Arterial Collapse during Thrombectomy for Stroke: Clinical Evidence and Experimental Findings in Human Brains and In Vivo Models.

BACKGROUND AND PURPOSE: Aspiration thrombectomy has become a preferred approach to recanalize large-vessel occlusion in stroke with a growing trend toward using larger-bore catheters and stronger vacuum pumps. However, the mechanical response of the delicate cerebral arteries to aspiration force has not been evaluated. Here, we provide preclinical and clinical evidence of intracranial arterial collapse in aspiration thrombectomy. MATERIALS AND METHODS: We presented a clinical case of arterial collapse with previously implanted flow diverters. We then evaluated the effect of vacuum with conventional aspiration catheters (with and without stent retrievers) in a rabbit model (n = 3) using fluoroscopy and intravascular optical coherence tomography. Then, in a validated human cadaveric brain model, we conducted 168 tests of direct aspiration thrombectomy following an experimental design modifying the catheter inner diameter (0.064 inch, 0.068 inch, and 0.070 inch), cerebral perfusion pressures (mean around 60 and 90 mm Hg), and anterior-versus-posterior circulation. Arterial wall response was recorded and graded via direct transluminal observation. RESULTS: Arterial collapse was observed in both the patient and preclinical experimental models. In the human brain model, arterial collapse was observed in 98% of cases in the M2 and in all the cases with complete proximal flow arrest. A larger bore size of the aspiration catheter, a lower cerebral perfusion pressure, and the posterior circulation in comparison with the anterior circulation were associated with a higher probability of arterial collapse. CONCLUSIONS: Arterial collapse does occur during aspiration thrombectomy and is more likely to happen with larger catheters, lower perfusion pressure, and smaller arteries.

Multi-modality gellan gum-based tissue-mimicking phantom with targeted mechanical, electrical, and thermal properties.

This study develops a new class of gellan gum-based tissue-mimicking phantom material and a model to predict and control the elastic modulus, thermal conductivity, and electrical conductivity by adjusting the mass fractions of gellan gum, propylene glycol, and sodium chloride, respectively. One of the advantages of gellan gum is its gelling efficiency allowing highly regulable mechanical properties (elastic modulus, toughness, etc). An experiment was performed on 16 gellan gum-based tissue-mimicking phantoms and a regression model was fit to quantitatively predict three material properties (elastic modulus, thermal conductivity, and electrical conductivity) based on the phantom material's composition. Based on these material properties and the regression model developed, tissue-mimicking phantoms of porcine spinal cord and liver were formulated. These gellan gum tissue-mimicking phantoms have the mechanical, thermal, and electrical properties approximately equivalent to those of the spinal cord and the liver.

Bioimpedance of soft tissue under compression.

In this paper compression-dependent bioimpedance measurements of porcine spleen tissue are presented. Using a Cole-Cole model, nonlinear compositional changes in extracellular and intracellular makeup; related to a loss of fluid from the tissue, are identified during compression. Bioimpedance measurements were made using a custom tetrapolar probe and bioimpedance circuitry. As the tissue is increasingly compressed up to 50%, both intracellular and extracellular resistances increase while bulk membrane capacitance decreases. Increasing compression to 80% results in an increase in intracellular resistance and bulk membrane capacitance while extracellular resistance decreases. Tissues compressed incrementally to 80% show a decreased extracellular resistance of 32%, an increased intracellular resistance of 107%, and an increased bulk membrane capacitance of 64% compared to their uncompressed values. Intracellular resistance exhibits double asymptotic curves when plotted against the peak tissue pressure during compression, possibly indicating two distinct phases of mechanical change in the tissue during compression. Based on these findings, differing theories as to what is happening at a cellular level during high tissue compression are discussed, including the possibility of cell rupture and mass exudation of cellular material.