Aneurysm Papers of the Month - October 1995

1. McMillan WD, Patterson BK, Keen RR, Pearce WH.  In
situ localization and quantification of 72 kDa Type IV
collagenase in aneurysmal, occlusive, and normal aorta. 
J Vasc Surg  1995; 22:295-305.

Abstract (condensed from authors): 

     Background:  72-kDa Type IV collagenase (MMP-2) is
a potent collagenase and elastase.  Alteration in
expression of MMP-2 or its inhibitor (TIMP-2) could
increase extracellular matrix degradation and contribute
to aneurysm formation.

     Methods:  Total RNA extracted from AAA (n=8),
Occlusive (n=9), and Normal (n=7) tissue was analyzed by
Northern blotting, with normalization of signals to
alpha-tubulin.  In-situ hybridization studies were
carried out in histological sections from a smaller
number of AAA and controls. 

     Results: Tissue MMP-2 levels were significantly
greater in AAA than in either OCC or NOR (p < .02 and
<.002 respectively).  Differences in TIMP-2 levels were
NS.   In situ studies localized MMP-2 and TIMP-2
expression to vascular smooth muscle cells and
macrophages surrounding inflammation in AAA adventitia;
whereas expression of these mRNA's occurred in
atherosclerotic plaque in OCC aorta.

     Conclusion: Differential patterns of expression of
MMP-2 are observed in AAA vs atherosclerotic occlusive
diseased aorta.

Comment by mdt:  The Pearce laboratory at Northwestern
continues its stream of important contributions to the
understanding of aneurysm disease.  Since our research
group (and also Thompson & colleagues in St. Louis) have
had rather similar results with MMP-9, the present
findings re MMP-2 are not surprising.  Based on the early
substrate gel enzymography approaches of Brophy et al and
Herron et al, I would guess that the more important
elastolytic activity of the two would be MMP-9.


2.  Wolf YG, Otis SM, Schwend RB, Bernstein EF. 
Screening for abdominal aortic aneurysms during lower
extremity arterial evaluation in the vascular laboratory. 
J Vasc Surg 22: 417-23, 1995.

*A MOMENT OF SILENCE PLEASE*

     To mark the passing of Gene Bernstein.  Gene was an
important contributor to the aneurysm field, especially
in his analyses related to aneurysmal enlargement.  He
was also a good friend.  I and everyone else in the
vascular surgical/biological community will miss him.


Abstract (condensed from authors): 

Purpose: To evaluate cost-effectiveness of screening for
AAA during routine noninvasive lower extremity
examinations.

Methods: 531 pateints screened over a 30 month period

Results:  See paper for a wealth of detail.  The most
important findings were that the prevalence of AAA was
6.7% in the population in whom the aorta was visualized. 
It was 15.2% in male smokers over 65 y/o.  Detection of
one aneurysm in the male smokers over 65 took an total of
36 minutes of screening time and cost about $240/AAA
identified.

Conclusion:  Screening for AAA during lower extremity
eval addresses a high-risk population, is cost-effective,
and should be consider appropriate and valuable.

Comment by mdt.   I agree completely, but I want to
mention something referred to in my Ottowa lecture as the
"fallacy of spurious causation."  This fallacy can occur
when one cause has joint observable effects.  This
population is high-risk, not necessarily because it is
atherosclerotic, but because AAA and athero are joint
observable effects of smoking.  One or both conditions
will be expressed in the phenotype depending on the
genetic susceptibilities to each disease.  More about
this in future communications, but a resident on research
time in my lab last year has developed an interesting new
theory about the effects of smoking on collagen and
elastin.