Background: Identifying sex-related differences/variables associated with 30 day/1 year mortality in patients with chronic limb-threatening ischemia (CLTI). Methods: Multicenter/retrospective/observational study. A database was sent to all the Italian vascular surgeries to collect all the patients operated on for CLTI in 2019. Acute lower-limb ischemia and neuropathic-diabetic foot are not included. Follow-up: One year. Data on demographics/comorbidities, treatments/outcomes, and 30 day/1 year mortality were investigated. Results: Information on 2399 cases (69.8% men) from 36/143 (25.2%) centers. Median (IQR) age: 73 (66–80) and 79 (71–85) years for men/women, respectively (p < 0.0001). Women were more likely to be over 75 (63.2% vs. 40.1%, p = 0.0001). More men smokers (73.7% vs. 42.2%, p < 0.0001), are on hemodialysis (10.1% vs. 6.7%, p = 0.006), affected by diabetes (61.9% vs. 52.8%, p < 0.0001), dyslipidemia (69.3% vs. 61.3%, p < 0.0001), hypertension (91.8% vs. 88.5%, p = 0.011), coronaropathy (43.9% vs. 29.4%, p < 0.0001), bronchopneumopathy (37.1% vs. 25.6%, p < 0.0001), underwent more open/hybrid surgeries (37.9% vs. 28.8%, p < 0.0001), and minor amputations (22% vs. 13.7%, p < 0.0001). More women underwent endovascular revascularizations (61.6% vs. 55.2%, p = 0.004), major amputations (9.6% vs. 6.9%, p = 0.024), and obtained limb-salvage if with limited gangrene (50.8% vs. 44.9%, p = 0.017). Age > 75 (HR = 3.63, p = 0.003) is associated with 30 day mortality. Age > 75 (HR = 2.14, p < 0.0001), nephropathy (HR = 1.54, p < 0.0001), coronaropathy (HR = 1.26, p = 0.036), and infection/necrosis of the foot (dry, HR = 1.42, p = 0.040; wet, HR = 2.04, p < 0.0001) are associated with 1 year mortality. No sex-linked difference in mortality statistics. Conclusion: Women exhibit fewer comorbidities but are struck by CLTI when over 75, a factor associated with short- and mid-term mortality, explaining why mortality does not statistically differ between the sexes.

Duodenal obstruction caused by abdominal aortic aneurysm was first described by Osler in 1905 and is named “aortoduodenal syndrome.” This condition has always been treated by open surgical repair. We report the first case of aortoduodenal syndrome successfully treated by endovascular aneurysm repair. A 74-year-old male patient referred to our hospital complaining postprandial vomit, reporting a consistent weight loss in the latest weeks. Enhanced computed tomography scans showed a small saccular abdominal aortic aneurysm compressing duodenum and inferior vena cava without any other evident pathological finding. As the patient underwent a successful endovascular treatment of the abdominal aortic aneurysm, symptoms immediately resolved so that he started back to feed and progressively gained body weight. Despite aortoduodenal syndrome is generally caused by large abdominal aortic aneurysm, this condition has to be suspected also in case of small abdominal aortic aneurysm. Differently from what has been reported in literature, endovascular aneurysm repair could be effective in the treatment of aortoduodenal syndrome.

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.

Late type II endoleaks (T2ELs) arising from the internal iliac artery (IIA) may present during follow-up after endovascular aortic repair (EVAR) of aortoiliac aneurysm and may warrant embolization if enlargement of the aneurysmal sac is demonstrated. When coverage of the IIA ostium has been made due to extensive iliac disease, access options can be challenging. Different treatment options have been reported over recent years, and a careful selection of the best one must be made based on the characteristics of each case. The present study reports a simple and reproducible sheathless percutaneous superior gluteal artery (SGA) access and provides a discussion based on a review of the existing literature on this topic.

Severe iliofemoral calcification can compromise emergency endovascular control of access‐site bleeding by preventing full covered‐stent expansion at the landing zone. A 78‐year‐old man developed hemodynamic instability, right‐flank pain, and severe anemia 6 h after ultrasound‐guided right transfemoral primary percutaneous coronary intervention for anterior ST‐segment elevation myocardial infarction. Contrast‐enhanced computed tomography demonstrated a large right retroperitoneal hematoma with active extravasation from the distal external iliac artery, immediately proximal to a bulky calcified plaque involving the proximal common femoral artery (CFA). Through ultrasound‐guided contralateral femoral access, an 8 mm × 60 mm self‐expanding covered stent achieved immediate sealing of the external iliac artery injury but remained markedly underexpanded distally at the calcified CFA landing zone. Conventional 8‐mm balloon post‐dilation was attempted, but residual underexpansion persisted; further high‐pressure dilation was avoided because of concern for rupture or perforation of the calcified iliofemoral segment and loss of the newly achieved seal. Bailout intravascular lithotripsy (IVL) with an 8 mm × 60 mm balloon consisted of 150 pulses delivered at 4 atm in repeated sequences, each followed by nominal‐pressure post‐dilation of the same balloon at 6 atm. Final angiography showed improved covered‐stent expansion with approximately 30% residual stenosis and no recurrent extravasation, dissection, perforation, or distal embolization. The patient was discharged on postoperative day 8. At 12‐month follow‐up, duplex ultrasound confirmed covered‐stent patency without edge stenosis, pseudoaneurysm, or hemodynamically significant restenosis. This case illustrates that IVL may provide a low‐pressure bailout option for calcium‐mediated peripheral covered‐stent underexpansion during emergency vascular access‐site repair; however, this off‐label use requires careful device sizing, attention to covered‐stent integrity, and structured imaging surveillance.