Abstract 11321: Very Late Vascular Response After Bare Metal Stent Implantation in Human Coronary Arteries
Background: Bare metal stents (BMSs) continue to be used in percutaneous coronary intervention, even after the introduction of drug-eluting stents; however, very long-term pathological findings, for example, beyond 10 years after their implantation, have yet to be clarified.
Methods and Results: Histopathological studies were performed in 22 lesions (les) obtained from 19 patients autopsied after noncardiac death 5-16 years (Y) poststenting. The interval between BMS implantation and death was distributed as follows: 5-8 Y, 5 les; 8-10 Y, 5 les; 10-12 Y, 4 les; 12-14 Y, 5 les; and 14-16 Y, 3 les. All examined BMS were stainless steel stents, such as Palmaz-Schatz, Multilink, and NIR stents. Neointima of the arteries that had been stented more than 5 Y showed full endothelial coverage, and the smooth muscle cells (SMCs) were atrophic and sparse, with abundant proliferation of collagen fibers. However, there was significant infiltration of inflammatory cells (T lymphocytes and macrophages (MΦ)) surrounding the stent struts. Although neointima beyond 7 Y resembled fibrotic scar with SMC depletion and replacement by collagen fibers, prominent infiltration by lipid-laden MΦ with strong collagen-degrading matrix metalloprotease immunoreactivity was evident around the struts. Beyond 10 Y, marked necrotic core formation with cholesterol clefts around the struts, and peristrut calcification including fine calcium deposits in the cytoplasm of many MΦ were evident. Furthermore, clusters of a lot of lipid-laden MΦ were also visible adjacent to the subendothelial spaces, accompanied by significant intimal thickening. In neointima beyond 13 Y, remarkable extracellular lipid core formation and calcification were typical in the superficial layer as well as the peristent area. In 4 of these lesions, advanced luminal narrowing occurred, and the luminal surface of the stented segments was focally disrupted and covered by nonocclusive mural thrombi in 2 other cases.
Conclusions: This extended late-phase (>10 Y) pathologic observation after BMS implantation demonstrated that neointima often transforms into lipid-laden tissue, and such advanced atherosclerotic progression may be associated with recurrence of myocardial ischemia, including ACS.
Author Disclosures: K. Inoue: None. M. Imai: None. K. Yamaji: None. K. Ando: None. M. Nobuyoshi: None. T. Kimura: None.
- © 2014 by American Heart Association, Inc.