Late type II endoleak (T2EL) arising from internal iliac artery (IIA) network may occur after endovascular aortic repair (EVAR) of aortoiliac aneurysm and may require embolization if sac enlargement is demonstrated. When direct antegrade access to ipsilateral IIA is not achievable due to previous vessel coverage and/or embolization, access to the nidus can be challenging. We report a case of T2EL originating from IIA network causing iliac sac enlargement in a patient previously treated by EVAR for artoiliac aneurysm with IIA embolization and coverage, in which embolization of the nidus was performed through a percutaneous sheathless access to ip-silateral superior gluteal artery (SGA). A literature review dealing with all cases of percutaneous direct SGA access for retrograde embolization of T2EL arising from IIA after previous EVAR is also reported. The research was conducted on Pubmed database using keywords “superior glu-teal artery access,” “transgluteal embolization” and “retrograde embolization for type II endo-leak”. Related articles and references were screened for suitable articles.

The hemodynamic consequences of the aortic stenosis (AS) on supraortic trunks may have a po-tential role in the diagnosis of concomitant internal carotid artery (ICA) stenosis by dampening blood flow velocity. To investigate the effect of AS on ICA blood flow we evaluated carotid and vertebral blood flow velocity indexes in patients undergoing transcatheter aortic valve implanta-tion (TAVI). Eighty-five patients admitted for endovascular treatment of a severe AS underwent supra-aortic Duplex ultrasound (DUS) examination prior and after TAVI to be enrolled in the study. Patients with other cardiac impairments that could configure a confounding factor were excluded. Pa-tients with symptomatic or severe ICA stenosis defined according to NASCET criteria were ex-cluded. Forty-five patients of a median age of 80 years met the study inclusion criteria. The peak systolic velocity (PSV) of the assessed supraortic arteries increased after TAVI: respectively common ca-rotid artery (CCA) 64 ± 17 cm/s vs 78 ± 23 cm/s, p= 0,01; ICA 68 ± 23 cm/s vs 96 ± 35 cm/s, p= 0,01; vertebral artery (VA) 45 ± 14 cm/s vs 52 ± 15 cm/s, p=0,03. Similarly, the end diastolic velocity (EDV) increased after TAVI: respectively CCA 13 ± 6 cm/s vs 15 ± 7 cm/s, p=ns; ICA 20 ± 9 cm/s vs 24 ± 9 cm/s, p= 0,01; VA 9 ± 4 cm/s vs 11 ± 4 cm/s, p=0,01. Consistently, the mean acceleration time (AC) decreased after TAVI: respectively CCA 0,17 ± 0,05 s vs 0,12 ± 0,05 s, p= 0.01; ICA 0,1 8 ± 0,05 s vs 0,12 ± 0,04 s, p= 0,01; VA 0,16 ± 0,05 s vs 0,11 ± 0,05 s, p=0,02. Severe AS significantly affects supra-aortic arteries blood flow as assessed by duplex, by de-creasing both PSV and EDV and increasing AC. This study suggests that carotid ultrasound cri-teria to assess ICA stenosis severity should be re-evaluated in larger multicenter studies to vali-date their predictive values in patients with concomitant AS.