Borrelli Enrico, Barresi Costanza, Ricardi Federico, Berni Alessandro, Grosso Domenico, Viggiano Pasquale, Marolo Paola, Introini Ugo, Reibaldi Michele, Bandello Francesco
IRCCS San Raffaele Scientific Institute, Milan, Italy.
Vita-Salute San Raffaele University, Milan, Italy.
Invest Ophthalmol Vis Sci. 2024 Mar 5;65(3):18. doi: 10.1167/iovs.65.3.18.
To explore the occurrence of macular atrophy (MA) in eyes with age-related macular degeneration (AMD)-associated Type 3 macular neovascularization (MNV) treated with anti-vascular endothelial growth factor (anti-VEGF) therapy. Importantly, we aimed at describing the existence of separate pathways leading to MA.
We analyzed 41 participants (41 eyes) with treatment-naïve Type 3 MNV who were followed up for a duration of 12 months after beginning the anti-VEGF therapy. At the one-year follow-up visit, optical coherence tomography (OCT) scans were reviewed for the presence of MA. MA regions of interest (ROIs) were selected and traced back to their original dominant baseline lesion (i.e., precursor) through previous serially captured OCT scans. Baseline lesions included precursors associated with the development and exudation of MNV and causes external to the neovascularization itself.
At the one-year follow-up visit, MA was graded to be present in 38 (92.7%) out of 41 eyes. These 78 MA ROIs were divided into two subgroups according to the precursor lesion, yielding a group of 53 MA lesions with precursors associated with the development and exudation of MNV (i.e., MA caused by physical harm from Type 3 neovessels, collapse of a serous pigment epithelium detachment, and fibrosis) and 25 MA regions with precursors external to the neovascularization itself (i.e., MA caused by drusen or subretinal drusenoid deposits).
Eyes with Type 3 MNV are commonly complicated by MA and precursors of MA include causes associated with the development and exudation of MNV, as well as lesions unrelated to the neovascularization process itself.
探讨接受抗血管内皮生长因子（抗VEGF）治疗的年龄相关性黄斑变性（AMD）相关3型黄斑新生血管（MNV）患者眼中黄斑萎缩（MA）的发生情况。重要的是，我们旨在描述导致MA的不同途径的存在。
我们分析了41例未经治疗的3型MNV患者（41只眼），这些患者在开始抗VEGF治疗后随访12个月。在一年的随访中，对光学相干断层扫描（OCT）图像进行回顾，以确定MA的存在。选择MA感兴趣区域（ROI），并通过先前连续采集的OCT图像追溯至其原始主要基线病变（即前驱病变）。基线病变包括与MNV发生和渗出相关的前驱病变以及新生血管本身以外的原因。
在一年的随访中，41只眼中有38只（92.7%）被判定存在MA。根据前驱病变，这78个MA ROI被分为两个亚组，一组是53个MA病变，其前驱病变与MNV的发生和渗出相关（即由3型新生血管的物理损伤、浆液性色素上皮脱离塌陷和纤维化引起的MA），另一组是25个MA区域，其前驱病变在新生血管本身以外（即由玻璃膜疣或视网膜下类玻璃膜疣沉积物引起的MA）。
3型MNV患者的眼睛常并发MA，MA的前驱病变包括与MNV发生和渗出相关的原因，以及与新生血管形成过程本身无关的病变。
