J. Vasc. Dis., Volume 4, Issue 4 (December 2025) – 3 articles

Chronic type B aortic dissection (cTBAD) is a challenging condition frequently complicated by persistent false lumen (FL) perfusion, leading to aneurysmal degeneration. Despite significant advances in thoracic endovascular aortic repair (TEVAR), long-term management remains challenging because of continuous FL backflow from distal re-entry tears and progressive aortic dilatation. We present the first documented case of FL exclusion using a custom-made false lumen occlusion device (FLOD). A 77-year-old male who had undergone TEVAR in 2017 underwent computed tomography angiography (CTA) in 2025, with the results revealing aneurysmal degeneration of the descending thoracic aorta (maximum diameter 58.5 mm) and two distal re-entry tears with substantial FL perfusion. Following multidisciplinary evaluation, the patient underwent endovascular reintervention with proximal stent graft extension and the deployment of a custom FLOD into the FL via femoral access. Completion angiography confirmed proper FL exclusion with preservation of visceral artery patency. Transesophageal echocardiography demonstrated rapid FL thrombosis. The patient was discharged on postoperative day 5 in good condition without complications. This case highlights that combining endograft extension with a dedicated FLOD is a safe and effective strategy for selected patients with complex cTBAD anatomy. Full article

Background: Cardiovascular disease (CVD) is the leading cause of mortality in chronic kidney disease (CKD), driven by mechanisms distinct from the general population. Fibroblast Growth Factor 23 (FGF-23), a phosphaturic hormone elevated early in CKD, has been mechanistically linked to left ventricular hypertrophy, vascular dysfunction, and disordered mineral metabolism. This study examines the associations between FGF-23 and key renal, mineral, and cardiovascular parameters and its utility in risk stratification. Methods: We conducted a cross-sectional study of 60 adults with CKD stages 1–5. Serum FGF-23 was quantified using ELISA, alongside measures of iPTH, phosphorus, calcium, and eGFR (Estimated Glomerular Filtration Rate). Cardiovascular evaluation included transthoracic echocardiography and carotid intima-media thickness (CIMT). Associations were analyzed using Spearman correlations, ROC analysis, and multivariable logistic regression. Results: FGF-23 levels were significantly associated with declining eGFR (r = –0.288; p < 0.05), elevated iPTH (Intact Parathyroid Hormone) (r = 0.361; p < 0.05), and serum phosphorus (r = 0.335; p < 0.05). Patients with structural cardiac abnormalities (left atrial enlargement or left ventricular hypertrophy) exhibited higher FGF-23 concentrations (154 vs. 128 pg/mL; p = 0.027). FGF-23 alone predicted high cardiovascular risk with moderate accuracy (AUC 0.70; sensitivity 76%; specificity 67%). A composite model including iPTH and eGFR improved discriminatory power (AUC 0.76). Conclusions: FGF-23 correlates with subclinical cardiovascular remodeling and key mineral abnormalities in CKD. Its integration with iPTH and eGFR enhances cardiovascular risk stratification, supporting its potential as a multidimensional biomarker in early CKD. However, the cross-sectional design and modest correlation strengths limit causal inference and generalizability of the findings. Full article

An ascending aortic aneurysm is a localized dilation of the ascending aorta, which poses a high risk of aortic dissection or rupture, with surgery recommended at diameters > 5.5 cm. However, events also occur at smaller sizes, suggesting additional factors—such as stenosis—may significantly influence aneurysm severity. To investigate this, a computational fluid dynamics (CFD) analysis was conducted using a patient-specific ascending aortic model (aneurysm diameter: 5.28 cm) under three aortic stenosis severities: mild, moderate, and severe. Results showed that the severe stenosis condition led to the formation of prominent recirculation zones and increased peak velocities, 2.36 m·s⁻¹ compared to 1.53 m·s⁻¹ for moderate stenosis and 1.37 m·s⁻¹ for mild stenosis. A significantly increased pressure loss coefficient was observed for the severe case. Additionally, the wall shear stress (WSS) distribution exhibited higher values along the anterior region and lower values along the posterior region. Peak WSS values were recorded at 43.46 Pa in the severe stenosis model, compared to 21.98 Pa and 13.87 Pa for the moderate and mild cases, respectively. Velocity distribution and helicity analyses demonstrate that increasing stenosis severity amplifies jet-induced flow disturbances, contributing to larger recirculation zones and greater helicity heterogeneity in the ascending aorta. Meanwhile, WSS results indicate that greater stenosis severity is also associated with elevated WSS magnitude and heterogeneity in the ascending aorta, with severe cases exhibiting the highest value. These findings highlight the need to incorporate hemodynamic metrics, alongside traditional diameter-based criteria, into rupture risk assessment frameworks. Full article