A 7-month-old Irish Setter underwent transcatheter therapy of a muscular ventricular septal defect (VSD) and pulmonary valve stenosis. Standard devices for muscular VSD closure could not span the interventricular septum due to right ventricular hypertrophy, and an Amplatzer post-infarction muscular VSD occluder with a wider waist was successfully implanted. Following VSD closure, inflation of the balloon dilation catheter during balloon pulmonary valvuloplasty resulted in iatrogenic embolization of the VSD occluder to the left ventricular outflow tract. Retrieval and reimplantation of the device was achieved using a snare catheter. This report describes a potential complication and management during intracardiac device implantation in a dog. Additionally, the case illustrates that the Amplatzer post-infarction muscular VSD occluder holds potential value in animals with a hypertrophied interventricular septum that cannot be spanned using a conventional device.
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http://dx.doi.org/10.1016/j.jvc.2015.08.003 | DOI Listing |
Catheter Cardiovasc Interv
December 2024
Department of Pediatric Cardiology, Heart Centre of Excellence, Al Jalila Children's Speciality Hospital, Dubai, United Arab Emirates.
We report the case of a 3-year-old asymptomatic girl (12 kg, 96 cm) who was diagnosed with a large iatrogenic left ventricular pseudoaneurysm (LVP) on follow-up ultrasound, 14 months after apical muscular ventricular septal defect (VSD) closure with a 10 mm Amplatzer Muscular VSD occluder (Abbott, USA) due to device erosion. The LVP was successfully occluded using detachable Penumbra coils, with complete thrombo-exclusion confirmed at 12-month follow-up.
View Article and Find Full Text PDFEuropace
December 2024
Department of Cardiology, Heart Lung Centre, Leiden University Medical Centre, P.O. Box 9600, 2300 RC Leiden, The Netherlands.
Aims: In repaired tetralogy of Fallot (rTOF), the septal anatomical isthmuses (AI), AI 3, between the ventricular septal defect (VSD) and pulmonary annulus, and AI 4, between the VSD and tricuspid annulus, are important ventricular tachycardia (VT) substrates when slow conducting. Our aim was to assess the influence of VSD characteristics, specifically the presence of muscular or fibrous tissue at its border, on the presence or absence of septal AIs, potentially related to VT.
Methods And Results: All consecutive rTOF patients who underwent electroanatomical mapping between January 2005 and March 2023 with an available surgical report providing VSD details (n = 91) were included.
Rev Cardiovasc Med
November 2024
Children's Heart Institute, UT Health McGovern Medical School, Houston, TX 77030, USA.
This review addresses the diagnosis and management of ventricular septal defects (VSDs). The VSDs are classified on the basis of their size, their number, and their location in the ventricular septum. Natural history of VSDs includes spontaneous closure, development of pulmonary hypertension, onset of infundibular obstruction, and progression to aortic insufficiency.
View Article and Find Full Text PDFWorld J Pediatr Congenit Heart Surg
January 2025
Queensland Pediatric Cardiac Service, Queensland Children's Hospital, South Brisbane, Queensland, Australia.
bioRxiv
September 2024
Department of Biomolecular Sciences, School of Pharmacy, University of Mississippi, Oxford, MS.
Voltage-gated sodium (Na) channels are pivotal for cellular signaling and mutations in Na channels can lead to excitability disorders in cardiac, muscular, and neural tissues. A major cluster of pathological mutations localizes in the voltage-sensing domains (VSDs), resulting in either gain-of-function (GoF), loss-of-function (LoF) effects, or both. However, the mechanism behind this functional divergence of mutations at equivalent positions remains elusive.
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