Background Non-ischemic cerebral enhancing (NICE) lesions have been reported as a rare complication of various neuroendovascular procedures, but information on their incidence after flow diversion is scant. It is unclear if specific devices or novel coating technologies may impact their occurrence. Methods We conducted a multicenter study on the incidence of NICE lesions after flow diverter (FD) implantation for cerebral aneurysm treatment. Results Eight centers identified 15 patients and provided detailed data. The clinical presentation ranged from asymptomatic to hemiplegia and cognitive impairment. The mean time to diagnosis after treatment was 65.1±101.5 days. Five centers disclosed information on all of their 1201 FD procedures during the inclusion period (2015–2022), during which 12 patients were diagnosed with NICE lesions in these institutions—that is, an incidence of 1%. FD coatings did not increase the incidence (6/591 patients (1%) treated with surface-modified FD vs 6/610 patients (1%) treated with bare FD; P=1.00). Significantly increased rates of 3.7% (6 cases in 161 procedures; P<0.01) and 3.3% (5 cases in 153 procedures; P<0.01) were found with stents of two specific product lines. The use of one product line was associated with a significantly lower incidence (0 cases in 499 procedures (0%); P<0.01). Conclusions Novel stent coatings are not associated with an increased incidence of NICE lesions. The incidence rate of 1% suggests that these lesions may occur more often after flow diversion than after other endovascular treatments. We found a concerning accumulation of NICE lesion cases when FDs from two product families were used.

Background: During the last decade, cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) was a current research focus without a standardized classification in digital subtraction angiography (DSA). This study was performed to investigate a device-independent visual cerebral vasospasm classification for endovascular treatment. Methods: The analyses are DSA based rather than multimodal. Ten defined points of intracranial arteries were measured in 45 patients suffering from cerebral vasospasm after SAH at three time points (hospitalization, before spasmolysis, control after six months). Mathematical clustering of vessel diameters was performed to generate four objective grades for comparison. Six interventional neuroradiologists in two groups scored 237 DSAs after a new visual classification (grade 0–3) developed on a segmental pattern of vessel contraction. For the second group, a threshold-based criterion was amended. Results: The raters had a reproducibility of 68.4% in the first group and 75.2% in the second group. The complementary threshold-based criterion increased the reproducibility by about 6.8%, while the rating deviated more from the mathematical clustering in all grades. Conclusions: The proposed visual classification scheme of cerebral vasospasm is suitable as a standard grading procedure for endovascular treatment. There is no advantage of a threshold-based criterion that compensates for the effort involved. Automated vessel analysis is superior to compare inter-group results in research settings.

The cytokine interleukin-6 (IL-6) plays a central role in the inflammation cascade as well as cardiovascular disease progression. Since myeloid cells are a primary source of IL-6 formation, we aimed to generate a mouse model to study the role of myeloid cell-derived IL-6 in vascular disease. Interleukin-6-overexpressing (IL-6^OE) mice were generated and crossed with LysM-Cre mice, to generate mice (LysM-IL-6^OE mice) overexpressing the cytokine in myeloid cells. Eight- to 12-week-old LysM-IL-6^OE mice spontaneously developed inflammatory colitis and significantly impaired endothelium-dependent aortic relaxation, increased aortic reactive oxygen species (ROS) formation, and vascular dysfunction in resistance vessels. The latter phenotype was associated with decreased survival. Vascular dysfunction was accompanied by a significant accumulation of neutrophils, monocytes, and macrophages in the aorta, increased myeloid cell reactivity (elevated ROS production), and vascular fibrosis associated with phenotypic changes in vascular smooth muscle cells. In addition to elevated Mcp1 and Cxcl1 mRNA levels, aortae from LysM-IL-6^OE mice expressed higher levels of inducible NO synthase and endothelin-1, thus partially accounting for vascular dysfunction, whereas systemic blood pressure alterations were not observed. Bone marrow (BM) transplantation experiments revealed that vascular dysfunction and ROS formation were driven by BM cell-derived IL-6 in a dose-dependent manner. Mice with conditional overexpression of IL-6 in myeloid cells show systemic and vascular inflammation as well as endothelial dysfunction. A decrease in circulating IL-6 levels by replacing IL-6-producing myeloid cells in the BM improved vascular dysfunction in this model, underpinning the relevant role of IL-6 in vascular disease. Myeloid cell-derived interleukin-6 (IL-6) overexpression was associated with systemic inflammation. Chronic myeloid cell-derived IL-6 evoked a significantly impaired endothelium-dependent aortic relaxation, increased aortic reactive oxygen species (ROS), and vascular dysfunction in resistance vessels. Vascular dysfunction was accompanied by a significant accumulation of myeloid cells in the aortic wall, an increased reactivity of myeloid cells, vascular fibrosis, and an altered vascular smooth muscle cell phenotype. This went in line with significantly elevated Mcp1, Cxcl1, and Rorc levels and an increased inducible NO synthase and endothelin-1 expression in LysM-IL-6^OE aortas. Bone marrow (BM) transplantation studies revealed that vascular dysfunction and ROS formation were driven by BM cell-derived IL-6 in a dose-dependent manner.

