Lanzino, Giuseppe

Background: Previous studies have linked pericoronary artery adipose tissue attenuation to major adverse cardiac event (MACE). However, the association between pericarotid artery fat and prognosis remains underexplored. This study aimed to investigate the association between preoperative pericarotid fat characteristics and the subsequent prognosis in patients undergoing carotid endarterectomy (CEA). Methods: This study included patients with preoperative computed tomography angiography (CTA) followed by CEA. Preoperative neck CTA images were obtained and analyzed with novel methods using 3D Slicer software. We segmented the common and internal carotid arteries. The segment was horizontally trimmed, isolating the region around the bifurcation, extending 15 mm above and 10 mm below. Pericarotid fat was defined as adipose tissue within a 5 mm radial distance from the outer vessel wall, with Hounsfield units (HU) between -190 and -30 (Figure 1, carotid segmentation [green] and pericarotid fat [yellow]) . For each patient, we calculated the HU average and the volume (mm3) of the pericarotid fat. MACE was defined as a composite of all-cause mortality, myocardial infarction, and cerebrovascular events. The relationship between both pericarotid fat characteristics and MACE was investigated. Results: Of the 43 patients initially included, one was excluded due to an inability to perform segmentation caused by chronic total occlusion, leaving 42 patients (age 73 [67-78] years, 33 [76.7%] male). The comparison of mean pericarotid fat HU between the ipsilateral and contralateral sides showed no significant difference (-60.3±11.0 HU vs. -60.9 ±11.3 HU, p=0.437). However, the median ipsilateral fat volume was significantly higher than the contralateral volume (528 [248, 1100] mm3 vs. 328 [184, 697] mm3, p=0.020). When comparing patients with and without MACE, those with MACE had a significantly lower ipsilateral fat density (-59.4±10.2 HU vs. -66.8 ±11.1 HU, p=0.022) and a higher fat volume (468 [233, 746] mm3 vs. 845 [458, 1451] mm3, p=0.044). Kaplan-Meier analysis revealed that higher volume and lower fat density than the median were significant predictors of MACE (log-rank p=0.015 and p=0.042, respectively) (Figure 2). Conclusions: Assessment of pericarotid fat using a novel CTA analytic method in patients undergoing CEA identified ipsilateral lower fat density and higher fat volume as predictors of adverse outcomes.

Background: Previous research has suggested pericarotid fat density to be significantly linked to atherosclerotic plaque components and cerebrovascular events. Inflammatory markers within the plaques are critical in the pathogenesis and progression of carotid artery disease. However, the association between pericarotid fat and inflammatory processes within atherosclerotic plaques remains underexplored. This study hypothesizes that pericarotid fat density is directly associated with the levels of inflammatory markers within atherosclerotic plaques. Methods: Carotid plaques were prospectively collected from patients with carotid artery disease undergoing carotid endarterectomy (CEA). The levels of inflammatory plaque cytokines (MCP-1, IL-8, IFN-γ, IL-10, IL-1β, IL-6, PDGF-AA, PDGF-AB/BB, TNF-α, VEGF) were measured in tissue homogenates using a customized 10-plex Luminex assay. Baseline demographics and clinical data of our population were extracted from electronic health records. We analyzed preoperative neck computed tomography angiography (CTA) images placing regions-of-interest (ROI) in the pericarotid fat on the slice showing maximal stenosis. For each patient, we calculated the average of Hounsfield Units (HU) within the ROI. Spearman correlation test was used to assess the correlation between variables. Results: Among the 43 patients included, the median age was 73 (67, 78) years, and 33 (76.7%) patients were male. Plaque levels of PDGF-AA and VEGF showed significant positive correlations with HU (r=0.330, p=0.030; r=0.380, p=0.011, respectively), as illustrated in Figure 1 . Although plaque levels of IFN-γ demonstrated a significant negative correlation with HU (r=-0.390, p=0.010), the most cases exhibited values close to zero. Conclusions: The assessment of pericarotid fat density on CTA may allow for the estimation of plaque inflammation, suggesting that more fat density is associated with increased inflammatory activity within atherosclerotic plaques.

