These findings are supported by experimental work that has shown late replacement of proliferating smooth muscle cells by relatively inactive ground matrix and fibrosis. The coupling of disease management and technological innovation is manifestly expressed in the field of endovascular neurosurgery. The development of small, flexible stents that can reach the intracranial circulation may revolutionize the management both of ischemic disease and aneurysmal subarachnoid hemorrhage. Clearly more work is necessary both in the laboratory and clinical arenas to better understand the long-term impact of such treatments.