A simple catheterization technique for producing suppression or block of atrioventricular (AV) conduction in dogs by neodymium:YAG (Nd:YAG) laser photocoagulation from the aortic root is described. In 14 canines, electrode catheters were percutaneously advanced to the high right atrium, to the His bundle area at the tricuspid valve (right His [RH]), and the noncoronary cusp of the aortic valve (left His [LH]). A 400 microns optical fiber was fed into the lumen of the LH catheter. Continuous wave Nd:YAG lasing at lambda = 1,064 nm at 15-20 watts was performed at the site of the largest recorded LH deflection, opposite to the RH catheter, until complete AV block (CAVB, group I, eight dogs) or persistent A-H prolongation (AHPr, group II, four dogs) occurred; in two animals, laser photoablation was unsuccessful. CAVB and AHPr were achieved in < 140 seconds of lasing. Mean lasing time was 51 +/- 41 seconds, total energy delivered, 776 +/- 601 J. There were no complications. Dogs were followed for up to 120 days. In group I, 6/6 dogs followed for at least 1 week continued to have CAVB (three AV nodal, five infra-His). In group II, 1/4 dog progressed to infra-His CAVB; 3/4 had depressed AV nodal function. AV block was not reversed by isoproterenol. Aortic root angiograms revealed intact valve function in all. Histology showed various degrees of damage and repair of AV junctional tissue. There were no valvular perforations. Transcatheter Nd:YAG laser photocoagulation of the AV junction from the aortic root is a fast, simple, and safe method for creating AV conduction block in dogs.
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http://dx.doi.org/10.1111/j.1540-8159.1993.tb01601.x | DOI Listing |
JACC Case Rep
January 2025
Heart, Vascular, and Thoracic Institute, Cleveland Clinic London, London, United Kingdom.
We describe the case of a 52-year-old man with radiation-induced severe mixed aortic and mitral valve disease, thickening of the aortomitral continuity, mitral annular calcification, and porcelain aorta with limited transcatheter treatment options. By replacing the aorta during circulatory arrest, we demonstrate that it is possible to clamp the ascending aorta to facilitate prosthetic aortic and mitral valve replacement.
View Article and Find Full Text PDFTrials
January 2025
Department of Vascular Surgery, The Fourth Affiliated Hospital, Zhejiang University School of Medicine, Yiwu, Zhejiang, China.
Background: Thoracic aortic pathologies involving the aortic arch are a great challenge for vascular surgeons. Maintaining the patency of supra-aortic branches while excluding the aortic lesion remains difficult. Thoracic EndoVascular Aortic Repair (TEVAR) with fenestrations provides a feasible and effective approach for this type of disease.
View Article and Find Full Text PDFJ Vasc Surg
January 2025
Division of Vascular and Endovascular Surgery, Mayo Clinic, Rochester MN, USA. Electronic address:
Objectives: Celiac artery (CA) incorporation during FB-EVAR for complex abdominal aortic aneurysms (cAAA) is typically performed with fenestrations. Double-wide scallops (DWS) can be used when appropriate. We aimed to assess outcomes of patients treated with DWS for the CA during FB-EVAR for cAAA.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
January 2025
Department of Cardiovascular Medicine, The University of Tokyo, Bunkyo-ku, Japan. (H. Yagi, H.A., Q.L., A.S.-K., M.U., H.K., R.M., A.S., S.O., H.T., Norifumi Takeda, I.K.).
Background: Marfan syndrome (MFS) is an inherited disorder caused by mutations in the gene encoding fibrillin-1, a matrix component of extracellular microfibrils. The main cause of morbidity and mortality in MFS is thoracic aortic aneurysm and dissection, but the underlying mechanisms remain undetermined.
Methods: To elucidate the role of endothelial XOR (xanthine oxidoreductase)-derived reactive oxygen species in aortic aneurysm progression, we inhibited in vivo function of XOR either by endothelial cell (EC)-specific disruption of the gene or by systemic administration of an XOR inhibitor febuxostat in MFS mice harboring the missense mutation p.
Cureus
December 2024
Internal Medicine, Icahn School of Medicine at Mount Sinai, Queens Hospital Center, New York, USA.
Marfan syndrome (MFS), an inherited connective tissue disorder, is caused by a mutation in the FBN1 gene. MFS is characterized by complex manifestations involving musculoskeletal, cardiovascular, and ocular systems. The usual presentation for suspecting diagnosis in an individual with aortic root disease is tall stature in addition to other features that fulfill Ghent criteria.
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