Neoatherosclerosis

Abstract

Since the advent of balloon angioplasty in the 1970s by Andreas Gruentzig, restenosis, or the excessive proliferation of smooth muscle cells into the intima, has been regarded as the primary limitation of percutaneous coronary intervention. The introduction of bare metal stents (BMS) in the 1990s reduced restenosis rates by eliminating elastic recoil and negative remodeling, and represented a significant advance. If one could escape the early risk of vessel renarrowing within the first 12 months after implantation, long-term outcomes appeared to be favorable, with late increases in luminal diameter between 1 and 3 years.1 However, data from a series of reports, including 1 in this issue, suggest the cellular response to stenting is a complex and dynamic phenomenon, not detectable by traditional luminography, that continues to evolve many years after stent placement and may be an important cause of late thrombotic events. These data enhance our understanding of how and why thrombosis within stents sometimes can occur late, many years after percutaneous coronary intervention. Article see p 47 Unlike angioplasty, stenting results in prolonged chronic inflammatory cell recruitment.2 In a series of human autopsy implants, Inoue et al3 reported that important temporal changes occur in the neointima after BMS placement in humans. Arteries that had been stented for 2 to 3 years demonstrated endothelial coverage with smooth muscle and collagen rich neointima. Chronic inflammation was observed and was characterized by macrophages, T cells, and giant cell infiltration. In stents implanted greater than 4 years, smooth muscle cells were sparse, with abundant collagen toward the lumen and evidence of foamy macrophages (so called “neoatherosclerosis”) around stent struts, which expressed metalloproteinases. These data suggest that neointima formation that occurs after metallic stent implants is subject to the same atherosclerotic forces that affect native vessels, and that macrophage mediated degradation …