gms | German Medical Science

7th International Symposium on AMD: Age-related Macular Degeneration – Understanding Pathogenetic Mechanisms of Disease

20.09. - 21.09.2019, Baden-Baden

Quantitative fundus autofluorescence (qAF) of SA secondary to AMD

Meeting Abstract

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  • R. Theodore Smith - New York/USA
  • K.B. Freund - New York/USA

7th International Symposium on AMD: Age-related Macular Degeneration - Understanding Pathogenetic Mechanisms of Disease. Baden-Baden, 20.-21.09.2019. Düsseldorf: German Medical Science GMS Publishing House; 2020. Doc19amd53

doi: 10.3205/19amd53, urn:nbn:de:0183-19amd539

Published: February 5, 2020

© 2020 Smith et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.


Outline

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Purpose: Quantitative autofluorescence (qAF) offers scaled, reproducible AF measurements between patients and over time. We studied qAF in lobules of geographic atrophy (GA) to correlate with two main pathways from intermediate age-related macular degeneration (iAMD) to two phenotypes of GA.

Methods: 23 eyes of 18 patients with GA underwent spectral-domain optical coherence tomography (SD-OCT) and qAF imaging on the Heidelberg Spectralis. We examined prior serial tracked OCT scans of 52 GA Regions-of-interest (ROIs) lobules or coalescent atrophic lobules (mean follow-up, 5.5 years) to divide them into 2 pathways by the dominant predecessor iAMD lesion type: soft drusen/ pigment epithelial detachment (PED), pathway 1, subretinal drusenoid deposits (SDD), pathway 2. Some ROIs arose from both pathways, and were assigned to a mixed group. Mean qAF values of GA ROIs were measured and compared between the 3 groups.

Results: The soft drusen/PED pathway (18/52) led to GA lesions that were “black” on AF, with lower mean qAF (35.88±12.75 qAF units), generally displaying the complete atrophy of the RPE and outer retina (cRORA) phenotype. The SDD pathway (12/52) led to GA lesions that were multilobular and “gray” on AF, with higher mean qAF (71.62±12.12 qAF units, P<0.001, t-test), generally displaying the incomplete atrophy of the RPE and outer retina (iRORA) phenotype. The mean qAF of ROIs from the mixed pathway (22/52) was intermediate (58.13±11.88 qAF units).

Conclusions: GA lesions can in most cases be divided by qAF (lower/higher) into 2 non-exclusive groups that correlate both with the precursor pathways (from drusen/PED or SDD, resp.) and their predominant final OCT atrophy classification (cRORA or iRORA), with remaining lesions arising from both forms of iAMD , with intermediate qAF. Thus, qAF of GA lobules reflects both their pathogenesis and structure, and would be an easily implemented and useful metric for clinical GA research.