A New Pan‐Nitinol Occluder for Transcatheter Closure of Ventricular Septal Defects in a Canine Model

Zhong-ru, Ding; Qin, Yong-wen; Hu, Jianqiang; Zhao, Xianxian; Yang, Zong-Xiao; Hongwu,; Cao, Jun

doi:10.1111/j.1540-8183.2009.00432.x

Cited by 7 publications

(6 citation statements)

References 13 publications

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“…All aspects of animal care were in accordance with the China's National Standard on “Laboratory animal‐requirements of environment and housing facilities” (GB 14925–2001). The VSD was created by a transcatheter puncture method as previously described in detail . Briefly, under general anesthesia with intravenous pentobarbital sodium, ventricular septal puncture was performed using an 8 F Mullins transseptal sheath and brockenbrough needle via the right jugular vein under fluoroscopic guidance.…”

Section: Methodsmentioning

confidence: 99%

Development and preclinical evaluation of a biodegradable ventricular septal defect occluder

Huang

Zhu

Cao

et al. 2012

Cathet Cardio Intervent

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Section: Methodsmentioning

confidence: 99%

Development and preclinical evaluation of a biodegradable ventricular septal defect occluder

Huang

Zhu

Cao

et al. 2012

Cathet Cardio Intervent

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“…In this study, we investigated the effect of MEG3 on autophagy in vivo study by using VSD rat model. The animal model was early established VSD rat model in our lab according to previous studies [27,28]. Eighteen adult male Sprague-Dawley rats were divided into three groups (n ¼ 6): control, VSD and VSD þ MEG3 mimics.…”

Section: Vsd Rat Modelmentioning

confidence: 99%

Uric acid and sphingomyelin enhance autophagy in iPS cell-originated cardiomyocytes through lncRNA MEG3/miR-7-5p/EGFR axis

Cao

Wen

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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2019) Uric acid and sphingomyelin enhance autophagy in iPS cell-originated cardiomyocytes through lncRNA MEG3/miR-7-5p/EGFR axis, Artificial Cells, Nanomedicine, and Biotechnology, 47:1, 3774-3785, ABSTRACTThis study aimed to determine the metabolites associated with ventricular septal defect (VSD) and the underlying mechanisms. Blood samples and thymus tissues were collected from VSD patients to perform LC-MS-based metabolomics assay and generate iPS cell-derived cardiomyocytes, respectively. VSD rat model was used in vivo study. RT-PCR, western blotting, immunohistochemistry, luciferase activity assay, GFP-LC3 adenovirus and GFP and RFP tfLC3 assay, and transmission electron microscopy were performed to investigate the underlying mechanisms. The metabolites uric acid (UA) and sphingomyelin (SM) increased in the serum of VSD patients, along with enhanced autophagy. The combination of UA and SM treatment could promote autophagy and inhibit EGFR and AKT3 expressions. Overexpression of EGFR and AKT3 suppressed autophagy in UA and SM-treated cardiomyocytes, respectively. Also, lncRNA MEG3 knockdown and overexpression could enhance and inhibit autophagy in UA and SM-treated cardiomyocytes, respectively, through targeting miR-7-5p. Moreover, miR-7-5p mimics and inhibitors promoted and inhibited autophagy in UA and SM-treated cardiomyocytes, respectively, via target EGFR. In VSD rat model, upregulation of MEG3 could reverse high level of autophagy and decrease serum UA and SM. In conclusion, UA and SM are essential VSD-associated metabolic biomarkers and MEG3/miR-7-5p/EGFR axis is critical to the regulation of autophagy in cardiomyocytes. ARTICLE HISTORY

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“…Structural components of the ASO might contribute to post-deployment sequelae. [23][24][25][26][27][28][29][30] In the ASO for ventricular septal defects, the fixed stainless-steel pin buttons at the center of the ASO discs might interfere with endothelialization and be a staging platform for thrombosis. 23 The ASO for ASDs has identical pin buttons.…”

Section: Discussionmentioning

confidence: 99%

Endocarditis and Incomplete Endothelialization 12 Years after Amplatzer Septal Occluder Deployment

Nguyen¹,

Palafox²,

Starr³

et al. 2016

Texas Heart Institute Journal

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A 4-year-old boy had a 15-mm atrial septal defect repaired percutaneously with use of an Amplatzer Septal Occluder. At age 16 years, he presented with a week's history of fever, chills, dyspnea, fatigue, and malaise. Cultures grew methicillin-sensitive Staphylococcus aureus. A transesophageal echocardiogram showed a 1.25 × 1.5-cm pedunculated mass on the left aspect of the atrial septum just superior to the mitral valve, and a smaller vegetation on the right inferior medial aspect of the septum. At surgery, visual examination of both sides of the septum revealed granulation tissue, the pedunculated mass, the small vegetation, and exposed metal wires that suggested incomplete endothelialization of the occluder. We removed the occluder and patched the septal defect. The patient returned to full activity after 4 months and was asymptomatic 3 years postoperatively. Our report reinforces the need for further investigation into prosthetic device endothelialization, endocarditis prophylaxis, and recommended levels of physical activity in patients whose devices might be incompletely endothelialized. In addition to reporting our patient's case, we review the medical literature on this topic.

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A New Pan‐Nitinol Occluder for Transcatheter Closure of Ventricular Septal Defects in a Canine Model

Cited by 7 publications

References 13 publications

Development and preclinical evaluation of a biodegradable ventricular septal defect occluder

Development and preclinical evaluation of a biodegradable ventricular septal defect occluder

Uric acid and sphingomyelin enhance autophagy in iPS cell-originated cardiomyocytes through lncRNA MEG3/miR-7-5p/EGFR axis

Endocarditis and Incomplete Endothelialization 12 Years after Amplatzer Septal Occluder Deployment

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