Bioresorbable vascular scaffold thrombosis in a consecutive cohort of 550 patients

Tröbs, Monique; Achenbach, Stephan; Röther, Jens; Klinghammer, Lutz; Schlundt, Christian

doi:10.1002/ccd.26569

Cited by 8 publications

(3 citation statements)

References 29 publications

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“…Although stents, a next-generation treatment, have decreased the incidence of thrombosis to approximately 0.2% [1], they fail to effectively control restenosis, which seriously affects the quality of life and long-term prognosis of patients after intervention. Therefore, minimizing the risk of in-stent restenosis and thrombosis has become the focus of research on and development of intervention apparatuses [2][3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Effect of Paclitaxel+Hirudin on the TLR4-MyD88 Signaling Pathway During Inflammatory Activation of Human Coronary Artery Smooth Muscle Cells and Mechanistic Analysis

Li¹,

Wang²,

Xu³

2018

Cell Physiol Biochem

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Background/Aims: Approximately 10%-20% of patients with acute cardiovascular disease who have received coronary intervention suffer restenosis and high inflammation. The stent compound paclitaxel+hirudin was prepared for the treatment of post-intervention restenosis. This study aimed to explore the anti-inflammatory and anti-restenosis mechanisms of paclitaxel+hirudin with regard to the TLR4/MyD88/NF-κB pathway. Methods: Human coronary artery smooth muscle cells (HCASMCs) at 4-6 generations after in vitro culture were used as a model. Lipopolysaccharide (LPS) was used as an inducer to maximally activate the TLR4/MyD88/NF-κB inflammation pathway. After MyD88 knockdown and selective blocking of MyD88 degradation with epoxomicin, the effects of paclitaxel+hirudin stenting on key sites of the TLR4/MyD88/NF-κB pathway were detected using ELISA, Q-PCR, and western blot analysis. Results: LPS at 1 μg/mL for 48 h was the optimal modeling condition for inflammatory activation of HCASMCs. Paclitaxel+hirudin inhibited the levels of key proteins and the gene expression, except for that of the MyD88 gene, of the TLR4-MyD88 pathway. The trend of the effect of paclitaxel+hirudin on the pathway proteins was similar to that of MyD88 knockdown. After epoxomicin intervention, the inhibitory effects of paclitaxel+hirudin on the key genes and proteins of the TLR4-MyD88 pathway were significantly weakened, which even reached pre-intervention levels. Paclitaxel+hirudin affected the MyD88 protein in a dosage-dependent manner. Conclusion: The paclitaxel+hirudin compound promotes MyD88 degradation in the TLR4/MyD88/NF-κB pathway to reduce the activity of TLR4 and NF-κB p65 and to weaken the LPS-initiated inflammatory reactions of IL-1β, IL-6, and TNF-α.

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Section: Introductionmentioning

confidence: 99%

Effect of Paclitaxel+Hirudin on the TLR4-MyD88 Signaling Pathway During Inflammatory Activation of Human Coronary Artery Smooth Muscle Cells and Mechanistic Analysis

Li¹,

Wang²,

Xu³

2018

Cell Physiol Biochem

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“…Furthermore, analysis of the data collected by several registries shows that this BVS associates with a high rate of early (within 30 days) definite or probable ST of 1.3-1.5% [106,107]. Moreover, 1 year after implantation, the definite or probable ST rates are markedly higher (up to 3.1%) than the rates detected by the randomized trials [108][109][110][111][112][113][114]. This apparently higher thrombogenicity may be caused by two major limitations of the first-generation thick-strut poly-lactic acid BVS.…”

Section: Drug-eluting Stentmentioning

confidence: 97%

“…The mean number and length of BVS implantation and its relation to the incidence of ST is illustrated in Figure 3, based on data from randomized controlled trials and registries with ≥100 patients that report a 6-12 month follow-up and BVS details [81,[101][102][103][104][106][107][108][109][110][111][112][113][114][117][118][119][120][121][122][123]. Only the ASSURE registry, which included 183 patients, reported no cases of ST at 1 year follow-up [119].…”

Section: Drug-eluting Stentmentioning

confidence: 99%

Bioresorbable Vascular Scaffolds—Dead End or Still a Rough Diamond?

Jeżewski

Kubisa

Eyileten

et al. 2019

JCM

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Percutaneous coronary interventions with stent-based restorations of vessel patency have become the gold standard in the treatment of acute coronary states. Bioresorbable vascular scaffolds (BVS) have been designed to combine the efficiency of drug-eluting stents (DES) at the time of implantation and the advantages of a lack of foreign body afterwards. Complete resolution of the scaffold was intended to enable the restoration of vasomotor function and reduce the risk of device thrombosis. While early reports demonstrated superiority of BVS over DES, larger-scale application and longer observation exposed major concerns about their use, including lower radial strength and higher risk of thrombosis resulting in higher rate of major adverse cardiac events. Further focus on procedural details and research on the second generation of BVS with novel properties did not allow to unequivocally challenge position of DES. Nevertheless, BVS still have a chance to present superiority in distinctive indications. This review presents an outlook on the available first and second generation BVS and a summary of results of clinical trials on their use. It discusses explanations for unfavorable outcomes, proposed enhancement techniques and a potential niche for the use of BVS.

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Use of a bioresorbable novolimus eluting vascular scaffold fails a hybrid PCI strategy with drug eluting stent

et al. 2017

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Bioresorbable vascular scaffold thrombosis in a consecutive cohort of 550 patients

Abstract: In a large real-world cohort treated with BVS, the rate of scaffold thrombosis was higher than published for randomized trials. A high rate of thrombosis was observed after combined implantation of BVS and stents within one vessel. © 2016 Wiley Periodicals, Inc.

Cited by 8 publications

References 29 publications

Effect of Paclitaxel+Hirudin on the TLR4-MyD88 Signaling Pathway During Inflammatory Activation of Human Coronary Artery Smooth Muscle Cells and Mechanistic Analysis

Effect of Paclitaxel+Hirudin on the TLR4-MyD88 Signaling Pathway During Inflammatory Activation of Human Coronary Artery Smooth Muscle Cells and Mechanistic Analysis

Bioresorbable Vascular Scaffolds—Dead End or Still a Rough Diamond?

Use of a bioresorbable novolimus eluting vascular scaffold fails a hybrid PCI strategy with drug eluting stent

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