Reactive tissue proliferation and damage of elastic lamina caused by hydrogel coated coils in experimental rat aneurysms

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Background and 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.


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.


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.


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.

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