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http://dx.doi.org/10.3174/ajnr.A5924 | DOI Listing |
Ann Vasc Surg
January 2025
Department of for Cardiovascular Surgery, University Heart Centre Freiburg - Bad Krozingen, University Medical Centre Freiburg, Freiburg, Germany; Faculty of Medicine, Albert Ludwigs University Freiburg, Freiburg, Germany.
Objectives: To report outcomes after the use of the Omniflow II biosynthetic graft (LeMaitre Vascular, Il, USA) for vascular reconstruction in patients with prosthetic infection at the aorto-iliac and femoropopliteal level.
Methods: Within a six-year period, all consecutive patients with aorto-iliac and femoro-popliteal graft infection treated by resection of the infected graft material, extensive local debridement and reconstruction using Omniflow II biosynthetic graft were retrospectively analzyed. Patient characteristics, intraoperative details, postoperative outcomes, and infection details were assessed.
J Vasc Surg Cases Innov Tech
April 2025
Unit of Vascular Surgery, Fondazione Policlinico Universitario Gemelli IRCCS, Rome, Italy.
Front Genet
January 2025
Sichuan Provincial Key Laboratory for Genetic Disease, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Marfan syndrome (MFS) is an inherited disorder that affects the connective tissues and mainly presents in the bones, eyes, and cardiovascular system, etc. Aortic pathology is the leading cause of death in patients with Marfan syndrome. The fibrillin-1 gene () is a major gene involved in the pathogenesis of MFS.
View Article and Find Full Text PDFJTCVS Open
December 2024
Division of Pediatric Cardiac Surgery, Department of Cardiothoracic Surgery, Stanford University, Palo Alto, Calif.
Objective: The study objective was to investigate the effect of free-edge length on valve performance in bicuspidization repair of congenitally diseased aortic valves.
Methods: In addition to a constructed unicuspid aortic valve disease model, 3 representative groups-free-edge length to aortic diameter ratio 1.2, 1.
Metabolic syndrome (MetS) is associated with osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs) and accumulation of arterial calcifications (ACs). Metformin (MET) inhibits this transdifferentiation in vitro. Here, we evaluate the in vivo efficacy of oral MET to reduce AC in a model of MetS.
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