BACKGROUND AND OBJECTIVES: Endoscopic endonasal surgery (EES) is the preferred approach for treating sellar and parasellar lesions due to its panoramic view and detailed anatomical definition. This study aims to review major arterial injuries during EES, a rare but critical complication associated with high mortality and morbidity rates. METHODS: A retrospective analysis was conducted, including 15 patients from 5640 EES procedures performed between August 1997 and February 2024 at in our center/Department of Neurosurgery. The study focuses on perioperative and postoperative management strategies, highlighting the use of oxidized regenerated cellulose (Surgicel®)/gelatin-thrombin matrix (Floseal®) and multidisciplinary collaboration to achieve hemostasis. RESULTS: The incidence of major arterial injury was 0.2%, with a mean patient age of 38.4 years and a female-to-male ratio of 10:5. The most common tumors were adenomas (n = 7) and chordomas (n = 5). The most commonly bleeding arteries in 6 patients each are the cavernous segment of the internal carotid artery and the paraclival carotid artery. Low-flow bleeding was observed in 10 of our patients, while high-flow bleeding was seen in 5 patients, 4 of whom were recurrent cases (P < .05). In 3 patients with high-flow bleeding from segments of the carotid artery, digital subtraction angiography was performed for stent placement or coil embolization, while in 1 patient with high-flow bleeding, digital subtraction angiography was used for monitoring cerebral blood flow. One of our patients died of a myocardial infarction at the 14th month of follow-up and 1 of our patients developed left-hemiparesis. CONCLUSION: The study underscores the importance of preoperative planning, surgical expertise, and multidisciplinary teamwork in managing major arterial injuries during EES. The authors advocate for the development of standardized treatment algorithms to improve outcomes in these patients. The findings contribute to the limited literature on managing internal carotid artery injuries in EES, emphasizing the need for ongoing research and algorithm development.

Background/Objectives: The interplay between cardiovascular risk factors and brain aging remains incompletely understood. We aimed to investigate the comparative associations of coronary artery calcium (CAC) and low-density lipoprotein cholesterol (LDL-C) with MRI-derived volumetric measures of the brain. Methods: In this retrospective, single-center, cross-sectional study, 84 participants who underwent coronary computed tomography for CAC scoring and brain magnetic resonance imaging within 90 days were included; LDL-C levels were available in 69 participants for LDL-based analyses. Brain volumetric measures were obtained using the automated lesionBrain pipeline within the volBrain platform, which performs fully automated tissue segmentation and lesion quantification based on multi-atlas and patch-based approaches. Associations were evaluated using Spearman’s correlation with false discovery rate correction and hierarchical multivariable regression, supported by bootstrap validation and post hoc power analysis. The cohort had a mean age of 58.0 ± 13.0 years (range 19–78) and was derived from routine clinical imaging. Results: LDL-C was positively associated with abnormal white matter volume (ρ = 0.334, p = 0.005), although this did not remain statistically significant after FDR correction (pFDR = 0.090). In fully adjusted models, LDL-C remained the only independent predictor (β = 0.006, 95% CI: 0.002–0.010, p = 0.007; standardized β = 0.225; partial R² = 11.7%), corresponding to a 6.2% increase in abnormal white matter volume per 10 mg/dL increase (derived from log-transformed models). CAC showed only a marginal association (p = 0.059). Post hoc power analysis demonstrated adequate power for LDL-C but insufficient power for CAC. Neither marker was associated with gray matter volume. Conclusions: In this cross-sectional cohort, higher LDL-C was independently associated with greater abnormal white matter volume after adjustment for cardiovascular risk factors, statin use, and CAC. No CAC–brain association was detected in this cohort, but limited statistical power means that small CAC effects cannot be excluded. These findings should be interpreted as associative rather than causal or mechanistic.