Infarct Topography and Reperfusion Injury After Endovascular Thrombectomy for Large Vessel Occlusion Stroke
Robert Regenhardt1, Anna Bonkhoff1, Markus Schirmer1, Alvin Das4, Adam Dmytriw2, Justin Vranic2, Rajiv Gupta2, James Rabinov2, Christopher Stapleton3, Thabele Leslie-Mazwi5, Aman Patel3, Natalia Rost 1
1Neurology, 2Radiology, 3Neurosurgery, Massachusetts General Hospital, 4Neurology, Beth Israel Deaconess Medical Center, 5Neurology, University of Washington
Objective:
To quantify region-specific volumes of infarcted tissue on MRI pre-endovascular thrombectomy (EVT), understand their importance for reperfusion injury and hemorrhagic transformation (HT), and identify associations with clinical and imaging characteristics. 
Background:
With continued expansion in indications for EVT, understanding the pathophysiology of reperfusion injury and HT becomes increasingly important. Pre-EVT infarct topography may have implications for treatment decisions acutely (e.g. stenting), and with post EVT care (e.g. antithrombotics). 
Design/Methods:
Patients were identified from a prospectively maintained database. Each patient’s diffusion weighted sequence underwent manual infarct delineation and was registered to a standard space for overlay with cortical, subcortical, and white matter atlases. HT was defined as ECASS PH1 or PH2. Variables with p<0.10 in univariate analyses were included in multivariable models. 
Results:
165 participants [median age 69 (IQR 56-79), 56% women] were identified. Intravenous alteplase was administered to 52%; 70% achieved TICI 2b-3 reperfusion. HT occurred in 8%. The distribution of pre-EVT infarcts was 48% (38-60%) white matter, 23% (6-47%) cortex, and 15% (4-28%) basal ganglia. Pre-EVT infarct volumes [median (IQR)] were 22 cc (12-43 cc) for total, 11 cc (6-19 cc) for white matter, 5 cc (1-19 cc) for cortex, and 3 cc (1-6 cc) for basal ganglia infarct. Paramagnetic sequences showed 3% had petechial hemorrhage and 40% had susceptibility vessel sign. Basal ganglia infarct volume was independently associated with HT (OR=1.342, 95%CI=1.002,1.797) in a model including white matter infarct volume, cortex infarct volume, smoking, and puncture-to-recanalization time. Basal ganglia infarct volume was linked to susceptibility vessel sign (Beta=0.233, p=0.006) and NIHSS (Beta=0.220, p=0.012), when controlling for total infarct volume. 
Conclusions:

Greater basal ganglia infarct volume was associated with a higher risk of HT when accounting for infarct volumes in other regions. Susceptibility vessel sign was associated with basal ganglia infarct volume, which may be related to acute middle cerebral artery perforator occlusion. 

10.1212/WNL.0000000000203704