Reactive tissue proliferation and damage of elastic lamina caused by hydrogel coated coils in experimental rat aneurysms.
OBJECTIVE
The HydroCoil Endovascular Aneurysm Occlusion and Packing Study clinical trial, comparing HydroCoil with platinum coils, reported an 8.6% reduction in significant recurrence following cerebral aneurysm coil embolization. We sought to better understand the mechanism of aneurysmal healing following HydroCoil implantation using the rat external carotid artery (ECA) sidewall aneurysm model.


METHODS
We ligated the proximal ECA, creating a blind pouch in our rat model. HydroCoil or bare platinum coil segments (5 mm) were inserted into aneurysms. Sham operated rats underwent identical procedures without coil insertion. 14 days after coil embolization, animals were sacrificed and the common carotid artery/internal carotid artery/ECA complex removed. Sac and surrounding vasculature underwent microscopic and histopathologic evaluation. Cellular and fibrotic components within the sac were defined as the organized area. Percentage of organized area and residual length of internal elastic lamina were calculated.


RESULTS
Organized tissue area in ECA sac 2 weeks following coil embolization was significantly greater in the HydroCoil group than the bare coil (60.42±22.58% vs 15.62±19.24%; p=0.01) and sham (60.42±22.58% vs 4.61±3.86%; p=0.002) groups. Elastic lamina was significantly reduced in the HydroCoil group compared with the sham and bare coil groups (21.67±16.50% vs 100% and 96.06±8.78%; both p<0.001). No significant difference was found between the bare coil and sham groups for organized tissue formation or reduction in elastic lamina. Greater numbers of B cells, T cells, and neutrophils were present within HydroCoil induced organized tissue compared with the platinum group; this difference was not statistically significant.


CONCLUSIONS
In the rat ECA sidewall aneurysm model, hydrogel coated coils cause more tissue reaction and organization compared with bare platinum coils, possibly attributed to observed elastic lamina damage and vascular smooth muscle cell proliferation.
Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan, USA Department of Neurosurgery, Huashan Hospital, Fudan University, China.
Chao
C
Zhang
Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan, USA Radiology, University of Michigan, Ann Arbor, Michigan, USA.
Neeraj
N
Chaudhary
Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan, USA Radiology, University of Michigan, Ann Arbor, Michigan, USA.
Joseph J
JJ
Gemmete
Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan, USA Radiology, University of Michigan, Ann Arbor, Michigan, USA.
B Gregory
BG
Thompson
Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan, USA.
Guohua
G
Xi
Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan, USA.
Aditya S
AS
Pandey
D000199:Actins / Q000096:biosynthesis; D000818:Animals; D001807:Blood Vessel Prosthesis / Q000009:adverse effects*; D002342:Carotid Artery, External / Q000473:pathology; D057510:Endovascular Procedures / Q000009:adverse effects*; D020100:Hydrogels / Q000009:adverse effects*; D002532:Intracranial Aneurysm / Q000473:pathology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley
D000199:Actins; D020100:Hydrogels; C498862:Acta2 protein, rat
Aneurysm; Coil