Dayu Teng1, Jeffrey Scott Pannell1, Robert C Rennert1, Jieying Li1, Yi-Shuan Li1, Victor W Wong1, Shu Chien2, Alexander A Khalessi2. 1. From the Division of Neurosurgery (J.S.P., R.C.R., V.W.W., A.A.K.), Department of Bioengineering and Institute of Engineering in Medicine (D.T., J.L., Y.-S., S.C.), University of California, San Diego. 2. From the Division of Neurosurgery (J.S.P., R.C.R., V.W.W., A.A.K.), Department of Bioengineering and Institute of Engineering in Medicine (D.T., J.L., Y.-S., S.C.), University of California, San Diego. akhalessi@ucsd.edu shuchien@ucsd.edu.
Abstract
BACKGROUND AND PURPOSE: Endovascular thrombectomy has shown promise for the treatment of acute strokes resulting from large-vessel occlusion. Reperfusion-related injury may contribute to the observed decoupling of angiographic and clinical outcomes. Iatrogenic disruption of the endothelium during thrombectomy is potentially a key mediator of this process that requires further study. METHODS: An in vitro live-cell platform was developed to study the effect of various commercially available endovascular devices on the endothelium. In vivo validation was performed using porcine subjects. RESULTS: This novel in vitro platform permitted high-resolution quantification and characterization of the pattern and timing of endothelial-cell injury among endovascular thrombectomy devices and vessel diameters. Thrombectomy devices displayed heterogeneous effects on the endothelium; the device performance assessed in vitro was substantiated by in vivo findings. CONCLUSIONS: In vitro live-cell artificial vessel modeling enables a detailed study of the endothelium after thrombectomy and may contribute to future device design. Large animal studies confirm the relevance of this in vitro system to investigate endothelial physiology. This artificial vessel model may represent a practical, scalable, and physiologically relevant system to assess new endovascular technologies.
BACKGROUND AND PURPOSE: Endovascular thrombectomy has shown promise for the treatment of acute strokes resulting from large-vessel occlusion. Reperfusion-related injury may contribute to the observed decoupling of angiographic and clinical outcomes. Iatrogenic disruption of the endothelium during thrombectomy is potentially a key mediator of this process that requires further study. METHODS: An in vitro live-cell platform was developed to study the effect of various commercially available endovascular devices on the endothelium. In vivo validation was performed using porcine subjects. RESULTS: This novel in vitro platform permitted high-resolution quantification and characterization of the pattern and timing of endothelial-cell injury among endovascular thrombectomy devices and vessel diameters. Thrombectomy devices displayed heterogeneous effects on the endothelium; the device performance assessed in vitro was substantiated by in vivo findings. CONCLUSIONS: In vitro live-cell artificial vessel modeling enables a detailed study of the endothelium after thrombectomy and may contribute to future device design. Large animal studies confirm the relevance of this in vitro system to investigate endothelial physiology. This artificial vessel model may represent a practical, scalable, and physiologically relevant system to assess new endovascular technologies.
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