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Differential Endothelial and Smooth Muscle Cell Proliferation on Metallic Substrates Used in Flow Diversion and Coil
John J Amusan1, Wasantha R Ranatunga2, Alexander A Oliver2
1From the Department of Radiology (J.J.A., A.A.O., Y.V., S.G., P.M., D.F.K., R.K.), Neurologic Surgery (J.J.A., W.R.R., S.G., R.K.), Mayo Clinic, Rochester, MN, USA. Amusan.John@mayo.edu.
Background And Purpose:
Endovascular treatment of intracranial aneurysms (IA) relies on flow diversion and coil embolization. The metallic substrates used in these devices directly contact endothelial cells (ECs) and smooth muscle cells (SMCs) and influence healing. Because controlled comparisons of vascular response across clinically used metals are limited, this study evaluated whether commonly used bare-metal substrates differentially affect EC and SMC proliferation.
Materials And Methods:
Flat coupons of nitinol, nitinol with a light thermal oxide (LTO) coating, 316LVM (stainless steel), 35NLT (cobalt-nickel-chromium), platinum, and cobalt were prepared. Human aortic ECs and SMCs were cultured on each surface. EC proliferation was assessed at 24, 48, and 72 hours, and SMC proliferation at 5, 7, and 10 days using a fluorometric live-dead viability assay and immunofluorescence microscopy. Group differences were analyzed by analysis of variance.
Results:
EC proliferation varied markedly by material and time. Nitinol, nitinol+LTO, 35NLT, and 316LVM supported robust endothelial growth (all p < 0.001), unlike platinum and cobalt. Immunofluorescence showed dense coverage on nitinol/stainless steel but sparse on platinum/cobalt. SMCs attached to most substrates except cobalt with limited, nonprogressive proliferation, indicating restrained neointimal expansion.
Conclusions:
EC proliferation differed across bare-metal substrates under static in vitro conditions, whereas SMC proliferation was comparatively limited. Nitinol, nitinol+LTO, 35NLT, and 316LVM supported greater EC proliferation than platinum and cobalt. These findings identify material-dependent vascular cell responses that warrant confirmation in flow-based, blood-contacting, device-level models before clinical extrapolation.

