Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Mar;67(3):271-276.
doi: 10.1007/s11748-019-01066-x. Epub 2019 Jan 28.

Etiology of aortic dissection

Affiliations
Review

Etiology of aortic dissection

Koichi Akutsu. Gen Thorac Cardiovasc Surg. 2019 Mar.

Abstract

We discuss the etiology of aortic dissection (AD) from various points of view. The development of AD requires two pathological conditions: medial degeneration and mechanical wall stress. First, histopathological findings of medial degeneration are hypothesized to be due to a loss of elastic fibers and interconnecting elastic fibers. Damage to the vasa vasorum plays a key role in creating an entry site. The clinical causes of medial degeneration include hypertension, aortic aneurysms, obstructive sleep apnea, and connective tissue disorders. Second, mechanical wall stress is supposedly induced by shear stress caused by blood flow, together with hypertension and aortic root movement. Further investigation is necessary in the search for mechanisms responsible for medial degeneration prior to AD development.

Keywords: Aortic dissection; Connective tissue disorder; Etiology; Medial degeneration; Shear wall stress; Vasa vasorum.

PubMed Disclaimer

References

    1. Circulation. 1999 Apr 27;99(16):2138-43 - PubMed
    1. JAMA. 2000 Feb 16;283(7):897-903 - PubMed
    1. Eur J Cardiothorac Surg. 2000 Apr;17(4):468-73 - PubMed
    1. Am J Respir Crit Care Med. 2003 Dec 15;168(12):1528-31 - PubMed
    1. Medicine (Baltimore). 1958 Sep;37(3):217-79 - PubMed

MeSH terms

LinkOut - more resources