Reducing aneurysm sac growth and secondary interventions following endovascular abdominal aortic aneurysm repair by preemptive coil embolization of the inferior mesenteric artery and lumbar arteries.

OBJECTIVE: Type II endoleak (EL-2) is the most common complication following endovascular aneurysm repair (EVAR), leading to continued sac growth and potential rupture. In this study, we examined the association between patency of the inferior mesenteric artery (IMA) and lumbar arteries (LAs) with respect to sac growth. The effect of preemptive embolization of the IMA and/or LAs on the need for secondary interventions for sac growth post-EVAR was also evaluated. METHODS: A retrospective cohort study was performed on consecutive patients who underwent EVAR for non-ruptured, infrarenal abdominal aortic aneurysms (AAAs) from January 2012 to December 2020. A select group of patients underwent preemptive embolization of the IMA and/or LA. Patients with any types I, III, or IV endoleaks were excluded. Patency of the IMA and LA on preoperative computed tomography angiogram (CTA) was evaluated on TeraRecon workstation. All secondary interventions to treat EL-2 were recorded. Sac growth was defined as centerline axial diameter increase of ≥5 mm on follow-up CTA. RESULTS: A total of 300 patients (mean age, 74 ± 8.5 years; 83.7% male) underwent EVAR. Ninety-nine patients had preemptive embolization of the IMA and/or LA. Mean follow-up of the cohort was 59.3 ± 30.5 months. Thirty-six patients (12%) demonstrated sac growth on follow-up; 12 of these (33.3%) had preemptive embolization. The median time until detection of sac growth was 28.8 months (interquartile range, 15.2-46.5 months), with a mean growth of 10.1 ± 6.4 mm. Sac growth was significantly associated with presence of EL-2: 27 of 36 (75%) with EL-2 vs 9 of 36 (25%) without EL-2 (P < .001). Patients with sac growth had a higher mean total number (2.6 ± 1.5) of patent lower LAs (L3, L4) compared with those without (2.0 ± 1.4; P = .03). Patency of L1, L2, and L3 LAs were not associated with sac growth. However, patency of at least one L4 LA was significantly associated with sac growth (14.8% vs 7.7%; P = .04). The highest incidence of sac growth (17.6%) was seen when both IMA and L4 LA were patent; significantly different from the lowest incidence (5.3%) when both were occluded preoperatively (P = .018). Preemptive coiling of the IMA and/or LA significantly reduced the need for post-EVAR secondary intervention for sac growth. Freedom from post-EVAR secondary intervention was achieved in 92 of 99 (92.9%) pre-EVAR coiled patients vs 163 of 201 (81.5%) patients who did not undergo pre-EVAR coiling (P = .009). CONCLUSIONS: Preemptive coil embolization of the IMA and LAs, especially L4 LA, reduces the need for secondary interventions for sac growth, potentially improving the long-term durability of EVAR.

Fat and exposure to 4-nitroquinoline-1-oxide causes histologic and inflammatory changes in murine livers.

Risk factors for liver cancer include tobacco use, alcohol consumption, obesity, and male sex. Administration of 4-nitroquinonline-1-oxide (4NQO) in drinking water mimics the effects of tobacco and leads to oral carcinoma in mice. This study compared the effects of diets high and low in saturated fat (HF and LF, respectively), and sex, on liver histopathology in 4NQO-treated mice and controls. We hypothesized that 4NQO would cause histopathological changes in liver, and that a HF diet would increase hepatic pathology when compared to the LF diet. Mice (C57Bl/6, 36/sex), were divided into a low fat (10 kcal% fat; LF) or high fat (60 kcal% fat, HF) diet. Mice were further subdivided into one of 3 water treatment groups for 17 weeks: water (control), vehicle (1.25% propylene glycol in water [PG]), or 4NQO in (50 µg/ml; 4NQO). All mice were subsequently given water alone for 6 more weeks. Upon euthanasia, livers were harvested, fixed, sectioned, and stained with hematoxylin and eosin (H&E). H&E slides were graded for histopathology; frozen liver samples were analyzed for triglyceride content. Trichrome stained sections were graded for fibrosis. CD3+ T cells, CD68+ macrophages, and Ly6+ neutrophils were detected by immunohistochemistry. Compared to water controls, 4NQO-treatment caused mouse liver histopathological changes such as fibrosis, and increases in hepatic neutrophils, T cells, and macrophages. HF diet exacerbated pathological changes compared to LF diet. Male controls, but not females, demonstrated severe steatosis and increased triglyceride content. 4NQO treatment decreased hepatic fat accumulation, even in animals on a HF diet. In conclusion, this murine model of oral cancer may serve as a model to study the effects of tobacco and diet on liver.