BACKGROUND AND PURPOSE: 3D high-resolution black-blood MRI or MR vessel wall imaging allows evaluation of the intracranial arterial wall and extraluminal pathology. We investigated the diagnostic accuracy and reliability of black-blood MRI for the intraluminal detection of large-vessel arterial occlusions. MATERIALS AND METHODS: We retrospectively identified patients with intracranial arterial occlusions, confirmed by CTA or DSA, who also underwent 3D black-blood MRI with nonenhanced and contrast-enhanced T1 sampling perfection with application-optimized contrasts by using different flip angle evolution (T1 SPACE) sequences. Black-blood MRI findings were evaluated by 2 independent and blinded neuroradiologists. Large-vessel intracranial arterial segments were graded on a 3-point scale (grades 0–2) for intraluminal baseline T1 hyperintensity and contrast enhancement. Vessel segments were considered positive for arterial occlusion if focal weak (grade 1) or strong (grade 2) T1-hyperintense signal and/or enhancement replaced the normal intraluminal black-blood signal. RESULTS: Thirty-one patients with 38 intracranial arterial occlusions were studied. The median time interval between black-blood MRI and CTA/DSA reference standard studies was 2 days (range, 0–20 days). Interobserver agreement was good for T1 hyperintensity (κ = 0.63) and excellent for contrast enhancement (κ = 0.89). High sensitivity (100%) and specificity (99.8%) for intracranial arterial occlusion diagnosis was observed with either intraluminal T1 hyperintensity or contrast-enhancement imaging criteria on black-blood MRI. Strong grade 2 intraluminal enhancement was maintained in >80% of occlusions irrespective of location or chronicity. Relatively increased strong grade 2 intraluminal T1 hyperintensity was noted in chronic/incidental versus acute/subacute occlusions (45.5% versus 12.5%, P = .04). CONCLUSIONS: Black-blood MRI with or without contrast has high diagnostic accuracy and reliability in evaluating intracranial large-vessel arterial occlusions with near-equivalency to DSA and CTA.

BACKGROUND: Experience with endoluminal flow diversion for the treatment of posterior circulation aneurysms is limited. PURPOSE: We sought to investigate factors associated with the safety and efficacy of this treatment by collecting disaggregated patient-level data from the literature. DATA SOURCES: PubMed, EMBASE, and Ovid were searched up through 2019 for articles reporting flow diversion of posterior circulation aneurysms. STUDY SELECTION: Eighty-four studies reported disaggregated data for 301 separate posterior circulation aneurysms. DATA ANALYSIS: Patient, aneurysm, and treatment factors were collected for each patient. Outcomes included the occurrence of major complications, angiographic occlusion, and functional outcomes based on the mRS. DATA SYNTHESIS: Significant differences in aneurysm and treatment characteristics were seen among different locations. Major complications occurred in 22%, angiographic occlusion was reported in 65% (11.3 months of mean follow-up), and good functional outcomes (mRS 0–2) were achieved in 67% (13.3 months of mean follow-up). Multivariate analysis identified age, number of flow diverters used, size, and prior treatment to be associated with outcome measures. Meta-analysis combining the current study with prior large nondisaggregated series of posterior circulation aneurysms treated with flow diversion found a pooled incidence of 20% (n = 712 patients) major complications and 75% (n = 581 patients) angiographic occlusions. LIMITATIONS: This study design is susceptible to publication bias. Use of antiplatelet therapy was not uniformly reported. CONCLUSIONS: Endoluminal flow diversion is an important tool in the treatment of posterior circulation aneurysms. Patient age, aneurysm size, prior treatment, and the number of flow diverters used are important factors associated with complications and outcomes.

BACKGROUND AND PURPOSE: Published data regarding embolic protection device efficacy is mixed, and its use during carotid artery stent placement remains variable. We, therefore, examined the frequency of embolic protection device use and its association with outcomes after carotid artery stent placement using a national quality improvement data base. MATERIALS AND METHODS: Patients undergoing carotid artery stent placement with or without embolic protection devices were identified in the American College of Surgeons National Surgical Quality Improvement Program data base. The primary outcome was the incidence of major adverse cardiovascular events (defined as death, stroke, or myocardial infarction/arrhythmia) within 30 days. Propensity scoring was used to create 2 matching cohorts of patients using demographic and baseline variables. RESULTS: Between 2011 and 2018, among 1200 adult patients undergoing carotid artery stent placement, 23.8% did not have embolic protection devices. There was no trend toward increased embolic protection device use with time. Patients without embolic protection device use received preoperative antiplatelets less frequently (90.6% versus 94.6%, P = .02), underwent more emergent carotid artery stent placement (7.2% versus 3.6%, P = .01), and had a higher incidence of major adverse cardiovascular events (OR = 1.81; 95% CI, 1.11–2.94) and stroke (OR = 3.31; 95% CI, 1.71–6.39). After compensating for baseline imbalances using propensity-matched cohorts (n = 261 for both), carotid artery stent placement without an embolic protection device remained associated with increased major adverse cardiovascular events (9.2% versus 4.2%; OR = 2.30; 95% CI, 1.10–4.80) and stroke (6.5% versus 1.5%; OR = 4.48; 95% CI, 1.49–13.49). CONCLUSIONS: Lack of embolic protection device use during carotid artery stent placement is associated with a 4-fold increase in the likelihood of perioperative stroke. Nevertheless, nearly one-quarter of patients in the American College of Surgeons National Surgical Quality Improvement Program underwent unprotected carotid artery stent placement. Efforts targeting improved embolic protection device use during carotid artery stent placement are warranted.

