The authors of this paper set out to investigate the prevalence of macular atrophy in treatment-naive patients with neovascular AMD undergoing aflibercept monotherapy (three monthly loading injections followed by subsequent treatment every two months). Case notes over a three year period were retrospectively reviewed. Masked graders assessed for macular atrophy at the 12 month mark using the following parameters to define atrophy: 1) its presence within the macular vascular arcade; 2) a roughly round or oval area of partial or complete depigmentation of the RPE, with thinning of the overlying neurosensory retina; 3) >=250µm in the longest linear dimension; 4) atrophic changes in the RPE and photoreceptor cells with increased choroidal signal beneath them on OCT; and 5) at least one of the additional characteristics: sharp demarcated borders, visibility of underlying choroidal vessels, or a uniformly reduced autofluorescence signal bounded by sharp borders on fundus autofluorescence. One hundred and twenty-three participants were included in the analysis of newly developed macular atrophy at 12 months. Thirteen eyes (10.6%, 95% confidence interval 5.7–17.4) of the 123 eyes developed new macular atrophy at 12 months. There was no significant difference in the occurrence of atrophy between idiopath polypoidal choroidal vasculopathy (IPCV) and typical AMD patients. The patients with newly developed macular atrophy were older, had worse vision at baseline, and had a larger lesion size than those who did not develop macular atrophy. Thinner subfoveal choroidal thickness, more intraretinal fluid and more subretinal hyper reflective material were all found to be prognostic for atrophy development.

Macular atrophy and macular morphology in aflibercept treated neovascular age-related macular degeneration.
Kuroda Y, Yamashiro K, Ooto S, et al.
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Saruban Pasu

Moorfields Eye Hospital, London, UK.

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