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A Systematic Histopathologic Evaluation of Type-A Aortic Dissections Implies a Uniform Multiple-Hit Causation
Nimrat Grewal1,2, Bart J J Velders1, Adriana C Gittenberger-de Groot2,3
1Department of Cardiothoracic Surgery, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.
Insights
Acute type A aortic dissection (TAAD) is linked to pre-existing medial defects in the ascending aorta. This suggests a developmental issue contributing to TAAD progression via a triple-hit mechanism.
Area of Science:
- Cardiovascular Pathology
- Aortic Diseases
- Histopathology
Background:
- The underlying pathophysiology of acute type A aortic dissection (TAAD) remains poorly understood.
- Investigating vessel wall defects is crucial for understanding TAAD.
- Systematic study of aortic specimens from TAAD patients was conducted.
Purpose of the Study:
- To systematically evaluate vessel wall defects in acute type A aortic dissection (TAAD).
- To identify histopathological differences between TAAD specimens and control tissues.
- To elucidate the pathophysiologic basis of TAAD.
Main Methods:
- Histopathological analysis of ascending aortic wall specimens from 58 TAAD patients.
- Comparison with 17 autopsy-obtained control aortic specimens.
- Systematic evaluation of medial and intimal layers.
Main Results:
- TAAD specimens exhibited significant elastic fiber fragmentation, thinning, degeneration, and medial degeneration.
- Mucoid extracellular matrix accumulation and smooth muscle cell nuclei loss were prevalent in TAAD.
- The dissection plane correlated with the vasa vasorum network, and the intimal layer was significantly thinner in TAAD patients.
Conclusions:
- TAAD is associated with diffuse, pre-existing medial defects in the ascending aorta.
- A hypothesis of a developmental defect underlying TAAD is proposed.
- TAAD progression is attributed to a triple-hit mechanism involving intimal tear, diseased media, and vasa vasorum propagation.
Abstract:
(1) Background: The pathophysiologic basis of an acute type A aortic dissection (TAAD) is largely unknown. In an effort to evaluate vessel wall defects, we systematically studied aortic specimens in TAAD patients. (2) Methods: Ascending aortic wall specimens (n = 58, mean age 63 years) with TAAD were collected. Autopsy tissues (n = 17, mean age 63 years) served as controls. All sections were studied histopathologically. (3) Results: Pathomorphology in TAAD showed predominantly moderate elastic fiber fragmentation/loss, elastic fiber thinning, elastic fiber degeneration, mucoid extracellular matrix accumulation, smooth muscle cell nuclei loss, and overall medial degeneration. The control group showed significantly fewer signs of those histopathological features (none-mild, p = 0.00). It was concluded that the dissection plane consistently coincides with the vasa vasorum network, and that TAAD associates with a significantly thinner intimal layer p = 0.005). (4) Conclusions: On the basis of the systematic evaluation and the consistent presence of diffuse, pre-existing medial defects, we hypothesize that TAAD relates to a developmental defect of the ascending aorta and is caused by a triple-hit mechanism that involves (I) an intimal tear; and (II) a diseased media, which allows (III) propagation of the tear towards the plane of the vasa vasorum where the dissection further progresses.
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