The Aneurysm Information Project

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    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.