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Spectral-Domain Optical Coherence Tomography Analysis of Fibrotic Lesions in Neovascular Age-Related Macular Degeneration.

脉络膜新生血管 光学相干断层摄影术 脉络膜 视网膜 病理 新生血管 视网膜 德鲁森
作者
Eric H Souied,Manar Addou-Regnard,Avi Ohayon,Oudy Semoun,Giuseppe Querques,Rocio Blanco-Garavito,Roxane Bunod,Camille Jung,Anne Sikorav,Alexandra Miere
出处
期刊:American Journal of Ophthalmology [Elsevier BV]
卷期号:214: 151-171 被引量:7
标识
DOI:10.1016/j.ajo.2020.02.016
摘要

Purpose To describe the spectral-domain optical coherence tomography (OCT) features of fibrotic lesions associated with neovascular age-related macular degeneration (nAMD) and to outline the progression pathways from initial macular choroidal neovascular lesions (CNVs) to fibrosis. Methods Patients with nAMD were retrospectively included when macular subretinal fibrosis was present. Fibrosis was categorized using spectral-domain OCT with respect to retinal pigment epithelium (RPE) in 836 spectral-domain OCT slices from 44 eyes of 39 patients. In addition, in 47 distinct eyes, 4181 spectral-domain OCT slices were retrospectively reviewed to longitudinally assess progression from the initial lesion to the final fibrosis. Results Cross-sectional analysis classified fibrosis on spectral-domain OCT slices, as type A if located underneath the RPE, as type B if located above the RPE, and as type C if the remaining RPE was undistinguishable. The longitudinal analysis series revealed 3 progression pathways from the original CNV: 1) progression to type A, followed by RPE erosion and subretinal hyperreflective material, then type B and type C fibroglial lesion (FGL; 17/47 eyes); 2) progression to type B then type C FGL (17/47 eyes); and 3) persistence of type A with development of a flat, fibroatrophic lesion (13/47 eyes). Subretinal hyperreflective material, macular hemorrhage, or RPE tear occurred in 14 of 47, 13 of 47, and 10 of 47 eyes, respectively. Conclusion This spectral-domain OCT analysis identified various patterns of macular fibrosis in eyes with nAMD. Three pathways of progression to fibrosis were described including the well-established pathway of type 2 CNV progression to FGL and the progression of type 1 fibrovascular CNV to FGL or fibroatrophic lesion.

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