To return to the home page, click here
Papers of the Month - August 1997
1. RA White, Donayre CE, Walot I, Kopchok GE, Wilson EP, deVirgilio
C. Regression of an AAA after endograft exclusion. J Vasc Surg
1997; 26: 133-7.
Abstract (adapted from authors). The authors describe the
regression of a 6.5 cm AAA in a 71 y/o patient within one year of
aortic endograft placement. The aneurysm decreased to 4 cm at 3
months, and it was 3.3 cm at 8 months. By one year it had
regressed completely, with mild shortening and angulation of the
unsupported body of the prosthesis.
Comment by mdt: Although others have described the phenomenon of
aneurysm regression after endoluminal exclusion, this may be the
first report of "complete" regression. Why should an aneurysm
regress once it is no longer under arterial pressure? I don't know
the answer, but, as usual, I am willing to speculate.
The most robust hypothesis that we have ever worked on in lab is
that the AAA is an autoimmune disease of maturity, like rheumatoid
arthritis. Over the last two years, we have partially
characterized four aortic proteins that appear to be autoantigens
(more about the last 3 in the September 97 Papers of the Month).
Two of these putative matrix proteins appear to resemble cell
adhesion molecules, in so far as they have lengthy (~100 residue)
immunoglobulin-like domains. Accordingly, we have suggested the
name "MatCAMs". We have examined the regional distribution of one
of the MatCAMs, and it appears to be limited to the aorta; in other
words, aorta-specific. So, how does the adventitial fibroblast
know that it is in the aorta, instead of someplace else like the
pulmonary artery? Perhaps pressure-induced or deformation-induced
signal transduction informs the fibroblast that it is in the aorta,
instead of some other place in the universe. We hypothesize that
the cell responds by making an aorta-specific MatCAM. Once the
pressure is off, the fibroblast downregulates autoantigen
production in the adventitia, and the inflammation resolves. The
same scenario might explain the regression of the tissue mass of
inflammatory aneurysms, once they are repaired. This hypothesis
would be testable by measuring MatCAM production by stretched and
unstretched fibroblasts in an in-vitro device.
2. Grange JJ, Davis V, Baxter BT. Pathogenesis of AAA: an update
and look toward the future. Cardiovascular Surgery 1997; 5: 256-
65.
Quoting the authors:
"Enhanced by the convergence of matrix biochemistry, cell biology
and immunology, this work is providing important new insight into
how matrix metabolism is regulated in the diseased aorta. The
focus is now on the inflammatory process and its regulation of the
matrix remodeling which occurs with AAA. .... Given the progress
of the past decade, we can expect the identification of aneurysm-
associated genes and clinical trials of anti-inflammatory
medications and protease inhibitors as we enter the 21st century."
Comment by mdt: This comprehensive, splendid paper is *must*
reading for every serious scientific student of AAA disease.