目的：识别新生血管性年龄相关性黄斑变性（neovascular age-related macular degeneration,NVAMD）患者接受抗血管内皮生长因子（vascular endothelial growth factor,VEGF）药物治疗后出现的黄斑萎缩事件，并评估其治疗前的眼部解剖结构变化。方法：回顾 2014 全年期间由采用抗 VEGF 药物治疗的所有 NVAMD 患者，这些患者的随访时间均超过 12 个月，并评估了从首次治疗（通常在 2014 年前）至 2018 年 6 月最后一次随访期间的所有谱域光学相干断层扫描（spectral domain-optical coherence tomography, SD-OCT）图像。结果：在既定的研究流程中，共识别出 278 例 NVAMD 患者的 342 眼，其中 47 眼发生了黄斑萎缩。从治疗开始到黄斑萎缩出现的中位时间为 29.6 个月（四分位距：17.7-43.4）。在发生萎缩的区域中，发现了三种黄斑结构改变（部分眼睛存在不止一种改变）：在 25 眼中观察到血管化色素上皮脱离（pigment epithelial detachment,PED）的塌陷和脉络膜新生血管（choroidal neovascularization，CNV）的消退；在 15 眼中观察到视网膜下高反射物质和(或)视网膜下纤维化的形成；在 13 眼中观察到黄斑萎缩与大玻璃膜疣及色素改变相关联，呈现出通常称为地图状萎缩的典型模式。结论：这些数据表明，在某些情况下，CNV 可能补偿脉络膜的缺血状态，而 CNV 的消退则可能使 RPE 细胞和光感受器暴露于缺血性损伤和萎缩的风险之中。

Background/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.