Endothelial repair process and its relevance to longitudinal neointimal tissue patterns: comparing histology with in silico modelling

• Published in: Journal of the Royal Society interface Vol. 11; no. 94; p. 20140022
• Main Authors: Tahir, Hannan, Bona-Casas, Carles, Narracott, Andrew James, Iqbal, Javaid, Gunn, Julian, Lawford, Patricia, Hoekstra, Alfons G.
• Format: Journal Article
• Language: English
• Published: England The Royal Society 06.05.2014
• Subjects: Animals; Computer Modelling; Coronary Vessels - metabolism; Coronary Vessels - pathology; Coronary Vessels - physiopathology; Endothelial Cells; Endothelium, Vascular - metabolism; Endothelium, Vascular - pathology; Endothelium, Vascular - physiopathology; In-Stent Restenosis; Models, Cardiovascular; Neointima - metabolism; Neointima - pathology; Neointima - physiopathology; Neointimal Patterns; Re-Endothelialization; Swine; neointimal patterns; endothelial cells; computer modelling; in-stent restenosis; re-endothelialization
• ISSN: 1742-5689; 1742-5662; 1742-5662
• DOI: 10.1098/rsif.2014.0022

Re-establishing a functional endothelium following endovascular treatment is an important factor in arresting neointimal proliferation. In this study, both histology (in vivo) and computational simulations (in silico) are used to evaluate neointimal growth patterns within coronary arteries along the axial direction of the stent. Comparison of the growth configurations in vivo and in silico was undertaken to identify candidate mechanisms for endothelial repair. Stent, lumen and neointimal areas were measured from histological sections obtained from eight right coronary stented porcine arteries. Two re-endothelialization scenarios (endothelial cell (EC) random seeding and EC growth from proximal and distal ends) were implemented in silico to evaluate their influence on the morphology of the simulated lesions. Subject to the assumptions made in the current simulations, comparison between in vivo and in silico results suggests that endothelial growth does not occur from the proximal and distal ends alone, but is more consistent with the assumption of a random seeding process. This may occur either from the patches of endothelium which survive following stent implantation or from attachment of circulating endothelial progenitor cells.