Predictive Factors Influencing the Evolution of Acquired Vitelliform Lesions in Intermediate Age-related Macular Degeneration Eyes.

In this study, we identify risk factors that predict the progression of AVL lesions over time. Retrospective cohort study SUBJECTS: 163 eyes of 132 patients with a diagnosis of iAMD with AVL METHODS: This retrospective study evaluated consecutive eyes with AMD from a retina clinic population and included 1181 patients and 2362 eyes. After excluding cases with associated geographic atrophy, macular neovascularization (MNV), vitreomacular traction, and those with less than two years of follow-up data, the final analysis cohort consisted of 163 eyes (132 patients) with at least one AVL lesion. The first available visit in which an AVL lesion was evident was considered the baseline visit, and follow-up data was collected from a visit 2years (+/- 3 months) later. Progression outcomes at the follow visit were classified into six categories: Resorbed, Collapsed, MNV, Stable, Increasing, and Decreasing. Subsequently, we analyzed the baseline characteristics for each category and calculated odds ratios to predict these various outcomes. The study focused on identifying predictive factors influencing the evolution of AVL in iAMD eyes. In total, 163 eyes with AVL had follow-up data at 2 years. The collapsed group demonstrated a significantly greater baseline AVL height and width compared to other groups (P < 0.001). With regards to qualitative parameters, subretinal drusenoid deposits (SDD) and intra-retinal hyper-reflective foci (IHRF) at the eye level, AVL located over drusen, and IHRF and ELM disruption over AVL were significantly more prevalent in the collapsed group compared to other groups (P< 0.05 for all comparisons). Odds Ratio for progressing to atrophy after 2 years of follow-up, compared to the resorbed group, were significant for SDD (OR = 2.82, P = 0.048) and AVL height (OR = 1.016, P = 0.006). The presence of SDD and greater AVL height significantly increases the risk of developing atrophy at the location of AVL after 2 years of follow-up. These findings may be of value in risk prognostication and defining patient populations for inclusion in future early intervention trials aimed at preventing progression to atrophy.

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