Why Do Aortas Cleave or Dilate? Clues from an Electronic Scanning Microscopy Study in Human Ascending Aortas

Author(s)

Borges, Luciano Figueiredo ^{[1, 2]} ; Blini, Joao Paulo Forato ^[1] ; Dias, Ricardo Ribeiro ^[3] ; Gutierrez, Paulo Sampaio ^[1]

Affiliation

^[1] Univ Sao Paulo, Fac Med, Hosp Clin, Pathol Lab, Sao Paulo - Brazil

^[2] Univ Fed Minas Gerais, Dept Morphol, Belo Horizonte, MG - Brazil

^[3] Univ Sao Paulo, Fac Med, Hosp Clin, Div Surg, Heart Inst InCor, Sao Paulo - Brazil

• Document type: Journal article
• Source: JOURNAL OF VASCULAR RESEARCH; v. 51, n. 1, p. 50-57, 2014.
• Web of Science Citations: 2

Abstract

In ascending aorta aneurysms (AscAA) the whole vessel wall dilates, while in aortic dissections (AD) the wall cleaves into two sheets. Both may present fine elastic fragmentation and a decrease in collagen. We analyzed whether alterations in the three-dimensional structure of these fibers could be involved in the pathogenesis of AscAA/AD. Specimens obtained at surgery for these diseases (n = 4 for each) and on coronary artery bypass surgery (controls, n = 4) were submitted to treatments which either preserve collagen or the elastic structure. These samples were examined by scanning electron microscopy. In all groups most of the collagen fibers were packed, forming laminar structures very similar to the elastic lamellae. In AscAA/AD, the fibers showed signs of degradation and/or fragmentation. Elastic tissue was distributed in large sheets with fenestrations, with smaller branches between them. In 1 of the dissection cases and 2 of the aneurysm cases elastic sheet fragmentation, which under light microscopy seems to be located at random, had a pattern of clefts which were irregular but approximately transversal to the main axis of the wall. The recognition of this pattern and the degradation/fragmentation of collagen and elastic fibrils facilitates understanding of why the wall is weak and affected by aneurysms and dissections. (C) 2013 S. Karger AG, Basel (AU)