Endovascular stent design dictates experimental restenosis and thrombosis

Vascular interventions that maximize initial lumen diameter provoke extensive neointimal hyperplasia but minimize its effects, causing long-term lumen size to be greater. Nevertheless, interventions such as endovascular stents, which increase lumen size above that achieved with balloon angioplasty, are subject to frequent thrombosis and restenosis. It has been unclear whether the response to stent-induced injury is determined solely by the degree of stent-induced arterial expansion or whether the geometric configuration of the stent or the material left in contact with the vessel wall also contribute.

We examined the vascular response to steel stents deployed in denuded rabbit iliac arteries for 14 days. In one set of experiments, the effects of sten configuration were examined, holding diameter, mass, surface area, and stent surface material constant. In another set, stent surface material was changed, with mass, configuration, and diameter unaltered. Changing stent configuration to reduce strut-strut intersections by 29% without affecting mass or surface area reduced vascular injury by 42%, thrombosis by 69%, and neointimal hyperplasia by 38%. Monocyte adhesion to stented arteries correlated linearly with vascular trauma and neointimal hyperplasia (r = .96, P < .01 for each). When the stainless steel surface was coated with an inert polymer material, vascular injury and neointimal hyperplasia were unchanged but thrombosis was eliminated.

Surface material and geometric configuration of stents may be more important than postplacement diameter in determining neointimal hyperplasia and thrombosis. Alterations in configuration affect vascular injury and neointimal hyperplasia, while surface material plays a greater role in thrombosis. Monocytes may be important modulators of stent-induced intimal thickening. Clinical confirmation of these findings may alter coronary stent deployment techniques and future stent designs.