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Background: We studied the evolution over time of diffusion weighted imaging (DWI) lesion volume and the factors involved on early and late infarct growth (EIG and LIG) in stroke patients undergoing endovascular treatment (EVT) according to the final revascularization grade. Methods: This is a prospective cohort of patients with anterior large artery occlusion undergoing EVT arriving at 1 comprehensive stroke center. Magnetic resonance imaging was performed on arrival (pre-EVT), Results: We included 98 patients (mean age 70, median National Institutes of Health Stroke Scale score 17, final mTICI≥2b 86%). Median EIG and LIG were 48 and 63.3 mL in patients with final mTICIρ =0.667; P ρ =0.614; P Conclusions: Infarct grows during and after EVT, especially in nonrecanalizers but also to a lesser extent in recanalizers. In recanalizers, number of passes and DWI volume influence EIG, while number of passes, DWI, and hypoperfused volume after the procedure determine LIG.

Introduction: We aimed to evaluate venous delay before and after treatment as a marker of radiological and clinical outcome in stroke patients receiving endovascular treatment (EVT). Methods: Prospective cohort of patients with anterior intracranial occlusion undergoing EVT. Brain MRI was performed on arrival (pre-EVT), Results: From 98 included patients (median NIHSS 17, final mTICI≥2b 86%), 89 pre-EVT dMRIs and 88 post-EVT dMRIs were evaluable. The median venous delay pre-EVT and post-EVT were -31.9[-58.1;-16.7]% and -13.5[-34.5;-7.5]%, respectively. Venous delay pre-EVT was not related to infarct volume or clinical outcome. When final mTICI≥2B, venous asymmetry decreased but still persisted. For each 10% of increment in venous delay post-EVT, there was an adjusted increase of 0.12[0.05-0.19]ml in the final infarct volume. Venous delay post-EVT was independently associated with mRS at 90 days (cOR 1.013 [95%CI 1.001-1.0256]). Conclusion: Cortical vein delay assessed after but not before EVT, is associated with a larger final infarct volume and with a worse clinical outcome.

Background: Laterality of the posterior cerebral artery (LPCA) in acute stroke has been related with a better leptomeningeal collateral circulation and with improved functional outcome at 6 months in patients treated with IV tPA. We aim to study the association between LPCA and the amount of brain tissue at risk of infarction in patients with anterior circulation arterial occlusion. Methods: From our prospective database of ischemic stroke we selected patients with anterior circulation arterial occlusion who underwent multimodal MRI < 12h of symptom onset. We considered LPCA when the following criteria were accomplished: a) ipsilateral PCA to the occlusion site was extended in 1 or more segments compared to the contralateral PCA and b) ipsilateral P4 segment was visible on axial TOF images. Two independent readers blinded to clinical data retrospectively assessed the presence of LPCA (k=0.65). We analyzed the association between LPCA and the volume of ischemic penumbra at baseline (Tmax>6s) and the final infarct volume (CT 24h). Good outcome was defined as mRS ≤ 2 at 90 days. Results: Seventy-two patients were included in the study (mean age 67y, 45% male). LPCA was present in 39 (54.1%). There were no differences between groups with or without LPCA, except a lower baseline NIHSS in the LPCA group (15 vs 19; p=0.003). Proportion of patients treated with reperfusion therapies was similar between groups. Patients with LPCA had a smaller lesion in Tmax>6s (54 vs 79cc; p=0.02), smaller final infarct volume (47 vs 111cc; p=0.013), and higher proportion of good outcome (52.8% vs 27.3%; p=0.03). In a multivariate analysis, LPCA was independently associated with smaller lesion volume on Tmax>6s (B -18, IC95% [-36,-0.3]), smaller final infarct volume (B -64.8, IC95% [-100,-29]) and better clinical outcome (OR 4.66, IC95% [1.04,20.8]). Conclusion: LPCA sign in patients with anterior circulation arterial occlusion is associated with smaller volume of brain tissue at risk resulting in smaller infarct volume and better clinical outcome. These findings suggest favorable leptomeningeal collaterals.

Background and Purpose— Intracranial atherosclerotic disease (ICAD) remains a challenge for stroke primary and secondary prevention. Molecular pathways involved in the development of ICAD from its asymptomatic stages are largely unknown. In our population-based study, we aimed to compare the risk factor and biomarker profiles associated with intracranial and extracranial asymptomatic cerebral atherosclerosis. Methods— The Asymptomatic Intracranial Atherosclerosis (AsIA) study cohort includes a random sample population of 933 white subjects >50 years with a moderate to high vascular risk (based on REGICOR score) and without a history of stroke (64% males; mean age, 66 years). Carotid and intracranial atherosclerosis were screened by cervical and transcranial color-coded Duplex ultrasound, being moderate to severe stenoses confirmed by MR angiography. We registered clinical and anthropometric data and created a biobank with blood samples at baseline. A panel of biomarkers involved in atherothrombogenesis was determined: C-reactive protein, asymmetric-dimethylarginine, resistin, and plasminogen activator inhibitor-1. Insulin resistance was quantified by Homeostasis Model Assessment index. Results— After multinomial regression analyses, male sex, hypertension, smoking, and alcoholic habits were independent risk factors of isolated extracranial atherosclerotic disease. Diabetes and metabolic syndrome conferred a higher risk for ICAD than for extracranial atherosclerotic disease. Moreover, metabolic syndrome and insulin resistance were independent risk factors of moderate to severe ICAD but were not risk factors of moderate to severe extracranial atherosclerotic disease. Regarding biomarkers, asymmetric-dimethylarginine was independently associated with isolated ICAD and resistin with combined ICAD–extracranial atherosclerotic disease. Conclusions— Our findings show distinct clinical and biological profiles in subclinical ICAD and extracranial atherosclerotic disease. Insulin resistance emerged as an important molecular pathway involved in the development of ICAD from its asymptomatic stage.