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Artery-to-artery embolism (AAE) is a common stroke mechanism in intracranial atherosclerotic disease (ICAD), associated with a considerable risk of recurrent stroke. We aimed to investigate cerebral hemodynamic features associated with AAE in symptomatic ICAD. Patients with anterior-circulation, symptomatic ICAD confirmed in CT angiography (CTA) were recruited. We classified probable stroke mechanisms as isolated parent artery atherosclerosis occluding penetrating artery, AAE, hypoperfusion, and mixed mechanisms, largely based on infarct topography. CTA-based computational fluid dynamics (CFD) models were built to simulate blood flow across culprit ICAD lesions. Translesional pressure ratio (PR = Pressurepost-stenotic/Pressurepre-stenotic) and wall shear stress ratio (WSSR = WSSstenotic-throat/WSSpre-stenotic) were calculated, to reflect the relative, translesional changes of the two hemodynamic metrics. Low PR (PR ≤ median) and high WSSR (WSSR ≥ 4th quartile) respectively indicated large translesional pressure and elevated WSS upon the lesion. Among 99 symptomatic ICAD patients, 44 had AAE as a probable stroke mechanism, 13 with AAE alone and 31 with coexisting hypoperfusion. High WSSR was independently associated with AAE (adjusted OR = 3.90; P = 0.022) in multivariate logistic regression. There was significant WSSR-PR interaction on the presence of AAE (P for interaction = 0.013): high WSSR was more likely to associate with AAE in those with low PR (P = 0.075), but not in those with normal PR (P = 0.959). Excessively elevated WSS in ICAD might increase the risk of AAE. Such association was more prominent in those with large translesional pressure gradient. Hypoperfusion, commonly coexisting with AAE, might be a therapeutic indicator for secondary stroke prevention in symptomatic ICAD with AAE. [ABSTRACT FROM AUTHOR]

Intracranial atherosclerotic disease (ICAD) is a major cause of ischemic stroke and transient ischemic attack (TIA) worldwide. The culprit of ICAD is frequently a high-grade intracranial atherosclerotic stenosis (ICAS) pertaining to the infarct territory, and by then, the ICAS is described as symptomatic. A high-grade ICAS may progressively limit cerebral perfusion downstream, demanding collateral compensation. Collateral circulation refers to the pre-existing and dynamic emergence of vascular channels that maintain and compensate for a failing principal vascular route. Collaterals through the Circle of Willis and leptomeningeal circulation are of utmost importance in this regard. In this article, we first discussed the epidemiology, stroke mechanisms, contemporary therapeutics, and prognosis of symptomatic ICAD. Then, we reviewed the collateral routes in ICAS, factors associated with recruitment and development of the collaterals and diagnostic imaging modalities in assessing the origin and function of collateral circulation. We discussed the associations between collateral circulation and clinical outcomes after acute reperfusion treatment in ICAD-related ischemic strokes with or without large vessel occlusion (LVO). We also conducted a systematic review and meta-analysis on the associations of collateral circulation with the risk of recurrent stroke and the functional outcome in symptomatic ICAS patients on medical treatment as secondary stroke prevention. Finally, we summarized current evidence in these aspects and proposed the future directions. [ABSTRACT FROM AUTHOR]

Background and Objective: Drug–drug interactions between direct oral anticoagulants (DOAC) and antiseizure medications via the cytochrome P450 (CYP) or the P-glycoprotein (P-gp) systems may lead to under-anticoagulation. The clinical relevance of these interactions is unclear. We aimed to elucidate the risk of thromboembolism with concurrent DOAC and CYP/P-gp modulating antiseizure medications. Methods: In this propensity score-weighted population-based retrospective cohort study, we used competing risk regression analyses to determine the risks of ischemic stroke, venous thromboembolism, and death in DOAC recipients taking CYP/P-gp-modulating antiseizure medications (phenytoin, valproate, levetiracetam, carbamazepine, or phenobarbital) versus those taking CYP/P-gp-neutral antiseizure medications (pregabalin, gabapentin, or clobazam). We also performed secondary analyses for the epilepsy and atrial fibrillation subgroups. Results: Among DOAC users, CYP/P-gp-modulating antiseizure medications were collectively associated with an increased risk of ischemic stroke (adjusted hazard ratio 1.28, 95% confidence interval 1.05–1.57, p = 0.017). In addition, phenytoin (adjusted hazard ratio 1.34, 95% confidence interval 1.07–1.68, p = 0.011) and valproate (adjusted hazard ratio 1.38, 95% confidence interval 1.10–1.74, p = 0.006) were associated with increased mortality. In the epilepsy subgroup, the risk of ischemic stroke and venous thromboembolism did not differ between CYP/P-gp-modulating and CYP/P-gp-neutral antiseizure medications. Conclusions: Although CYP/P-gp-modulating antiseizure medications were associated with an increased risk of ischemic stroke when paired with DOAC in the primary analysis, such a phenomenon was not found among patients with epilepsy who took phenytoin, valproate, or levetiracetam with DOAC. Therefore, these antiseizure medication options among patients with epilepsy with concurrent DOAC should not be restricted solely based on their potential drug–drug interactions. Yet, the increased mortality during concurrent use of DOAC with phenytoin or valproate might call for caution. [ABSTRACT FROM AUTHOR]

Objectives: We aimed to investigate the correlation between an overall cerebral small vessel disease (CSVD) burden and outcomes after endovascular treatment (EVT) for patients with acute ischemic stroke (AIS) due to large vessel occlusion (LVO). Methods: In a multicenter registry study, we enrolled patients with EVT for anterior-circulation LVO-stroke. In 3.0-T MR imaging, we assessed 4 CSVD imaging markers, lacunes, white matter hyperintensities, cerebral microbleeds, and enlarged perivascular spaces, each assigned a score of 0 or 1 and summed up to an overall CSVD burden score of 0–4. We dichotomized the overall CSVD severity as none to mild (score 0–2) and moderate to severe (3–4). Primary outcome was 90-day functional dependence or death (modified Rankin Scale (mRS) 3–6). Secondary outcomes included increase in NIH Stroke Scale ≥ 4 within 24 h (early neurological deterioration (END)) and within 7 days, symptomatic intracranial hemorrhage, 90-day mRS 2–6, and 90-day mortality. Results: Among 311 patients (63.0% male; mean age 65.1 ± 12.7 years), 260 (83.6%) had none-to-mild and 51 (16.4%) had moderate-to-severe overall CSVD burden. Moderate-to-severe CSVD burden was not significantly associated with the primary outcome (47.1% versus 45.4%; p > 0.05 in univariate and multivariate logistic regression), or the secondary outcomes except for a higher risk of END (11.8% versus 3.1%; p < 0.05 in multivariate analyses). Sensitivity analyses with 0–1 versus 2–4 of the CSVD burden score, and the score as an ordinal variable, showed similar results. Conclusions: An overall moderate-to-severe CSVD burden was not associated with 90-day functional dependence or death, after EVT for anterior-circulation LVO. Trial registration: ChiCTR1900022154 Key Points: • Moderate-to-severe cerebral small vessel disease burden on MRI should not be an exclusion indicator in determining the eligibility of an acute ischemic stroke patient for endovascular treatment. [ABSTRACT FROM AUTHOR]