Abstract WP66: Impaired Collaterals Are Associated With Intracranial Thrombus Extension: Evidence From MRI, Catheter Angiography, and Retrieved Thrombus Composition

Abstract

Background: Clot propagation after initial occlusion may increase target thrombus burden and its pathophysiologic basis has not been extensively studied in acute human ischemic stroke. We investigated whether clot characteristics on MRI, catheter angiography, and thrombus histopathology indicated that impaired collaterals may be associated with extension of acute intracranial occlusions via stasis clotting in slow flow arterial segments. Methods: Analysis of consecutive AIS-LVO endovascular thrombectomy patients at 2 academic medical centers with: 1) pretreatment MRI, and 2) retrieved thrombi. GRE MR susceptibility vessel sign presence and extent of ASITN collateral scores were rated by blinded assessors. Extracted clots were fixed in formalin, stained by hematoxylin and eosin, and RBC, WBC and fibrin percent composition quantified by a neuropathologist blinded to clinical details. We evaluated the correlation of collateral grade with clot size by susceptibility vessel sign (SVS) and clot composition by RBC%. Non-parametric values were computed via Spearman correlation. Results: Among the 48 patients, mean age was 71.4 (SD 17.7), 56.3% female, and mean presenting NIHSS was 15.5 (SD 7.41). A susceptibility vessel sign was present in 65%, with mean SVS length 15.6 mm (SD 8.3). Collateral scores were mean 2.3 (SD 1.2). The number of passes per procedure was mean 1.98 (SD 1.30) The presence of a susceptibility vessel sign correlated with higher RBC% in retrieved thrombi (r s =0.36 p=0.011). Worse collateral grades correlated with longer SVS length (r s =-0.50 p=0.004) and greater SVS width (r s =-0.54 p=0.002). Worse collateral grade also trended toward correlation with higher RBC% in retrieved clots (r s =-0.19 p=0.18). Conclusion: Impaired angiographic collaterals are associated with longer RBC-rich thrombi on susceptibility imaging and trend toward association with higher RBC% in retrieved thrombi. These findings support that, in LVO acute ischemic stroke, clot propagation after initial occlusion occurs by stasis clotting accelerated by impaired collaterals.