Introduction: Iatrogenic cervical artery dissection (CeAD) may result from various procedures such as procedural and diagnostic angiography. Due to the rarity of iatrogenic CeAD, existing literature on management and outcomes is limited. This observational cohort study investigates clinical approaches and long-term outcomes of iatrogenic CeAD after endovascular interventions. Methods: We conducted a retrospective chart review to analyze patients who underwent endovascular treatments at the Mayo Clinic from 1998 to 2021. We focused on patients with iatrogenic CeAD resulting from interventions. Pertinent patient factors were extracted. Descriptive statistics highlighted the relationship between treatments and long-term clinical outcomes. Results: Between 1998 and 2021, 21,191 patients underwent catheter cerebral angiography. Among them, 32 had iatrogenic CeAD (30 identified as white, 23 women, median age 59 [range 40.5–92.9]). Common comorbidities included hypertension (62.5%), smoking (56.3%), and hyperlipidemia (46.9%). Of the 32 patients, 9(28.1%) had dissection with diagnostic angiograms, 6(18.8%) endovascular thrombectomy, 15(46.9%) aneurysm treatment, and 2(6.3%) angioplasty with or without stenting. The location of dissections was dependent upon the intervention: 17(53.1%) had internal carotid artery dissection, 13(40.6%) vertebral artery dissection, and 2(6.3%) common carotid dissection. One patient was symptomatic with neck pain. All dissections were diagnosed by cerebral angiography during the same session as the initial intervention. Only 4(12.5%) were treated with hyperacute stenting. Following diagnosis, 30(93.7%) were placed on antithrombotic therapy, including aspirin alone (34.4%) or dual antiplatelet therapy with aspirin and clopidogrel (37.5%). The median duration of acute treatment was 3 months. The median duration of imaging follow up was 1022 days. Follow-up imaging showed an excellent radiological course, with complete or nearly complete dissection remodeling. Conclusions: Iatrogenic CeAD with endovascular interventions is rare and typically benign. Most cases are managed medically without significant clinical complications or long-term negative outcomes. Single or dual antiplatelet therapies remain preferred treatments, in line with current trends. Key factors influencing clinical decision-making include location, occlusion rate, pseudoaneurysm formation, intracranial extension, distal collateral circulation, and ischemia.

Background: The bovine aortic arch is a vascular variant in which the left common carotid artery originates from the brachiocephalic trunk rather than directly from the aortic arch. The bovine anatomical variation may alter the blood flow dynamics, potentially contributing to the formation and progression of carotid plaques. In this study, we evaluated the association of the bovine aortic arch and the severity of carotid stenosis. Methods: In this retrospective study, we included patients with carotid artery disease undergoing carotid endarterectomy (CEA) and pre-surgical computed tomography angiography (CTA). CTAs were reviewed to assess the carotid stenosis and the anatomy of the aortic arch. The left carotid artery was classified as normal if it originated from the aortic arch and as bovine if it originated from the brachiocephalic trunk (Figure 1) . Unlimited propensity score matching was performed to balance baseline characteristics between patients with bovine and normal anatomies. The Mann-Whitney U test was applied to compare carotid stenosis between bovine and normal arteries. Results: A total of 203 patients (bovine:23, normal:180) were initially enrolled. Using propensity score matching, 20 patients with bovine anatomy were matched to 45 patients with normal anatomy (Figure 2) . Among the 65 patients included, 47 (74.6%) were male, with a median age of 70 [IQR:65.0-76.0] years. Left-sided carotid artery disease was more prevalent in the bovine compared to normal group (N=12, 66.7% vs. N=16, 36.4%; p=0.030). Additionally, the severity of carotid stenosis in CEA-treated side was higher in patients with bovine arch compared to normal controls (82.5% [76.2-88.7] vs. 70.0% [50.0-95.0]; p=0.030) (Figure 3) . Conclusions: The association of a bovine aortic arch with more severe carotid stenosis suggests that this anatomical variant may be a marker for increased cerebrovascular risk.

Introduction/Purpose The multicenter, prospective, single‐arm, controlled, non‐randomized SCENT trial on flow diverter (FD) treatment for intracranial aneurysms (IA) was analyzed for patients’ age and IA characteristics impacting stroke and occlusion rates over 5 years. Materials and Methods Impact on major ipsilateral stroke and IA occlusion was studied by stratifying age as </= 65 years versus >65 years. Twice as many subjects treated were </= 65 years old (n=119/180). Product‐limit (Kaplan‐Meier) estimates of time to both endpoints, stratified by age group, were created. Univariate predictors of time to stroke were identified by including candidate variables in univariable proportional hazards regression models. Those variables found to be significant (p<0.10) at the univariate level were entered into a multivariable survival model to identify independent predictors. The stepwise selection produced a final reduced model with a significance level to both enter and stay set at 0.05. Results When parent artery stenosis and IA size were entered into a multiple‐stepwise survival model, only stenosis remained as an independently significant predictor of time to stroke. At 3‐year follow‐up, there were a total of 23 strokes (12.8%), with 11 (47.8%) occurring in subjects </= 65 years; there was a greater risk for seniors (HR1.96, 95% CI 0.83‐4.78, p=.122). Four patients (4/180; 2.2%) experienced aneurysm ruptured within the first week post‐treatment, with 3 being </= 65 and the fourth aged 66 years. No new strokes were reported between 3 and 5 years. Complete IA occlusion rates for seniors were 60.0% (33/55), 67.6% (25/37), and 85.7% (18/21) at 12, 36, and 60 months, respectively, as compared to 79.1% (87/110), 82.5% (66/80), and 91.8% (56/61) for younger subjects. The time to complete IA occlusion was shorter in younger patients (HR1.53, 95% CI 1.07‐2.19, p=.020). Five subjects (2.8%) underwent retreatment, 2 in 60‐year‐old patients, and one each aged 64, 70, and 75. Conclusion Stroke, early rupture risk, and aneurysm occlusion in patients treated with FD are related to age and pre‐existing parent artery stenosis, IA size, and location. With demographic shifts, future treatments need to focus on expedited and improved healing.

