Peristrut microhemorrhages: a possible cause of in-stent neoatherosclerosis?

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• 作者：Zaven Terzian^a ; ^b ; T. Christian Gasser^c ; Francis Blackwell^a ; ^b ; Fabien Hyafil^a ; ^b ; Liliane Louedec^a ; Catherine Deschildre^a ; Walid Ghodbane^b ; Richard Dorent^a ; ^b ; Antonino Nicoletti^a ; Marion Morvan^a ; Mohammed Nejjari^a ; ^d ; Laurent Feldman^a ; ^b ; Graciela Pavon-Djavid^a ; ^e ; Jean-Baptiste Michel^a ; ^{jean-baptiste.michel@inserm.fr}
• 关键词：Coronary artery disease ; Stent ; Neoatherosclerosis ; Hemorrhage ; Hemoglobin ; Cholesterol
• 刊名：Cardiovascular Pathology
• 出版年：2017
• 出版时间：January-February 2017
• 年：2017
• 卷：26
• 期：Complete
• 页码：30-38
• 全文大小：2598 K
• 卷排序：26

文摘

In-stent neoatherosclerosis is characterized by the delayed appearance of markers of atheroma in the subintima, but the pathophysiology underlying this new disease entity remains unclear.Methods and resultsWe collected 20 human coronary artery stents by removal from explanted hearts. The mean duration of stent implantation was 34 months. In all samples, neoatherosclerosis was detected, particularly in peristrut areas. It consisted of foam cells and cholesterol clefts, with or without calcification, associated with neovascularization. Iron and glycophorin-A were present in peristrut areas, as well as autofluorescent ceroids. Moreover, in response to neoatherosclerosis, tertiary lymphoid organs (tissue lymphoid clusters) often developed in the adventitia. Some of these features could be reproduced in an experimental carotid stenting model in rabbits fed a high-cholesterol diet. Foam cells were present in all samples, and peristrut red blood cells (RBCs) were also detected, as shown by iron deposits and Bandeiraea simplicifiola isolectin-B4 staining of RBC membranes. Finally, in silico models were used to evaluate the compliance mismatch between the rigid struts and the distensible arterial wall using finite element analysis. They show that stenting approximately doubles the local von Mises stress in the intimal layer.ConclusionsWe show here that stent implantation both in human and in rabbit arteries is characterized by local peristrut microhemorrhages and finally by both cholesterol accumulation and oxidation, triggering together in-stent neoatherosclerosis. Our data indicate that these processes are likely initiated by an increased mechanical stress due to the compliance mismatch between the rigid stent and the soft wall.