BACKGROUND AND PURPOSE: High call frequency can lead to inadequate sleep, fatigue, and burnout, resulting in detrimental effects on physicians and patients. We aimed to assess the correlation between the frequency and burden of neurointerventional surgery calls and sleep deprivation with physician burnout, physical and driving safety, and fatigue-related medical errors. MATERIALS AND METHODS: We sent an online questionnaire to the members of the 2 neurointerventional surgery societies comprising 50 questions and spanning 3 main topics: 1) overnight/weekend call burden, 2) sleeping patterns, and 3) Copenhagen Burnout Inventory. RESULTS: One hundred sixty-four surveys were completed. Most (54%) neurointerventional surgeons reported burnout. Call burden of ≥1 every 3 days and being in practice >10 years were independent predictors of burnout. Thirty-nine percent reported falling asleep at the wheel, 23% reported a motor vehicle crash/near-crash, and 34% reported medical errors they considered related to call/work fatigue. On multivariate logistic regression, high call burden (called-in >3 times/week) was an independent predictor of sleeping at the wheel and motor vehicle crashes. Reporting <4 hours of uninterrupted sleep was an independent predictor of motor vehicle crashes and medical errors. Most neurointerventional surgeons recommended a maximum call frequency of once every 3 days. CONCLUSIONS: Call frequency and burden, number of years in practice, and sleep deprivation are associated with burnout of neurointerventional surgeons, sleeping at the wheel, motor vehicle crashes, and fatigue-related medical errors. These findings contribute to the increasing literature on physician burnout and may guide future societal recommendations related to call burden in neurointerventional surgery.

BACKGROUND AND PURPOSE: Acute stroke intervention refractory to mechanical thrombectomy may be due to underlying vessel wall pathology including intracranial atherosclerotic disease and intracranial arterial dissection or recalcitrant emboli. We studied the prevalence and etiology of refractory thrombectomy, the safety and efficacy of adjunctive interventions in a North American–based cohort. MATERIALS AND METHODS: We performed a multicenter, retrospective study of refractory thrombectomy, defined as unsuccessful recanalization, vessel reocclusion in <72 hours, or required adjunctive antiplatelet glycoprotein IIb/IIIa inhibitors, intracranial angioplasty and/or stenting to achieve and maintain reperfusion. Clinical and imaging criteria differentiated etiologies for refractory thrombectomy. Baseline demographics, cerebrovascular risk factors, technical/clinical outcomes, and procedural safety/complications were compared between refractory and standard thrombectomy groups. Multivariable logistic regression analysis was performed to determine independent predictors of refractory thrombectomy. RESULTS: Refractory thrombectomy was identified in 25/302 cases (8.3%), correlated with diabetes (44% versus 22%, P = .02) as an independent predictor with OR = 2.72 (95% CI, 1.05–7.09; P = .04) and inversely correlated with atrial fibrillation (16% versus 45.7%, P = .005). Refractory etiologies were secondary to recalcitrant emboli (20%), intracranial atherosclerotic disease (60%), and/or intracranial arterial dissection (44%). Four (16%) patients were diagnosed with early vessel reocclusion, and 21 patients underwent adjunctive salvage interventions with glycoprotein IIb/IIIa inhibitor infusion alone (32%) or intracranial angioplasty and/or stenting (52%). There were no significant differences in TICI 2b/3 reperfusion efficacy (85.7% versus 90.9%, P = .48), symptomatic intracranial hemorrhage rates (0% versus 9%, P = .24), favorable clinical outcomes (39.1% versus 48.3%, P = .51), or mortality (13% versus 28.3%, P = .14) versus standard thrombectomy. CONCLUSIONS: Refractory stroke thrombectomy is encountered in <10% of cases, independently associated with diabetes, and related to underlying vessel wall pathology (intracranial atherosclerotic disease and/or intracranial arterial dissection) or, less commonly, recalcitrant emboli. Emergent salvage interventions with glycoprotein IIb/IIIa inhibitors or intracranial angioplasty and/or stenting are safe and effective adjunctive treatments.