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Ortner's Syndrome: Secondary Laryngeal Paralysis Caused by a Great Thoracic Aorta Aneurysm.

ABSTRACT: Introduction Recurrent laryngeal nerve injury caused by cardiovascular disease is a rare condition, and often it is the only prominent sign of an imminent break of an aortic artery aneurysm. Objective To report left laryngeal paralysis caused by a great aortic arch aneurysm and to highlight the importance of an otorhinolaryngologic evaluation along with a thoracic radiologic study. Resumed Report A 42-year-old man complained of thickness of his voice and dysphagia for 3 months, but no thoracic pain or other relevant complaints. Video laryngoscopy revealed immobility of his left vocal fold in the paramedian position. Imaging was obtained for investigation, including magnetic resonance imaging of his thorax, which showed a fusiform aneurysm in the aortic arch, leading to recurrent compression of the left laryngeal nerve. The patient was successfully treated with endovascular repair of the aneurysm. At 2-month follow-up, there was still no recovery of the laryngeal mobility. Conclusion An aortic artery aneurysm can suddenly break, requiring emergency heart surgery, and the results can be fatal in many cases. We suggest routine exam of the vocal folds in all patients with a heart condition, and we review the literature and suggest the use of imaging to reduce the number of emergency procedures.

SUBMITTER: Zangirolami AC

PROVIDER: S-EPMC4399202 | biostudies-other | 2015 Apr

REPOSITORIES: biostudies-other

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Project description:Mutations in lysyl oxidase (LOX) are associated with thoracic aortic aneurysm and dissection (TAAD). Mice that do not express Lox (Lox-/- ) die soon after birth and have 60% and 40% reductions in elastin- and collagen-specific cross-links, respectively. LOX inactivation could also change the expression of secreted factors, the structural matrix, and matrix-associated proteins that constitute the aortic matrisome. We hypothesized that absence of Lox will change the mechanical behavior of the aortic wall because of reduced elastin and collagen cross-linking and alter the expression levels of matrisome and smooth muscle cell (SMC) genes in a vascular location-specific manner. Using fluorescence microscopy, pressure myography, and gene set enrichment analysis, we visualized the microarchitecture, quantified the mechanical behavior, and examined matrisome and SMC gene expression from ascending aortas (AAs) and descending aortas (DAs) from newborn Lox+/+ and Lox-/- mice. Even though Lox-/- AAs and DAs have fragmented elastic laminae and disorganized SMCs, the unloaded outer diameter and wall thickness were similar to Lox+/+ AAs and DAs. Lox-/- AAs and DAs have altered opening angles, circumferential stresses, and circumferential stretch ratios; however, only Lox-/- AAs have increased pressurized diameters and tangent moduli. Gene set enrichment analysis showed upregulation of the extracellular matrix (ECM) regulator gene set in Lox-/- AAs and DAs as well as differential expression of secreted factors, collagens, ECM-affiliated proteins, ECM glycoproteins, and SMC cell cycle gene sets that depend on the Lox genotype and vascular location. These results provide insights into the local chemomechanical changes induced by Lox inactivation that may be important for TAAD pathogenesis.NEW & NOTEWORTHY Absence of lysyl oxidase (Lox) causes thoracic aortic aneurysms. The aortic mechanical behavior of Lox-/- mice is consistent with reduced elastin and collagen cross-linking but demonstrates vascular location-specific differences. Lox-/- aortas show upregulation of matrix remodeling genes and location-specific differential expression of other matrix and smooth muscle cell gene sets.

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Ortner's Syndrome: Secondary Laryngeal Paralysis Caused by a Great Thoracic Aorta Aneurysm.

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