Intravascular ultrasound assessment of stent edge restenosis mechanisms and treatment outcomes following percutaneous coronary intervention

Abstract This study aimed to elucidate the biological or mechanical causes of stent edge restenosis (SER) via intravascular ultrasound (IVUS). A retrospective assessment was conducted on 126 SER lesions that underwent IVUS prior to revascularization. The primary mechanisms of SER were categorized. (...

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Main Authors: Xi Wu, Zhe Liu, Haobo Huang, Mingxing Wu, He Huang, Lei Wang
Format: Article
Language:English
Published: Nature Portfolio 2025-05-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-01381-9
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author Xi Wu
Zhe Liu
Haobo Huang
Mingxing Wu
He Huang
Lei Wang
author_facet Xi Wu
Zhe Liu
Haobo Huang
Mingxing Wu
He Huang
Lei Wang
author_sort Xi Wu
collection DOAJ
description Abstract This study aimed to elucidate the biological or mechanical causes of stent edge restenosis (SER) via intravascular ultrasound (IVUS). A retrospective assessment was conducted on 126 SER lesions that underwent IVUS prior to revascularization. The primary mechanisms of SER were categorized. (1) neointimal hyperplasia (NIH); (2) neoatherosclerosis; (3) uncovered lesion; (4) stent underexpansion; or (5) a protruding calcified nodule (CN). The predominant biological or mechanical causes of SER were NIH in 42.9% (n = 54) of lesions, neoatherosclerosis in 32.5% (n = 41), uncovered lesion in 14.3% (n = 18), stent underexpansion in 7.9% (n = 10), and protruding CN in 2.4% (n = 3). The 2-year device-oriented clinical endpoints (DoCE) incidence was 7.1% (n = 9). The group with biological causes treated via drug-coated balloons (DCB) exhibited a comparable DoCE rate (9.5%) to those with biological causes treated with drug-eluting stents (DES) and mechanical causes managed with or without restenting (6.0%, HR 2.78, 95% CI: 0.91–9.21; p = 0.161). The majority of the analyzed SERs were attributed to biological causes, including NIH, neoatherosclerosis, and uncovered lesions. The 2-year DoCE rate within patients receiving DCB for mechanically or biologically induced SER was similar to that observed in patients receiving new DES.
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spelling doaj-art-3d51455a43ef42e4b3ddc02829a390992025-08-20T01:49:33ZengNature PortfolioScientific Reports2045-23222025-05-0115111310.1038/s41598-025-01381-9Intravascular ultrasound assessment of stent edge restenosis mechanisms and treatment outcomes following percutaneous coronary interventionXi Wu0Zhe Liu1Haobo Huang2Mingxing Wu3He Huang4Lei Wang5Department of Cardiology, Xiangtan Central Hospital (the affiliated hospital of Hunan University)Department of Cardiology, Xiangtan Central Hospital (the affiliated hospital of Hunan University)Department of Cardiology, Xiangtan Central Hospital (the affiliated hospital of Hunan University)Department of Cardiology, Xiangtan Central Hospital (the affiliated hospital of Hunan University)Department of Cardiology, Xiangtan Central Hospital (the affiliated hospital of Hunan University)Department of Cardiology, Xiangtan Central Hospital (the affiliated hospital of Hunan University)Abstract This study aimed to elucidate the biological or mechanical causes of stent edge restenosis (SER) via intravascular ultrasound (IVUS). A retrospective assessment was conducted on 126 SER lesions that underwent IVUS prior to revascularization. The primary mechanisms of SER were categorized. (1) neointimal hyperplasia (NIH); (2) neoatherosclerosis; (3) uncovered lesion; (4) stent underexpansion; or (5) a protruding calcified nodule (CN). The predominant biological or mechanical causes of SER were NIH in 42.9% (n = 54) of lesions, neoatherosclerosis in 32.5% (n = 41), uncovered lesion in 14.3% (n = 18), stent underexpansion in 7.9% (n = 10), and protruding CN in 2.4% (n = 3). The 2-year device-oriented clinical endpoints (DoCE) incidence was 7.1% (n = 9). The group with biological causes treated via drug-coated balloons (DCB) exhibited a comparable DoCE rate (9.5%) to those with biological causes treated with drug-eluting stents (DES) and mechanical causes managed with or without restenting (6.0%, HR 2.78, 95% CI: 0.91–9.21; p = 0.161). The majority of the analyzed SERs were attributed to biological causes, including NIH, neoatherosclerosis, and uncovered lesions. The 2-year DoCE rate within patients receiving DCB for mechanically or biologically induced SER was similar to that observed in patients receiving new DES.https://doi.org/10.1038/s41598-025-01381-9Stent edge restenosisPercutaneous coronary interventionIntravascular unltrasound
spellingShingle Xi Wu
Zhe Liu
Haobo Huang
Mingxing Wu
He Huang
Lei Wang
Intravascular ultrasound assessment of stent edge restenosis mechanisms and treatment outcomes following percutaneous coronary intervention
Scientific Reports
Stent edge restenosis
Percutaneous coronary intervention
Intravascular unltrasound
title Intravascular ultrasound assessment of stent edge restenosis mechanisms and treatment outcomes following percutaneous coronary intervention
title_full Intravascular ultrasound assessment of stent edge restenosis mechanisms and treatment outcomes following percutaneous coronary intervention
title_fullStr Intravascular ultrasound assessment of stent edge restenosis mechanisms and treatment outcomes following percutaneous coronary intervention
title_full_unstemmed Intravascular ultrasound assessment of stent edge restenosis mechanisms and treatment outcomes following percutaneous coronary intervention
title_short Intravascular ultrasound assessment of stent edge restenosis mechanisms and treatment outcomes following percutaneous coronary intervention
title_sort intravascular ultrasound assessment of stent edge restenosis mechanisms and treatment outcomes following percutaneous coronary intervention
topic Stent edge restenosis
Percutaneous coronary intervention
Intravascular unltrasound
url https://doi.org/10.1038/s41598-025-01381-9
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