A Systematic Histopathologic Evaluation of Type-A Aortic Dissections Implies a Uniform Multiple-Hit Causation.

Nimrat Grewal,Bart J J Velders,Adriana C Gittenberger-De Groot,Jan H N Lindeman,Robert J M Klautz,Robert Poelmann,Thomas J Van Brakel

doi:10.3390/jcdd8020012

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.

Highlights

An acute aortic dissection is a medical catastrophe [1] with an estimated mortality of 26% in patients undergoing acute surgery and up to 58% in patients not receiving surgical treatment [2]
Chi-square test was used to compare the morphology between the dissection and the control group
Putative aortic wall abnormalities in TAAD were mapped according to the revised, consensus nomenclature for noninflammatory, degenerative aortic histopathologies [9]. Conclusions for this systematic evaluation of TAAD wall and control aorta are summarized in Table 3 and Figure 3

Summary

Introduction

An acute aortic dissection is a medical catastrophe [1] with an estimated mortality of 26% in patients undergoing acute surgery and up to 58% in patients not receiving surgical treatment [2]. Reported incidences of an aortic dissection vary between 3 and 9 per. An aortic dissection is hallmarked by a tear in the intimal layer, which allows blood to access the middle layer of the wall, causing the vascular layers to separate (dissect) from one another, resulting in formation of a ‘’false” lumen. One or multiple re-entry tears downor upstream allow flow in the false lumen. Pressure build-up in the false lumen may result in compression of the aortic side branches. Depending on the degree of occlusion, and the side branches involved, this may result in life-threatening ischemia

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Conclusion