Deployment of
drug-eluting stents instead of bare-
metal stents has dramatically reduced restenosis rates, but rates of very late
stent thrombosis (>1 year postimplantation) have increased. Vascular endothelial cells normally provide an efficient barrier against
thrombosis,
lipid uptake, and
inflammation. However, endothelium that has regenerated after
percutaneous coronary intervention is incompetent in terms of its integrity and function, with poorly formed cell junctions, reduced expression of antithrombotic molecules, and decreased
nitric oxide production. Delayed arterial healing, characterized by poor endothelialization, is the primary cause of late (1 month-1 year postimplantation) and very late
stent thrombosis following implantation of
drug-eluting stents. Impairment of vasorelaxation in nonstented proximal and distal segments of stented coronary arteries is more severe with
drug-eluting stents than bare-
metal stents, and
stent-induced flow disturbances resulting in complex spatiotemporal shear stress can also contribute to increased thrombogenicity and
inflammation. The incompetent endothelium leads to late
stent thrombosis and the development of in-
stent neoatherosclerosis. The process of neoatherosclerosis occurs more rapidly, and more frequently, following deployment of
drug-eluting stents than bare-
metal stents. Improved understanding of vascular biology is crucial for all cardiologists, and particularly interventional cardiologists, as maintenance of a competently functioning endothelium is critical for long-term vascular health.