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主动脉夹层动脉瘤的发病机制。中膜改变意义的比较组织病理学研究。

Pathogenesis of dissecting aneurysm of aorta. Comparative histopathologic study of significance of medial changes.

作者信息

Schlatmann T J, Becker A E

出版信息

Am J Cardiol. 1977 Jan;39(1):21-6. doi: 10.1016/s0002-9149(77)80005-2.

Abstract

In previous investigation of the normal aging aorta, the claimed specificity of alterations in the media in the pathogenesis of dissecting aneurysm of the aorta was challenged. The concept was promoted that these changes are nonspecific and caused by general hemodynamic events within the aorta. In this investigation the aortic media was studied in patients with a dilated ascending aorta, whose hemodynamic profile is known to be altered. The results were compared with data obtained from the study of aortas with complete or incomplete dissection and aortas from patients with Marfan's syndrome, a condition known to predispose to dissection. Only quantitative differences were found between the normal "aging" aorta and the overtly abnormal aorta. The pathogenesis of dissected aneurysm, therefore, is considered to be initiated by processes if injury and repair within the aortic wall, consequent to hemodynamic forces. The histologic features of the media previously implicated as the specific underlying defect appear to represent the morphologic substrate of this traumatizing and reparative process. This process may gradually lead to dilatation of the aorta and, according to Laplace's law, a vicious cycle may ensue that may lead to further complications. Local circumstances determine whether a dilated aorta will rupture or whether an incomplete or complete dissection will occur. The fact that the aorta in patients with Marfan's syndrome shows basically the same structural alterations supports the concept proposed. The underlying connective tissue disorder in these patients will lead to complications at an earlier age. Dissecting aneurysm therefore is part of a spectrum of lesions that have as a common denominator the process of injury and repair.

摘要

在先前对正常衰老主动脉的研究中,有人对主动脉中膜改变在主动脉夹层动脉瘤发病机制中所宣称的特异性提出了质疑。有人提出这样一种观点,即这些改变是非特异性的,是由主动脉内一般的血流动力学事件引起的。在本研究中,对升主动脉扩张患者的主动脉中膜进行了研究,已知这些患者的血流动力学特征发生了改变。将结果与从完全或不完全夹层的主动脉以及马方综合征患者的主动脉研究中获得的数据进行了比较,马方综合征是一种已知易发生夹层的疾病。在正常“衰老”主动脉与明显异常的主动脉之间仅发现了数量上的差异。因此,夹层动脉瘤的发病机制被认为是由血流动力学力量导致的主动脉壁内损伤和修复过程引发的。先前被认为是特定潜在缺陷的中膜组织学特征似乎代表了这种创伤和修复过程的形态学基础。这个过程可能会逐渐导致主动脉扩张,根据拉普拉斯定律,可能会形成一个恶性循环,进而导致进一步的并发症。局部情况决定了扩张后的主动脉是否会破裂,或者是否会发生不完全或完全夹层。马方综合征患者的主动脉显示出基本相同的结构改变这一事实支持了所提出的概念。这些患者潜在的结缔组织疾病会在更早的年龄导致并发症。因此,夹层动脉瘤是一系列以损伤和修复过程为共同特征的病变的一部分。

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