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Chronic Type A aortic dissection: could surgical intervention be guided by molecular markers?

机译:慢性A型主动脉夹层:能否在分子标记物的指导下进行外科手术?

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摘要

Aortic dissection, occurring following a separation of the layers constituting the complex vascular walls, leads to the formation of a 'false' lumen and disrupts the regulation of aortic wall homeostasis and function. This clinical condition still represents an important health problem and is associated with high mortality. Its natural history mandates surgical intervention when exceeding 55 mm in diameter and involving the ascending portion of the aorta (Type A), on the bases of an anatomical classification dated back to 1965. An intriguing question rising is whether a dissection that overcomes that critic acute phase has still the indication to surgical intervention. Molecular analysis of chronic dissected aortic walls could help in understanding how morphology and structure are affected and whether tissue homeostasis is re-established. Thus, pursued by this consideration, we made a histological and immunohistochemical characterization of a chronic Type A dissection, reporting three major findings: endothelial cells line the aortic primitive lumen, as well as the 'false' one; walls of primitive and 'false' lumina are comparable in thickness; vascular layers in the 'false' lumen are made up of terminally differentiated cells. This evidence obtained in a single specimen encourages a meditation on the compulsory indication for surgical intervention. © 2011 The Authors Journal of Cellular and Molecular Medicine © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
机译:在构成复杂血管壁的层分离之后发生的主动脉夹层导致“假”管腔的形成,并破坏了主动脉壁稳态和功能的调节。这种临床状况仍然代表着重要的健康问题,并伴有高死亡率。它的自然历史要求对直径超过55毫米并累及主动脉上升部分(A型)的外科手术进行干预,其历史可追溯到1965年。根据这个解剖学分类,一个令人感兴趣的问题是,能否通过解剖来克服这种批评阶段仍是手术干预的指征。慢性解剖主动脉壁的分子分析可以帮助理解形态和结构如何受到影响以及组织稳态是否得以重建。因此,出于这种考虑,我们对慢性A型夹层进行了组织学和免疫组织化学表征,报告了三个主要发现:内皮细胞系在主动脉原始管腔内,还有“假”管腔。原始和“假”灯的壁厚可比。 “假”管腔中的血管层由终末分化的细胞组成。在单个标本中获得的这一证据鼓励人们冥想对手术干预的强制性指征。 ©2011作者,细胞与分子医学杂志©2011细胞与分子医学基金会/ Blackwell PublishingLtd。

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