The structural atrophy of the aneurysm wall in secondary expanding aortic aneurysms with endoleak type II

Background: Abdominal aortic aneurysm (AAA) has an age-dependent prevalence of 2% to 11% and is a leading cause of death in men aged >65 years if not treated surgically. Today, endovascular aneurysm repair (EVAR) is performed in up to 80% of elective cases and 60% of ruptured cases. Although EVAR improves perioperative, early, and midterm outcomes, it is associated with specific complications, especially endoleaks (ELs). Type II EL occurs in up to 30% of procedures; however, aneurysm sac expansion and rupture are rare, and currently nothing is known about the morphologic changes in this condition. In this study, we investigate the aneurysm wall morphology in secondary expanding human AAA samples after EVAR with persistent type II EL in comparison to nonaneurysmatic control aortic and AAA samples. Methods: Samples were acquired from the aneurysm sac during retroperitoneal feeder vessel ligation in a cohort of 10 patients with secondary expansion after EVAR and type II EL diagnosed by computed tomography and contrast-enhanced ultrasound. Control tissues included 42 AAAs and 13 control aortae published previously. Hematoxylin and eosin staining and immunohistochemistry for CD3/4/31/68 and Ki67 were performed for morphologic analysis. Terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling (TUNEL) assays allowed quantification of apoptosis. Reverse transcription-polymerase chain reaction was used to quantify gene expression and Western blot to quantify collagen expression. Results: Secondary expansion of 33.8% +/- 6 30% during 5 years was seen after EVAR before reoperation. The aneurysm wall after expansion shows significant thinning of the intima-media layer accompanied by a scarcity of cells, with only a little chronic inflammation left compared with AAA samples. Macrophages are seen in abundance, and matrix metalloproteinase expression is significantly upregulated. Relevant apoptosis is not noticed. Fibrous tissue is reduced, and a collagen turnover to different subtypes is noted in comparison to nonaneurysmatic control aorta and AAA. In addition, the transcription factors vascular endothelial growth factor, Kruppel-like factor 4, and BCL2, elevated in AAA, are significantly reduced after secondary expansion. Conclusions: The aneurysm sac morphology after EVAR with persistent type II EL is characterized by atrophy and proteolysis suggestive of structural weakening. These results should be considered for the follow-up schedule as well as for the potential treatment of this most frequent EVAR complication.