American journal of ophthalmology · 2018
The Border of Macular Atrophy in Age-Related Macular Degeneration: A Clinicopathologic Correlation.
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Dolz-Marco Rosa, Balaratnasingam Chandrakumar, Messinger Jeffrey D, Li Miaoling, Ferrara Daniela, Freund K Bailey, Curcio Christine A
Аннотация
PURPOSE: To correlate in vivo imaging to histology in an eye with macular atrophy owing to age-related macular degeneration (AMD; complete retinal pigment epithelium [RPE] and outer retinal atrophy [cRORA]) to evaluate the utility of new optical coherence tomography (OCT) suggested by previous histology.
DESIGN: Case study with clinicopathologic correlation.
METHODS: In vivo eye-tracked cross-sectional OCT scans at 13 and 8 months before death were compared to postmortem histopathology. On OCT, the atrophy border was identified as either the descent of the external limiting membrane (ELM) toward the Bruch membrane (BrM) (representing gliosis) or the presence of choroidal hypertransmission (representing lack of shadowing by RPE). Thicknesses of RPE, basal laminar deposit (BLamD), and BrM were measured at 500 and 100 μm on the nonatrophic and atrophic sides of these borders, on in vivo eye-tracked OCT and histology matched to the same location.
RESULTS: In all OCT scans, the ELM descent was visible. The RPE-BLamD band significantly thickened toward it (P < .005), over time (P = .015 and P = .043, at 500 and 100 μm, respectively). On OCT, the ELM descent delineated a smaller atrophic area than did hypertransmission. RPE-BLamD thicknesses manually measured on OCT overestimated histologic thicknesses. BrM visibility varied with RPE status.
CONCLUSION: Visible on OCT, the ELM descent is a histopathologic atrophy border supporting new terminology of cRORA, whereas hypertransmission reveals RPE degeneration. RPE-BLamD thickening across the macula, toward the atrophy and over time is confirmed. The presence of gliosis and thick RPE-BLamD suggests that macular atrophy is a late stage in disease progression, encouraging anatomic endpoints at earlier AMD stages than atrophy enlargement.
DESIGN: Case study with clinicopathologic correlation.
METHODS: In vivo eye-tracked cross-sectional OCT scans at 13 and 8 months before death were compared to postmortem histopathology. On OCT, the atrophy border was identified as either the descent of the external limiting membrane (ELM) toward the Bruch membrane (BrM) (representing gliosis) or the presence of choroidal hypertransmission (representing lack of shadowing by RPE). Thicknesses of RPE, basal laminar deposit (BLamD), and BrM were measured at 500 and 100 μm on the nonatrophic and atrophic sides of these borders, on in vivo eye-tracked OCT and histology matched to the same location.
RESULTS: In all OCT scans, the ELM descent was visible. The RPE-BLamD band significantly thickened toward it (P < .005), over time (P = .015 and P = .043, at 500 and 100 μm, respectively). On OCT, the ELM descent delineated a smaller atrophic area than did hypertransmission. RPE-BLamD thicknesses manually measured on OCT overestimated histologic thicknesses. BrM visibility varied with RPE status.
CONCLUSION: Visible on OCT, the ELM descent is a histopathologic atrophy border supporting new terminology of cRORA, whereas hypertransmission reveals RPE degeneration. RPE-BLamD thickening across the macula, toward the atrophy and over time is confirmed. The presence of gliosis and thick RPE-BLamD suggests that macular atrophy is a late stage in disease progression, encouraging anatomic endpoints at earlier AMD stages than atrophy enlargement.