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Experimental Model of Dissecting Aneurysms

Takeshi Okamotoa, Shigeru Miyachia, Makoto Negoroa, Goro Otsukaa, Osamu Suzukia, Hiroomi Keinoa and Jun Yoshidaa

a From the Department of Neurosurgery, Nagoya University Graduate School of Medicine, Japan (T.O., S.M., M.N., G.O., O.S., J.Y.), and the Department of Perinatology, Institute of Developmental Research, Aichi, Japan (H.K.)



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  		FIG 1. Drawings illustrate the method used for creating the experimental dissections.

A, In a canine CCA, a small incision is made in the adventitial layer.

B, The adventitia is dissected from the media by using a thin probe that is passed through the adventitial incision.

C, After the two layers are sufficiently dissected, a longitudinal slitlike or elliptical defect is made in the intima.

D, The adventitial incision is tightly closed.

E, Cross-sectional view of the result.



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  		FIG 2. Bar graph summaries the serial angiographic changes. A indicates the acute stage; C, chronic stage; S, subacute stage.



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  		FIG 3. Example of aneurysm formation, with persistent stenosis (group I-C 6-mm elliptical defect).

A, Angiogram shows a double shadow due to a massive adventitial hematoma that formed immediately after lesion creation.

B, Angiogram obtained 2 hours later shows a subadventitial hematoma with the characteristics of an aneurysmal pouch.

C, Angiogram obtained 1 week later shows that the hematoma has become a saccular aneurysm.

D, Chronic-stage (3-month) angiogram shows that the aneurysm is smaller.

E, Photograph shows external protrusion of the aneurysm (arrow).

F, Chronic-stage photograph obtained in shows that part of the intimal defect extends to the aneurysm orifice (arrow).

G, Chronic-stage photomicrograph shows that the inner layer of the aneurysm dome (asterisk) is covered with organized clots and fully endothelialized (elastica van Gieson stain, original magnification x5). Arrows indicate the adventitia; single arrowheads, media; double arrowheads, intima.

H, Scanning electron micrograph shows endothelialization (original magnification x700).



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  		FIG 4. Example of persistent stenosis (group I-C 6-mm elliptical defect).

A, Angiogram obtained just after lesion creation shows a subadventitial hematoma that is compressing the arterial lumen.

B, Angiogram obtained 2 hours later shows that the subadventitial hematoma has spontaneously thrombosed, but it is still compressing the arterial lumen.

C, Angiogram obtained in the chronic stage shows that the stenosis has improved.



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  		FIG 5. Example of occlusion (group I-D 8-mm elliptical defect).

A, Photograph obtained immediately after lesion creation shows that the arterial lumen is compressed. It has a serpentine configuration, and a subadventitial hematoma is present.

B, Angiogram shows an occlusion.

C, Angiogram obtained after 2 hours shows that the vessel lumen has transiently recanalized.

D, Angiogram shows that the lumen has become occluded again in the subacute stage.

E, Photomicrograph shows that the subadventitial hematoma, which is already organized, compresses the arterial lumen (arrow) to cause a crescentic cross-sectional profile (elastica van Gieson stain, original magnification x5).



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  		FIG 6. Diagrams show hypothetical schemes of aneurysm formation (left) and persistent stenosis (right).

Left, Hemodynamic stress from vortex flow inside the cavity may cause external protrusion of the adventitia, which results in a saccular aneurysm.

Right, A large entry zone can produce a massive, widespread subadventitial hematoma of sufficient size to compress the true lumen and result in abrupt occlusion. When the hematoma is large, the artery is likely to remain thrombosed.





Copyright © 2009 by the American Society of Neuroradiology. Print ISSN: 0195-6108 Online ISSN: 1936-959X