Histopathologic and immunohistochemical comparison of human, rabbit, and swine aneurysms embolized with platinum coils.
OBJECTIVE
The purpose of this study was to clarify the cellular mechanisms of aneurysmal healing by comparing histologic and immunohistochemical findings in experimental rabbit and swine aneurysms to a human aneurysm embolized with platinum coils.


METHODS
Swine sidewall aneurysms (n = 5, harvested at 12 weeks) and elastase-induced rabbit aneurysms (n = 6, harvested at 24 weeks) were created and embolized. A single human aneurysm, embolized 6 years before death, was harvested following autopsy. All specimens were processed by using a modified paraffin embedding technique. Tissue was sectioned and stained with hematoxylin and eosin and Masson trichrome. Immunohistochemistry and immunofluorescence were performed with multiple antibodies, including alpha smooth muscle actin, myosin heavy chain, desmin, vimentin, and CD31.


RESULTS
The human aneurysm's dome was filled with loose, hypocellular, amorphous tissue. The aneurysm's neck was completely covered with a thin layer of hypocellular tissue. Collagen and myofibroblasts were sparse in both the dome and neck. Rabbit aneurysms' domes were also filled with a loose, hypocellular tissue, amorphous matrix. In 5 of 6 aneurysms, a thin layer of hypocellular tissue ran along the neck. Collagen and myofibroblasts were sparse in the dome. Swine aneurysms were filled with densely infiltrated tissue, including chronic inflammatory tissue and extensive, attenuated collagen fiber bundles associated with myofibroblasts. Thick layers of myofibroblasts entirely bridged the necks.


CONCLUSIONS
Absence of collagen deposition and scant myofibroblastic reaction to platinum coil embolization are seen in the rabbit model but not in swine aneurysms. The elastase-induced aneurysm model in rabbits is more suitable than sidewall swine aneurysms for testing of modified devices aimed at improving intra-aneurysmal fibrosis.
Dai
Daying
D
Neuroradiology Research Laboratory, Department of Radiology, Mayo Clinic, Rochester, MN 55905, USA.
Ding
Yong Hong
YH
Danielson
Mark A
MA
Kadirvel
Ramanathan
R
Lewis
Debra A
DA
Cloft
Harry J
HJ
Kallmes
David F
DF
D000199:Actins / Q000378:metabolism; D000368:Aged; D017542:Aneurysm, Ruptured / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D000818:Animals; D020771:Anterior Cerebral Artery / Q000378:metabolism / Q000473:pathology; D017536:Carotid Artery, Common / Q000378:metabolism / Q000473:pathology; D003893:Desmin / Q000378:metabolism; D004621:Embolization, Therapeutic / Q000295:instrumentation / Q000379:methods*; D004847:Epithelial Cells / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D002532:Intracranial Aneurysm / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D008297:Male; D032389:Myocytes, Smooth Muscle / Q000378:metabolism* / Q000473:pathology; D018995:Myosin Heavy Chains / Q000378:metabolism; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D010984:Platinum / Q000627:therapeutic use*; D011817:Rabbits; D034421:Sus scrofa; D014746:Vimentin / Q000378:metabolism
D000199:Actins; D003893:Desmin; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D014746:Vimentin; D010984:Platinum; D018995:Myosin Heavy Chains