Surv Ophthalmol. 2026 Aug 6:S0039-6257(26)00116-5. doi: 10.1016/j.survophthal.2026.08.002. Online ahead of print.
ABSTRACT
Macular atrophy (MA) is a major cause of long-term visual decline in neovascular age-related macular degeneration (nAMD), despite the ability of anti-vascular endothelial growth factor (anti-VEGF) therapy to control exudation. We summarize current evidence on the definition, epidemiology, risk factors, imaging features, and functional consequences of MA in nAMD. Optical coherence tomography (OCT) has improved the identification of atrophic changes and supports distinguishing complete retinal pigment epithelium and outer retinal atrophy from fibro-atrophy, a proposed OCT-based category in which outer retinal and RPE loss occur beneath hyperreflective or fibrotic tissue that makes choroidal hypertransmission absent or unassessable. In treated eyes, long-term studies show that MA becomes increasingly common over time and is a major factor limiting durable visual benefit, yet epidemiologic estimates remain difficult to compare because MA definitions, imaging modalities, lesion-size thresholds, and terminology varies substantially across studies. Important risk factors include older age, poor baseline visual acuity, type 3 macular neovascularization, intraretinal fluid, subretinal hyperreflective material, and early atrophic signs on baseline imaging, whereas type 1 neovascularization may be associated with slower atrophy progression. Once established, MA substantially affects visual function, not only reducing visual acuity, but also impairing reading speed and other visual functions. A major unresolved controversy is whether cumulative anti-VEGF exposure contributes independently to MA, rather than reflecting more severe or recurrent exudative disease. Future progress will depend on standardized definitions, multimodal imaging, and predictive models to guide personalized management and develop therapies targeting atrophy.
PMID:42562278 | DOI:10.1016/j.survophthal.2026.08.002