Purpose: Type II endoleaks (T2EL) are a leading cause of aneurysmal sac enlargement following an EVAR, raising concerns about potential late rupture. Despite their clinical relevance, treatment options for T2EL remain limited due to an incomplete understanding of their pathophysiology. This study examines inflammatory biomarkers within the excluded aneurysm sac to uncover mechanisms driving T2EL persistence and identify potential therapeutic targets for AAA management. Methodology: A prospective cohort study of 28 patients was undertaken at Royal Prince Alfred Hospital, Sydney. Participants were grouped into T2EL (n = 5), EVAR without sac enlargement (n = 12), and control group of peripheral arterial intervention (PAI; n = 11). Blood was collected from a peripheral artery, vein, and intervention site, and an enzyme-linked immunosorbent assay was undertaken for Vascular Endothelial Growth Factor (VEGF), interleukin 6 (IL-6), interleukin-1 beta (IL-1β) and TNF-related apoptosis-inducing ligand (TRAIL). Results: VEGF levels were notably elevated at the intervention site in the T2EL group (57.19 ± 25.51 pg/mL) compared to EVAR (17.65 ± 10.73 pg/mL, p=0.15) and PAI (21.15 ± 28.91 pg/mL, p=0.21). In contrast, peripheral VEGF concentrations were similar between the T2EL, EVAR and PAI cohorts, suggesting localised VEGF-driven angiogenesis within the expanding sac. Inflammatory markers (IL-6, IL-1β, and TRAIL) showed no significant differences between groups or sampling sites. To standardise for inflammation, VEGF levels were normalised to TRAIL. The VEGF/TRAIL ratio was significantly higher (p<0.05) in the T2EL group compared to the combined non-T2EL cohort (EVAR and PAI cohorts). Conclusion: This study is among the first to implicate local VEGF-mediated angiogenesis, rather than inflammation, as a potential mechanism sustaining T2EL and driving sac expansion. Targeting VEGF may represent a novel therapeutic strategy to halt T2EL progression and reduce AAA-related risk.