Flow diversion (FD) is a novel endovascular technique based on the profound alteration of cerebrovascular hemodynamics, which emerged as a promising minimally invasive therapy for intracranial aneurysms. However, delayed post-procedural stroke remains an unexplained concern. A consistent follow-up-regimen has not yet been defined, but is required urgently to clarify the underlying cause of delayed ischemia. In the last two years, 223 patients were treated with six different FD devices in our center. We identified subacute, FD-induced segmental vasospasm (SV) in 36 patients as a yet unknown, delayed-type reaction potentially compromising brain perfusion to a critical level. Furthermore, 86% of all patients revealed significant SV approximately four weeks after treatment. In addition, 56% had SV with 25% stenosis, and 80% had additional neointimal hyperplasia. Only 13% exhibited SV-related high-grade stenosis. One of those suffered stroke due to prolonged SV, requiring neurocritical care and repeated intra-arterial (i.a.) biochemical angioplasty for seven days to prevent territorial infarction. Five patients suffered newly manifested, transient hemicrania accompanying a compensatorily increased ipsilateral leptomeningeal perfusion. One treated vessel obliterated permanently. Hence, FD-induced SV is a frequent vascular reaction after FD treatment, potentially causing symptomatic ischemia or even stroke, approximately one month post procedure. A specifically early follow-up-strategy must be applied to identify patients at risk for ischemia, requiring intensified monitoring and potentially anti-vasospastic treatment.

The advent of endovascular thrombectomy has significantly improved outcomes for stroke patients with intracranial large vessel occlusion, yet individual benefits can vary widely. As demand for thrombectomy rises and geographical disparities in stroke care access persist, there is a growing need for predictive models that quantify individual benefits. However, current imaging methods for estimating outcomes may not fully capture the dynamic nature of cerebral ischaemia and lack a patient-specific assessment of thrombectomy benefits. Our study introduces a deep learning approach to predict individual responses to thrombectomy in acute ischaemic stroke patients. The proposed models provide predictions for both tissue and clinical outcomes under two scenarios: one assuming successful reperfusion and another assuming unsuccessful reperfusion. The resulting simulations of penumbral salvage and difference in National Institutes of Health Stroke Scale (NIHSS) at discharge quantify the potential individual benefits of the intervention. Our models were developed on an extensive dataset from routine stroke care, which included 405 ischaemic stroke patients who underwent thrombectomy. We used acute data for training (n = 304), including multimodal CT imaging and clinical characteristics, along with post hoc markers such as thrombectomy success, final infarct localization and NIHSS at discharge. We benchmarked our tissue outcome predictions under the observed reperfusion scenario against a thresholding-based clinical method and a generalized linear model. Our deep learning model showed significant superiority, with a mean Dice score of 0.48 on internal test data (n = 50) and 0.52 on external test data (n = 51), versus 0.26/0.36 and 0.34/0.35 for the baselines, respectively. The NIHSS sum score prediction achieved median absolute errors of 1.5 NIHSS points on the internal test dataset and 3.0 NIHSS points on the external test dataset, outperforming other machine learning models. By predicting the patient-specific response to thrombectomy for both tissue and clinical outcomes, our approach offers an innovative biomarker that captures the dynamics of cerebral ischaemia. We believe this method holds significant potential to enhance personalized therapeutic strategies and to facilitate efficient resource allocation in acute stroke care.

A threshold-based classification of cerebral vasospasm needs reference values for intracranial vessel diameters on digital subtraction angiography (DSA). We aimed to generate adjusted reference values for this purpose by retrospectively analyzing angiograms and potential influencing factors on vessel diameters. Angiograms of the anterior circulation were evaluated in 278 patients aged 18–81 years. The vessel diameters of 453 angiograms (175 bilateral) were gathered from nine defined measuring sites. The effect sizes of physical characteristics (i.e., body weight and height, body mass index, gender, age, and cranial side) and anatomical variations were calculated with MANOVA. Segments bearing aneurysms were excluded for the calculation of reference values. Adjusted vessel diameters were calculated via linear regression analysis of the vessel diameter data. Vessel diameters increased with age and body height. Male and right-sided vessels were larger in diameter. Of the anatomical variations, only the hypoplastic/aplastic A1 segment had a significant influence (p < 0.05) on values of the anterior cerebral artery and the internal carotid artery with a small effect size (|ω²| > 0.01) being excluded from the reference values. We provide gender-, age-, and side-adjusted reference values and nomograms of arterial vessel diameters in the anterior circulation.