OBJECTIVE: To develop a new saccular aneurysm model in vitro using ela
stase to study aneurysm initiation, growth, and rupture and to create
a new in vivo aneurysm model to test endovascular therapies. METHODS:
Seventeen common carotid arteries excised from freshly killed pigs and
sheep were treated with seven different methods of elastase delivery.
The arteries were mounted in a saline-filled flow chamber. They recei
ved pulsatile flow for 48 hours, or until the resulting aneurysms rupt
ured. Changes were continuously monitored with video camera recordings
and validated with histological sections. RESULTS: All eight arteries
treated topically, either on the intimal or on the adventitial surfac
e, with elastase concentrations greater than 1 U/mm(2), developed sacc
ular aneurysms; five of them ruptured within 48 hours. All four arteri
es treated with surface concentrations of 0.1 U/mm(2) via microcathete
r infusion into the lumen developed fusiform aneurysms. None of the ar
teries that received surface concentrations less than 0.1 U/mm(2) deve
loped aneurysms. Histological sections revealed a reduced number of ce
llular elements in a stretched collagen matrix at the dome of the sacc
ular aneurysms. CONCLUSION: After empirically testing several methods
of elastase delivery, we were able to induce saccular, bifurcation-typ
e aneurysms in animal arterial specimens. These aneurysms are histolog
ically similar and more authentic than surgical models. The procedure
is easy and reproducible. Our results suggest a possible enzymatic rol
e in aneurysm formation and highlight the dramatic effects of selectiv
e arterial elastic damage. Also, the rapid growth of our experimental
aneurysms may reflect the speed of the natural process.