Abstract 18707: Neointima After Stent Implantation and Pathological Morphology of Underlying Plaque in Stent Edge Site
Introductions: Previous study have shown penetration of stent struts into a lipid core was associated with increased neointimal thickness compared with stent struts in contact with fibrous plaque. Therefore, recent intravascular imaging guided percutaneous coronary intervention (PCI) suggested to avoid the stent edge landing at the site of lipid core plaque. Although, it remains unclear whether pathological morphology underlying plaque is associated with neointimal thickening especially at the stent edge. The objective of our study is to clarify pathological underlying morphological predictors of exaggerated intimal hyperplasia at the edges of the stents.
Methods: We examined histopathological details of 24 stents in 16 coronary arteries from 8 autopsy cases. Coronary arteries were fixed with 10% formalin, embedded with plastic, and cut at 2-mm intervals along the entire length of the stents. The most proximal and distal sections were stained by hematoxylin and eosin, and Elastica van Gieson, and analyzed as the proximal and distal stent edges. Intima elastic lamina area, stent area, in-stent neointima, and underlying plaque area such as fibrous, calcified and atheroma tissue were measured.
Results: The mean duration after stent implantation was 19.3 months. Lipid core penetration by stent struts was present in 7 edges. Lipid core penetration was not associated with an increased neointimal thickness compared with struts in contact with fibrous plaque (1.43 ± 0.97 mm2 versus 0.97 ± 0.64 mm2, P=0.43). There is no significant relationship identified between neointimal area and underlying plaque area such as lipid and calcification.
Conclusions: The underlying plaque burden, including lipid area and calcified area, did not correlate with the amount of intimal hyperplasia at the proximal and distal edge of the stents. It is not necessary to avoid the stent edge landing at the site lipid core plaque and calcified plaque in DES era.
Author Disclosures: R. Kawakami: None. K. Fuji: None. M. Shibuya: None. T. Imanaka: None. K. Kawai: None. T. Saita: None. M. Ishihara: None. T. Masuyama: None. S. Hirota: None.
- © 2016 by American Heart Association, Inc.