Acute Aortic Disease.. - Index of

206 Shahriari and Farkas
properties of the aorta, whereas collagen provides tensile strength. Histologic
examination of human aneurysmal aortic tissue has documented fragmentation
and decreased concentration of elastin. While this compromise in the quality and
quantity of the elastin contributes to the dilatation of the aorta (6–8), it does not
markedly decrease the tensile strength. As demonstrated in rodent experiments,
transgenic animals that do not produce elastin will form aortic aneurysms, yet will
not succumb to rupture. If there is degradation of the collagen in the same
elastin-deficient animal, however, susceptibility to rupture is demonstrated. The
loss of the elastic properties in the aortic wall seems to be compensated by an
increase in collagen synthesis during the early stages of aneurysm formation (9).
Later in the disease process, collagen degradation exceeds its synthesis and this
culminates in rupture (10).
Over the last decade, much research has been focused on the enzymes involved
in the degradation of elastin and collagen. The imbalance between proteases such as
matrix metalloproteinases (MMPs) and their inhibitors [e.g., tissue inhibitors of
metalloproteinases-2, Plasminogen activator inhibitor (PAI)] (11) has been suggested
as a possible mechanism (12–14). New insight into immunologic mechanisms
underlying aneurysm formation and rupture has resulted in emerging
hypotheses regarding the interactions between Th1/ Th2 cytokines (15–18).
Understanding these complex relationships may assist in altering the natural history
of aortic aneurysmal disease in the future.
EPIDEMIOLOGY
Thoracic Aortic Aneurysms
According to a Swedish study (19), the prevalence of asymptomatic thoracic
aortic aneurysms (TAAs) is highest in males 75 to 79 years of age, with a peak
incidence occurring 10 years later in females. Thirty-nine percent of the males
and 27% of the females have coexisting abdominal aortic aneurysms (AAA) or
iliac artery aneurysms. Bickersatff et al. (20) estimated the prevalence of TAA to
be 5.9/100,000 population per year. The incidence of rupture was calculated to
be 5.0/100,000 population per year (21). Our own institutional database outlining
the characteristics of over 1600 patients with TAA has previously shown (22)
a growth rate of 0.19 cm per year, and a mean annual rate of rupture or dissection
of 3% for aneurysms measuring 5.0 to 5.9 cm, and 7.0% for aneurysms greater
than 6.0 cm (Fig. 1) (23).
Risk factors for rupture include vascular disease, female gender, pulmonary
disease, hypertension, size of the aneurysm, chronic obstructive pulmonary disease,
the presence of symptoms, and dissection within the aneurysm (21–23). In
one series (24) 12% of thoracic aortic ruptures were associated with dissection in
aortas less than 5.0 cm. Our institution addressed the impact of relative aortic size
by developing the “aortic size index,” which incorporates the patient’s body
surface area in the measurement (25). Increasing aortic size index was found to