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January, 1998
l. Matsumura JS and Pearce WH. Endovascular grafting for aortic
aneurysms: the learning curve and long-term outcome.
Cardiovascular Surgery 1997; 5: 557-8.
Abstract (adapted from authors):
"As with all new technology, there is a learning curve, and,
perhaps more important, the long-term outcome of the endovascular
graft is unknown." The authors proceed to ennumerate some of the
most important lessons of scaling the learning curve, including 1)
the sentinel significance of the "endoleak", 2) widespread
convergence of design of rigid support for bifurcated limb grafts,
3) the use of stiff guidewires during insertion, 4) re-engineering
attachment systems prone to metal fatigue, 5) improved patient
selection (eg excluding candidates with thrombus within the
anticipated attachment system deployment site; 6) and the role of
thin-cut computed tomography with delayed images and careful size
surveillance during long-term followup.
The authors express serious concern that five groups have now
reported on the phenomenon of gradual expansion of the aorta at the
deployment site during long term followup. There have also been
reports of patients who initially appear to have had a complete
thrombosis of the aneurysm sac and then develop a subsequent
endoleak. "...it is possible that the dilatation of the aortic
waist will lead to unsealing of an endovascular graft from the
wall, with development of reperfusion of the aneurysm sac, aneurysm
growth, and rupture. Delayed rupture recently has been identified
in the EVT trial."
Comment by mdt: The authors express some of the same concerns that
have been articulated by ourselves and others on this homepage. We
are still a long way from having the confidence that the long-term
results of the stent graft will prove to be as durable as the
conventional surgical repair.
2. Weck KE, Canto AJD, Gould JD, et al. Murine gamma-herpesvirus
68 causes severe large-vessel arteritis in mice lacking interferon-
gamma responsiveness. A new model for virus induced vascular
disease. Nature Medicine, 1997; 3: 1346-1353.
Abstract (from authors):
Fundamental issues remain unresolved regarding the possible
contribution of viruses to vascular pathology... Here we
demonstrate that infection of mice with gammaHV68 provides a novel
model for addressing these issues. IFN-g null mice died weeks to
months after infection with severe large vessel panarteritis. ...
These studies demonstrate that IFN-g is essential for control of
chronic vascular pathology induced by this virus.
Comment by mdt: The above very brief description of this paper
does not do justice to anything other than the principal finding,
so for those interested in the field of inflammation and vascular
disease, I recommend a close reading of the original. Among many
other interesting findings, the authors observe that the aortic
smooth muscle cell may be a site of latent virus, and that the
subendothelium of IFN-g null mice becomes infiltrated with lipid as
in human atherosclerosis. For someone like myself with an interest
in the role of inflammation in AAA disease, I was impressed by the
amount of chronic inflammatory change in the adventitia. Although
the authors mention parallels of the observed lesions with those of
Kawasaki's Disease, they do not comment on any aneurysmal
dilatations in this model. We raised the hypothesis in 1996 that
herpes may be implicated in aneurysm pathobiology as a molecular
mimic, as herpes and CMV have amino acid sequence motifs that occur
in some of the aortic-adventitial-specific proteins that we have
recently described. Thus, we continue to watch developments in
this field with keen interest.