The Residual Lipid-Rich Coronary Atheroma Behind the Implanted Newer-Generation Drug-Eluting Stent and Future Stent-Related Event Risks

Murai, Kota; Kataoka, Yasufumi; Nicholls, Stephen J.; Puri, Rishi; Nakaoku, Yuriko; Nishimura, Kunihiro; Kitahara, Satoshi; Iwai, Takamasa; Sawada, Kenichiro; Matama, Hideo; Honda, Satoshi; Fujino, Masashi; Yoneda, Shuichi; Takagi, Kensuke; Nishihira, Kensaku; Otsuka, Fumiyuki; Asaumi, Yasuhide; Tsujita, Kenichi; Noguchi, Teruo

doi:10.1016/j.cjca.2022.07.004

Cited by 3 publications

(1 citation statement)

References 29 publications

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“…Residual plaque burden and lipid-rich plaque are also associated with edge restenosis after DES implantation. 16 Other lesion factors include a lipid arc of >185° and a minimum stent area of 4.1 mm 2 . 16 …”

Section: Predisposing Factors For In-stent Restenosismentioning

confidence: 99%

In-stent restenosis after percutaneous coronary intervention: emerging knowledge on biological pathways

Pelliccia,

Zimarino,

Niccoli

et al. 2023

European Heart Journal Open

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Percutaneous coronary intervention (PCI) has evolved significantly over the past four decades. Since its inception, in-stent restenosis (ISR) – the progressive reduction in vessel lumen diameter after PCI – has emerged as the main complication of the procedure. Although the incidence of ISR has reduced from 30% at 6 months with bare-metal stents (BMS) to 7% at 4 years with drug-eluting stents (DES), its occurrence is relevant in absolute terms because of the dimensions of the population treated with PCI. The aim of this review is to summarize the emerging understanding of the biological pathways that underlie ISR. ISR is associated with several factors, including patient-related, genetic, anatomic, stent, lesion and procedural characteristics. Regardless of associated factors, there are common pathophysiologic pathways involving molecular phenomena triggered by the mechanical trauma caused by PCI. Such biologic pathways are responses to the denudation of the intima during balloon angioplasty and involve inflammation, hypersensitivity reactions, and stem cell mobilization in particular of endothelial progenitor cells (EPCs). The results of these processes are either vessel wall healing or neointimal hyperplasia and/or neoatherosclerosis. Unraveling the key molecular and signal pathways involved in ISR is crucial to identify appropriate therapeutic strategies aimed at abolishing the ‘Achille’s heel’ of PCI. With this regard, we discuss novel approaches to prevent DES restenosis. Indeed, available evidence suggests that EPCs-capturing stents promote a rapid stent re-endothelisation, which in turn has the potential to decrease the risk of stent thrombosis and allow the use of a shorter duration of dual antiplatelet therapy.

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Section: Predisposing Factors For In-stent Restenosismentioning

confidence: 99%