Aims: To identify incident macular atrophy and evaluate antecedent anatomic alterations in eyes with neovascular age-related macular degeneration (NVAMD) that were treated with anti-vascular endothelial growth factor (anti-VEGF) agents. Methods: All patients treated with anti-VEGF agents for NVAMD by one of the authors during the 2014 calendar year who had follow up ≥ 12 months had evaluation of all SD-OCT scans from first treatment (usually prior to 2014) to last follow up through June 2018. Results: The ascertainment procedure identified 342 eyes of 278 patients with NVAMD among which 47 developed macular atrophy. The median time from treatment initiation to development of macular atrophy was 29.6 (interquartile range, 17.7-43.4) months. Three macular alterations were identified in areas that developed atrophy (some eyes had more than one); collapse of a vascularized pigment epithelial detachment (PED) and regression of choroidal neovascularization (CNV) in 25 eyes, development of subretinal hyper-reflective material and/or subretinal fibrosis in 15 eyes, or atrophy occurring in association with large drusen and pigmentary changes resulting in an arc of atrophy in a pattern typically referred to as geographic atrophy in 13 eyes. Conclusions: These data suggest that in some instances CNV may compensate for choroidal ischemia and the loss of CNV may expose retinal pigmented epithelial cells and photoreceptors to ischemic damage and atrophy.

Aims: To identify incident macular atrophy and evaluate antecedent anatomic alterations in eyes with neovascular age-related macular degeneration (NVAMD) that were treated with anti-vascular endothelial growth factor (anti-VEGF) agents. Methods: All patients treated with anti-VEGF agents for NVAMD by one of the authors during the 2014 calendar year who had follow up ≥ 12 months had evaluation of all SD-OCT scans from first treatment (usually prior to 2014) to last follow up through June 2018. Results: The ascertainment procedure identified 342 eyes of 278 patients with NVAMD among which 47 developed macular atrophy. The median time from treatment initiation to development of macular atrophy was 29.6 (interquartile range, 17.7-43.4) months. Three macular alterations were identified in areas that developed atrophy (some eyes had more than one); collapse of a vascularized pigment epithelial detachment (PED) and regression of choroidal neovascularization (CNV) in 25 eyes, development of subretinal hyper-reflective material and/or subretinal fibrosis in 15 eyes, or atrophy occurring in association with large drusen and pigmentary changes resulting in an arc of atrophy in a pattern typically referred to as geographic atrophy in 13 eyes. Conclusions: These data suggest that in some instances CNV may compensate for choroidal ischemia and the loss of CNV may expose retinal pigmented epithelial cells and photoreceptors to ischemic damage and atrophy.