Papers of the Month - March 96

This month is a bonanza, all based on last month's issue
of the JVS.  There are three clinical and two research
papers notable for comment.  First the clinical papers...

1. White GH, et al (Sydney, Australia).  Historic control
comparison of outcome for matched groups of patients
undergoing endoluminal versus open repair of abdominal
aortic aneurysms.  JVS 1996; 23:201-12.

Abstract (adapted from authors):

Purpose: To analyze outcomes of two matched groups of
patients with AAA, one with open repair and the other
with endoluminal repair.

Methods:  The historical cohort was selected from
consecutive patients who underwent open repair between
1991-2, who would have been suitable for endoluminal
repair under the same criteria applied to those who did
undergo endoluminal repair in 1992-4.  Approximately the
same number of patients (27-28) were evaluated in each
group.

Results:  Five of 28 patients in the endoluminal group
had complications requiring early operative repair (3) or
late revision (2).  ...The incidence of local/vascular
complications was significantly greater for the group
with endoluminal repair.

Conclusion:  "In this early experience with prototype
devices, patients who were medically suitable for open
surgical procedures did not derive benefit from the less
invasive endoluminal technique..."

Comment by mdt:  I am often asked by readers of the AIP
home page whether endoluminal repair of AAA is as safe as
conventional repair.  So far, this paper is
representative of the reported experience.  Technological
advances will no doubt come as time goes on, but for the
present the endoluminal procedure has to still be
considered to be investigational.

2. Brown PM, et al (Kingston, Ontario, Canada). 
Selective management of AAA's in a prospective
measurement program.  JVS 1996; 23: 213-22.

Abstract (adapted from authors):

Purpose:  To clarify recommended treatment of patients
with small AAA's < 5 cm in diameter.....

Methods:  492 patients with AAA's < 5 cm were entered
into a prospective measurement program...

Results:  201 patients came to operation because of
increase in size to 5 cm or greater, or for other
reasons.  291 have not undergone operation at a mean
follow-up of 3 1/2 years.  [Although this point was not
emphasized by the authors, only one rupture occurred in
one of the patients entered into the small AAA
surveillance study; and this patient had progressed to 5
cm]

Comment by mdt:  The authors conclude that a
recommendation for elective operation should be strongly
considered for AAA's between 4.5-5.0 cm in a fit patient;
but I can't help wondering whether this bottom line
really follows from the information presented.  Over 1000
life-years accumulated (approximately) in the group under
surveillance, and the cumulative total would no doubt
have been less if a more aggressive surgical policy had
been recommended at the time.

3. Kazmers A, et al.  AAA repair in VA medical centers. 
JVS 1996; 23: 191-200.  

Abstract (adapted from authors):

Purpose:  To define outcomes after AAA repair in the
Veterans Affairs medical centers from 1991-4.

Methods:  All patients with DRG's 110 & 111....

Results: Approximately 5% mortality in 3419 elective
repairs and 47% mortality in 268 rupture repairs.  ....
"Although many lower-volume centers had excellent
results, centers that performed 32 or more repairs tended
to have lower mortality rates."

Conclusions:  Mortality rates were comparable to those
reported in other large series.  Outcomes for veterans
may improve by referring to centers with a greater
operative volume or to lower-volume centers that have
proven excellent results.  

Comment by mdt:  As an academic surgeon who once attended
every third month at a university-affiliated VA hospital,
I applaud the results as reported.  The results are at
least as good and probably better than results overall in
hospitals-in-general throughout the USA.  Our VA has many
critics, who would probably like to see the hospital
system dismantled and turned over to unbridled
entrepreneurship in the private sector.  In the present
era, when providing medical care to patients goes against
the bottom line of insurance companies (and is,
accordingly, discouraged), the VA remains a sanctuary
where patients can be treated according to their needs,
and without regard to whether their "insurance" will
cover what should be done in their best interest.  

About papers 4 and 5:  I will comment on these two papers
briefly in advance of writing very short summaries.  At
the New York Academy of Sciences Symposium on aneurysm
disease a couple of weeks ago, it was evident that the
rat model of AAA  developed by Sammy Anidjar of France in
collaboration with Phil Dobrin of Chicago (at least until
recently: he's moving to Salt Lake City) had become
highly useful as a tool for evaluating potential
pharmacological interventions to modify the natural
history of the diseae in susceptible persons.  Of course,
the rats aren't really susceptible "persons", but you
have to start somewhere....

4. Petrinec D, et al.  Doxycycline inhibition of
aneurysmal degeneration in an elastase-induced rat model
of AAA: Preservation of aortic elastin associated with
suppressed production of 92 kD gelatinase.  JVS  1996:
23: 336-46.

Comment by mdt:  Several studies noted in previous Papers
of the Month have documented the important role of matrix
metalloproteinases (MMP's) in the enzymatic destruction
of the aorta that occurs during progression of AAA
disease.  Some members of the family of antibiotics
related to tetracycline (like doxycycline) have the
interesting property of inhibiting the activity of MMP's
by mechanisms distinct from their antimicrobial
properties.  In the experimental model, the incidence of
AAA was reduced from 83% (control, saline) to 8%
(doxycycline).  The reader is referred to the original
article to enjoy this beautifully illustrated scientific
paper.


5. Ricci MA et al.  Anti-CD 18 monoclonal antibody slows
experimental aneurysm expansion.  JVS  1996; 23: 301-7.

Comment by mdt:  The rationale for this experiment was
quite similar to the one above, but these investigators
took a different approach to blocking the inflammatory
process in the experimental model.  The 92 kDa MMP
referenced above is a product of the activated
macrophage, so Ricci et al performed this experiment to
determine whether an antibody broadly directed against
the macrophage and other leukocytes would blunt the
aneurysm-forming response in the Anidjar/Dobrin model. 
It did; reducing the size of the aorta by about 50% at 14
days.  This study and the preceding one are steps on the
way to developing interventions that may stop the
progression of small aneurysms to a size where there is
significant risk of rupture.