Aneurysm Papers of the Month - October 1996

1. Cole CW, Hill GB, Millar WJ, Laupacis A, Johnston KW.  Selective
screening for AAA.  Chronic Diseases in Canada  (1996) 17: 51-55.

Abstract (based on wording of authors):

Introduction:  AAA meets the criteria as a possible target for
early detection by screening (high prevalence, high case-fatality
rate, treatable, preclinical phase when detectable safely, and
acceptable to target population); but cost-effectiveness, meaning
that money spent would not be better spent in some other way, has
never been proven.  The cost-effectiveness of screening might be
enhanced by focusing on people with higher than average risk of
harboring latent disease.

Method: Data from a hospital-based, case-control study involving 78
men with AAA and 99 male controls were used to derive a risk
function based on age, smoking, high blood pressure, history of
heart disease, body mass index, and serum high-density lipoprotein. 
The risk of AAA was estimated and multiplied by the expectation of
life to give a measure of potential benefit, and the proportion of
the total potential benefit that would be obtained screening only
those with a given level of risk was calculated.

Result: In order to obtain 80% of the total potential benefit among
men, 52% of the elderly population would have to be examined if
using a risk function based on age alone.  If age plus smoking were
used, 35% would have to be screened.  If age plus all risk factors
were used, only  17% would require screening.

Conclusion: Selective screening appears to be a promising strategy;
but a prospective study would be required to demonstrate that the
predictions are valid.

Comment by mdt: Interesting approach.  Nice work.

2. Predictors of death in nonruptured and ruptured AAA's.  Chen JC,
Hildebrand HD, Salvian AJ, Taylor DC, Strandberg S, Myckatyn TM,
Hsiang YN.  J Vasc Surg 1996; 24: 614-23.

Abstract (condensed from authors):

A consecutive review of all patients having AAA surgery (478
nonruptured, 157 ruptured) at Vancouver General Hospital from Jan
84 to Dec 93.  Independent predictors of perioperative death
(overall 3.8%) in nonruptured cases were prolonged ventilation,
perioperative myocardial infarction, history of peripheral vascular
disease, perioperative renal dysfunction, and a history of
congestive heart failure.  In  ruptured cases (overall mortality
46%), the preoperative predictors were age, level of consciousness,
and cardiac arrest.  For unconscious patients who had sustained a
cardiac arrest, the mortality rates were 88% at age 60, 93% at age
70, 96% at age 80, and 99% at age 90.  

Comment by mdt: Sounds like getting old may be dangerous for your
health.  As the authors point out in the Discussion: "The decision
to withhold therapy or to terminate aggressive life support must
never be a simple reflex response derived by some general formula
or criteria.  However, mortality risk estimates can be helpful as
a reference point for both the surgeon and the patient's family
when such options are contemplated."  

Papers like this are probably noticed by the insurance providers
who appear to be systematically engaged in rationalizations to deny
medical benefits to their "covered lives."  

3. Elastase-induced matrix degradation in arterial organ cultures:
An in-vitro model of AAA disease.  Wills A, Thompson MM, Crowther
M, Brindle NP, Nasim A, Sayers RD, Bell PRF.  J Vasc Surg 1996; 24:
667-79.

Abstract (condensed from authors):

Porcine aortic organ cultures were preincubated with pancreatic
elastase before culture in standard conditions for up to 14 days. 
Although exogenous elastase was removed after 24 hours, substantial
degradation of the aortic ECM occurred in the subsequent 13 days,
with elastin degradation occurring in a time-dependent manner (p <
.001) not confined to the initial phase of exogenous elastase
activity.  There was a time related release of MMP's, and MMP's
1,2,3, and 9 were detected by Western blots.  The vascular SMC was
the source of MMP's 1,2, and 3.  Addition of autogenous leucocytes
initiated an inflammatory infiltrate, which enhanced matrix
degradation and MMP production (P < 0.001).  

Comment by mdt: *VERY* nice work.  The development of an in-vitro
model is a *major* contribution to the field and should lead to a
much better understanding of the molecular signals that are
exchanged among the cell types involved.  The authors add the
disclaimer that the "model cannot be regarded as analagous to human
aneurysmal disease because of the lack of an atherosclerotic
component," but I don't think they should spend much time worrying
about that.  We will be publishing a brief communication in the
soon forthcoming Annals of the New York Academy of Sciences
(devoted to AAA), with the hypothesis that ! aneurysms cause
atherosclerosis.