Abstract Number ‐ 34: Basal ganglia infarct volume and risk of hemorrhagic transformation after endovascular thrombectomy

Abstract

Introduction As more large vessel occlusion stroke patients are treated with endovascular thrombectomy (EVT), understanding the pathophysiology of reperfusion injury and the risks of hemorrhagic transformation (HT) are increasingly important. Pre‐EVT infarct topography may have implications for acute interventional treatments such as stenting, and post thrombectomy care such as antithrombotic choice. We sought to quantify region‐specific volumes of infarcted tissue on pre‐EVT MRI, understand their importance for HT, and identify associations with clinical and imaging characteristics. Methods Patients with pre‐EVT MRI were identified retrospectively 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. Structure‐specific lesion volumes were determined. HT was defined as PH1 or PH2 hemorrhage by ECASS criteria. Variables with p< 0.10 in univariate analyses were included in multivariable models. Logistic regression was performed for associations with hemorrhagic transformation and linear regressions for infarct volumes. Results 165 participants [median age 69 years (interquartile range, IQR 56–79), 56% women] were identified. Risk factors included hypertension (70%), diabetes (20%), atrial fibrillation (34%), and prior stroke/TIA (13%). 52% were treated with intravenous alteplase; 70% achieved TICI 2b‐3 reperfusion. HT occurred in 8%. 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. Pre‐EVT infarcts [median (IQR)] were made up of 48% (38‐60%) white matter, 23% (6‐47%) cortex, and 15% (4‐28%) basal ganglia. 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‐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 In this cohort, greater basal ganglia infarct volume was associated with a higher risk of hemorrhagic transformation, even when accounting for infarct volume in other regions. Susceptibility vessel sign was associated with basal ganglia infarct volume, which may be related to acute middle cerebral artery thrombus occlusion of perforators. These findings require further study in larger cohorts.