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논문번호 39
논문제목(영문) Origin of restenosis after drug-eluting stent implantation in hyperglycemia is inflammatory cells and thrombus.
국내외구분 국외 SCI여부 SCI(E)
연구책임자역할 공저자
주저자명 Kwon JS
교신저자명 Ahn Y
공동저자명 Kwon JS, Kim YS, Cho AS, Kim JS, Jeong SY, Hong MH, Jeong MH, Ahn Y;
게제년월일 2011-01-21
ISSN 1340-3478
Impact Factor 2.733
학술지명 J Atheroscler Thromb. 2011;18(7):604-615.
서지사항 0집 / 18권 / 7호,   페이지(604 - 615)
요약초록문
(Abstract) 입력		 AIMS:
The cellular and molecular mechanisms and safety after drug-eluting stent (DES) implantation in diabetic patients are still poorly understood; therefore, in this study, we evaluated the pathologic responses of the sirolimus-eluting stent (SES) or paclitaxel-eluting stent (PES) in a type I diabetes mellitus (DM) rat model.
METHODS:
The type I DM rat model was manipulated by intra-peritoneal streptozotocin injection. Two weeks later, DES was implanted in the aorta of rats with hyperglycemia or not as a control. Four weeks after DES implantation, the stented aorta was isolated and histomorphometric analysis was performed.
RESULTS:
On histomorphometric analysis, increased thrombus, inflammatory cell infiltration, and neointimal hyperplasia (NIH) without change of the smooth muscle cell number after DES implantation were observed in DM rats compared with non-DM (NDM) rats. Furthermore, delayed coverage of mature endothelial cells defined as a von Willebrand factor expression and increased immature endothelial cells as a c-kit expression after DES implantation were observed in DM rats compared with NDM rats. Increased fibrin deposition and decreased hyaluronic acid accumulation at NIH after DES implantation were also observed in DM rats compared with NDM rats.
CONCLUSIONS:
In conclusion, the main mechanism of restenosis after DES implantation under hyperglycemic conditions was initial thrombus with changes of the extracellular matrix rather than SMC proliferation. These results provided a therapeutic clue for the selection of DES and application of combination therapy using anti-thrombotic and anti-inflammatory drugs in diabetic patients.
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