Abstract Cardiovascular disease remains a prominent cause of disability and premature death worldwide. Within this spectrum, carotid artery atherosclerosis is a complex and multifaceted condition, and a prominent precursor of acute ischaemic stroke and other cardiovascular events. The intricate interplay among inflammation, oxidative stress, endothelial dysfunction, lipid metabolism, and immune responses participates in the development of lesions, leading to luminal stenosis and potential plaque instability. Even non-stenotic plaques can precipitate a sudden cerebrovascular event, regardless of the degree of luminal encroachment. In this context, carotid imaging modalities have proved their efficacy in providing in vivo characterization of plaque features, contributing substantially to patient risk stratification and clinical management. This review emphasizes the importance of identifying high-risk individuals by use of current imaging modalities, biomarkers, and risk stratification tools. Such approaches inform early intervention and the implementation of personalized therapeutic strategies, ultimately enhancing patient outcomes in the realm of cardiovascular disease management.

Abstract Adult primary leptomeningeal gliomatosis (PLG) is a rare, rapidly progressive and fatal disease characterized by prominent leptomeningeal infiltration by a glial tumor without an identifiable parenchymal mass. The molecular profile of adult PLG has not been well‐characterized. We report the clinical, pathological, and molecular findings of six adult PLG patients (five males and one female), median age 58 years. All cases exhibited pathological leptomeningeal enhancement at presentation. Leptomeningeal biopsy was diagnostic in five (of six) cases, revealing infiltration by an astrocytic glioma with mitotic activity, lacking microvascular proliferation or necrosis. One case was diagnosed at autopsy. All tumors were IDH‐wildtype, with five harboring TERT promoter mutations. Additional mutations identified were PTEN in one case, TP53 in two cases, and NF1 in two cases. A chromosome profile with +7/−10 was found in four cases, whereas the remaining two showed either chromosome 7 or 7p gain only. Four cases showed chromosome 9p loss with CDKN2A/B homozygous deletion, one case showed hemizygous CDKN2A/B loss, and one case showed intact chromosome 9 and CDK4/GLI1 amplification. DNA methylation profiling was performed in four cases and revealed a match to glioblastoma (GBM) family and mesenchymal typical class with high confidence scores in two cases; the other two cases showed only suggestive combined scores for GBM family and mesenchymal atypical class. The molecular profile of all cases closely aligned with that of adult‐type GBM, IDH‐wildtype, CNS WHO grade 4. All patients succumbed to the disease. In five cases with extensive leptomeningeal disease at diagnosis, the course was rapid, with median survival of 24 days following palliative care. Only one case, with relatively localized disease at diagnosis, received chemoradiation therapy and survived 535 days, raising the possibility that early diagnosis and timely treatment could improve outcome. A detailed list of previously reported cases is provided in a supplementary table.

Background Iatrogenic cervical artery dissection (CeAD) results from various procedures including interventional angiographic procedures and diagnostic angiography. Iatrogenic CeAD is rare, resulting in limited literature on management and outcomes. This observational cohort study investigates approaches and outcomes of iatrogenic CeAD after endovascular interventions. Methods We conducted a retrospective review for patients who underwent endovascular intervention with resulting iatrogenic CeAD at Mayo Clinic, Rochester, MN, from 1998 to 2021. Pertinent patient factors were extracted and descriptive statistics generated. Results Between 1998 and 2021, 21,191 patients underwent catheter-based cerebral angiography. Thirty-two had iatrogenic CeADs (23 women; median age 59 [range 40.5–92.9]). Common comorbidities included hypertension (62.5%), smoking (56.3%), and hyperlipidemia (46.9%). Nine (28.1%) had dissection with diagnostic angiograms, 6 (18.8%) endovascular thrombectomy, 15 (46.9%) intracranial aneurysm treatment/coiling, and 2 (6.3%) intracranial angioplasty with/without stenting. All dissections were diagnosed by cerebral angiography during the same session as initial interventions. Four (12.5%) underwent hyperacute stenting. Thirty (93.7%) were placed on antithrombotic therapy with aspirin alone (34.4%) or dual-antiplatelet therapy with aspirin and clopidogrel (37.5%). Median duration of acute treatment was three months. Follow-up imaging showed excellent radiological course. Conclusions Iatrogenic CeAD with endovascular interventions is rare and typically benign. Most are managed medically without complications or long-term negative outcomes. Oral single or dual-antiplatelet therapies are preferred compared to previous studies which emphasize intravenous anticoagulation. The duration of acute therapy varied from three months to lifelong. Key factors influencing clinical decision-making may include occlusion rate, pseudoaneurysm formation, intracranial extension, distal collateral circulation, and resultant ischemia.