E-015 Failure mechanisms of current thrombectomy devices identified in a human brain model: iatrogenic embolization, residual and recurrent large vessel occlusion, persistent perforating artery occlusion, and arterial collapse, traction and avulsion

Abstract

Introduction Complete recanalization in large vessel occlusion (LVO) strokes with suction catheters and stent retrievers has remained at 50% despite improved technologies and accumulating operator experience. About 40% of patients experience poor neurological outcomes and many cannot be recanalized at the first attempt. In this experimental study, we aimed to analyze the interaction between the arteries/emboli/devices in human brains and to provide mechanistic explanations of failures and complications of current interventions in a human brain LVO model. Method Elastic, fragment-prone and stiff embolus analogs were fabricated using a multilinear regression model derived from analysis of LVO emboli. Then, 105 LVO were generated in 12 fresh human brains pressurized by a pulsatile pump and recanalization attempted in 61 cases using aspiration thrombectomy (ACETM 68; Penumbra) and in 44 cases using stent/aspiration technique (SolitaireTM Platinum, Medtronic and ACETM 68, Penumbra). Results First pass complete (34%), successful (71%) and complete (60%) recanalization rates in this model were consistent with the literature. Devices loaded the emboli with tensile forces leading to elongation and intravascular fragmentation with downstream embolization to the microcirculation causing recurrent (15%) and residual (73%) occlusions, or both (12%). Moreover: a) residual emboli remained in small branching and perforating arteries in alleged complete recanalization (28%); b) vacuum caused arterial collapse at physiological pressures (43%); c) device withdrawal caused arterial traction (41%); and d) severe arterial traction provoked avulsion of perforating arteries. Conclusion Stents and suction catheters load emboli with tensile forces leading to fragmentation, embolization and residual occlusion and cause significant arterial deformation, collapse and traction. Disclosures L. Savastano: 4; C; Endovascular Engineering. D. Gebrezgiabhier: None. J. Arturo Larco: None. S. Madhani: None. A. Shahid: None. Y. Liu: 2; C; Endovascular Engineering.