2013
DOI: 10.1253/circj.cj-12-1259
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Mechanism of Edge Restenosis After Drug-Eluting Stent Implantation

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Cited by 26 publications
(7 citation statements)
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“…We reckon that sufficient plaque debulking and DCB angioplasty are effective to obtain large lumen area and to inhibit neointimal hyperplasia which is the main cause of restenosis in nonstented vessels. On the other hand, several mechanisms of stent edge restenosis have been reported including negative remodeling, mechanical injury at stent edge due to hinge motion, and local changes in shear stress [11][12][13]. In particular, all the TLR cases in the current study of stent edge restenosis at the LAD ostium had a low %PA following DCA.…”
Section: Discussionmentioning
confidence: 59%
“…We reckon that sufficient plaque debulking and DCB angioplasty are effective to obtain large lumen area and to inhibit neointimal hyperplasia which is the main cause of restenosis in nonstented vessels. On the other hand, several mechanisms of stent edge restenosis have been reported including negative remodeling, mechanical injury at stent edge due to hinge motion, and local changes in shear stress [11][12][13]. In particular, all the TLR cases in the current study of stent edge restenosis at the LAD ostium had a low %PA following DCA.…”
Section: Discussionmentioning
confidence: 59%
“…For instance, tortuous lesions are a risk factor for restenosis or stent fracture after stent implantation [ [31][32][33]. Moreover, SER can occur stent implantation due to physical stress at the stent edge segment in tortuous vessels [4]. Thus, SER may be associated with tortuous vessels.…”
Section: Discussionmentioning
confidence: 99%
“…Stent edge restenosis (SER) is a type of ISR observed at the edge of the stent and identified as the prevailing limitation of ISR after stent implantation. It has been reported that the mechanism of SER was related to vessel injury by ballooning or stent implantation, the residual plaque, and the small lumen area in the stent edge segments [4][5][6][7]. In addition, mechanical stresses due to hinge motion are risk factors for SER incidents [8].…”
Section: Introductionmentioning
confidence: 99%
“…It has been suggested that this arises from mechanical injury and chronic local inflammation at the stent edge induced by hinge motion between stented and unstented segments of the vessel with every heart contraction. 8 It has also been suggested that straightening of a curved artery upon stenting changes the WSS distribution at the stent edge, leading to endothelial dysfunction and edge restenosis. 19 Moreover, finite element analysis of a curved bifurcation model suggested that the straightening effect is attenuated by making the stent more flexible, thereby reducing the mechanical stress to the artery, in particular at the distal end of the stent and the side branch ostium.…”
Section: Discussionmentioning
confidence: 99%
“…[3][4][5] This high restenosis rate in bifurcation lesions could stem from chronic inflammation due to continuous mechanical stress from the stent on the artery. [6][7][8] Alternatively, restenosis could be caused by the delay in re-endothelialization and endothelial dysfunction due to flow disturbances and the concomitant change in wall shear stress (WSS) on endothelial cells (ECs). 9 In either case, stent flexibility is likely a key contributing factor because a rigid stent would straighten the artery, increasing mechanical stress and the change of WSS.…”
Section: Introductionmentioning
confidence: 99%