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Note to the reader: For a while I have been trying to put up
direct pointers to the referenced papers, but unfortunately
they move around and the links often fail to work. Accordingly,
I am going back to the old format. To retreive the abstract or
order a copy of the paper, the reader may always search one
or more of the authors, or a title keyword, on MedLine. There
is a pointer to MedLine at the bottom of my homepage.
#1. Dobrin PB. Animal models of aneurysms. Annals of
Vascular Surgery 1999; 13: 641-648.
Comment by mdt: This comprehensive reference is highly
recommended for laboratory workers interested in the problem
of aneurysms. Dobrin has made pioneering contributions of
his own toward the development of the elastase-infusion
model (in collaboration with Anidjar), and among all of the
animal models, this one is perhaps the most informative.
#2. Lawrence PF, et al. THe epidemiology of surgically
repaired aneurysms in the United States. J Vasc Surg
1999; 30: 632-40.
Comment by mdt: Lawrence and colleagues have prepared
an extensive report based on data collected from the
National Hospital Discharge Survey, which is a
comprehensive database of patients hospitalized in
non-federal acute-care hospitals in the USA. In 1994
there were 51,949 non-cerebral aneurysm repairs in
the USA. Seventy-five % (about 39,000) were for AAA.
Operative mortalities were 8.4% for elective, and 68%
for emergency repair. The reader is referred to the source
for additional interesting detail re effects of geographical
distribution and hospital size.
#3. Hirose H, Tilson MD. Negative genetic risk factor
for AAA: HLA-DQ3, a Japanese study. J Vasc Surg
1999; 30: 959.
Comment by mdt: This brief communication was a letter
to the Editor of the JVS regarding a followup finding
among the AAA patients previously reported. The
initial report suggested that HLA-DR 15 was a positive
risk factor; and the present report suggests that
HLA-DQ3 is a negative risk factor. Altogether, 89%
of 36 patients were either DR15 positive or DRQ3
negative. It remains to be seen whether these genes
have etiologic significance in AAA disease or whether
they are markers for the presence of other pathogenetic
genes. It also remains to be seen whether the
effects are independent or due to linkage disequilibrium.
Finally, it remains to be seen whether findings in
the relatively homogeneous population of Japan will
apply to the more mixed population of North America.