Use of the AFX Stent Graft in Patients with Extremely Narrow Aortic Bifurcation: A Multicenter Retrospective Study.

INTRODUCTION: This study analyzed the patient outcomes following endovascular aortic aneurysm repair (EVAR) for infrarenal aortic pathologies with very narrow aortic bifurcations using the AFX stent graft. METHODS: The data was retrieved from the archived medical records of 35 patients treated for abdominal aortic aneurysm (AAA) (48.6%) or penetrating aortic ulcer (PAU) (51.4%) with very narrow aortic bifurcation between January 2013 and May 2020. Patient survival, freedom from endoleak (EL), and limb occlusion were estimated applying the Kaplan-Meier method. RESULTS: The mean follow-up time was 20.4 ± 22.8 months. The mean aortic bifurcation diameter was 15.8 ± 2.2 mm. Technical success was 100%, and no procedure-related deaths occurred. Two type II ELs occurred within 30-day follow-up. We observed one common iliac artery stenosis at four months and one type III EL at 54 months in the same patient, both of which required re-intervention. Overall patient survival was 95 ± 5% (AAA: 100%; PAU: 89 ± 10%), freedom from limb occlusion was 94 ± 5% (AAA: 91 ± 9%; PAU: 100%), freedom from type II EL was 94 ± 4% (AAA: 88 ± 8%; PAU: 100%), and freedom from EL type III was 83 ± 15% (AAA: 80 ± 18%; PAU: 100%) at the end of the follow-up period. CONCLUSIONS: Very narrow aortic bifurcations may predispose patients to procedure-related complications following EVAR. Our results suggest a safe use of the AFX stent graft in such scenarios. The overall short- and long-term procedure-related patient outcomes are satisfying albeit they may seem superior for PAU when compared to AAA.

Pathophysiology of chronic limb ischemia.

Chronic ischemia of the lower extremities is an everyday problem in vascular surgery clinics. In Germany, approximately 3% of all hospitalizations are due to peripheral artery disease (PAD), with critical limb ischemia (CLI) in particular showing a rapid increase. The consequences of chronic undersupply range from reduced walking distance to loss of limbs. At the beginning there are stress factors, such as hyperlipidemia (LDL), free radicals, arterial hypertension, infections or subclinical inflammation that interfere with endothelial homeostasis and cause endothelial dysfunction with increased permeability. Cells of the immune system are attracted and migrate into the vascular wall, where they lead to the degradation of matrix components and destabilization of the plaque. By changing the phenotype of smooth muscle cells and macrophages towards osteoclast-like cells, bone-like hardening of the vessel wall takes place. Above a vessel wall thickness of approximately 100 µm, hypoxia-induced factor (HIF-1α) is intensified by the lack of oxygen, which leads to an increase in growth factors, such as vascular endothelial growth factor (VEGF). This promotes angiogenesis, but it is not sufficient to compensate for a stenosed artery. Arteriogenesis refers to the growth of existing collateral vessels. The driving forces are the pressure gradient before and after the stenosis and the shear forces acting on the vessel walls. In the case of progressive stenosis, the compensatory capacities can be overtaxed and a manifest hypoxia in the tissue with regression of the obtained vascular structures and tissue atrophy occurs.