Marion R Munk1,2,3, Lala Ceklic1,2, Andreas Ebneter1, Wolfgang Huf4, Sebastian Wolf1,2, Martin S Zinkernagel1,2. 1. Department of Ophthalmology, Department of Clinical Research, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. 2. Bern Photographic Reading Center, University Hospital Bern, Bern, Switzerland. 3. Department of Ophthalmology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA. 4. Center for Medical Physics and Biomedical Engineering, Medical University of Vienna, Vienna, Austria.
Abstract
PURPOSE: To identify the prevalence and progression of macular atrophy (MA) in neovascular age-related macular degeneration (AMD) patients under long-term anti-vascular endothelial growth factor (VEGF) therapy and to determine risk factors. METHOD: This retrospective study included patients with neovascular AMD and ≥30 anti-VEGF injections. Macular atrophy (MA) was measured using near infrared and spectral-domain optical coherence tomography (SD-OCT). Yearly growth rate was estimated using square-root transformation to adjust for baseline area and allow for linearization of growth rate. Multiple regression with Akaike information criterion (AIC) as model selection criterion was used to estimate the influence of various parameters on MA area. RESULTS: Forty-nine eyes (47 patients, mean age 77 ± 14) were included with a mean of 48 ± 13 intravitreal anti-VEGF injections (ranibizumab:37 ± 11, aflibercept:11 ± 6, mean number of injections/year 8 ± 2.1) over a mean treatment period of 6.2 ± 1.3 years (range 4-8.5). Mean best-corrected visual acuity improved from 57 ± 17 letters at baseline (= treatment start) to 60 ± 16 letters at last follow-up. The MA prevalence within and outside the choroidal neovascularization (CNV) border at initial measurement was 45% and increased to 74%. Mean MA area increased from 1.8 ± 2.7 mm2 within and 0.5 ± 0.98 mm2 outside the CNV boundary to 2.7 ± 3.4 mm2 and 1.7 ± 1.8 mm2 , respectively. Multivariate regression determined posterior vitreous detachment (PVD) and presence/development of intraretinal cysts (IRCs) as significant factors for total MA size (R2 = 0.16, p = 0.02). Macular atrophy (MA) area outside the CNV border was best explained by the presence of reticular pseudodrusen (RPD) and IRC (R2 = 0.24, p = 0.02). CONCLUSION: A majority of patients show MA after long-term anti-VEGF treatment. Reticular pseudodrusen (RPD), IRC and PVD but not number of injections or treatment duration seem to be associated with the MA size.
PURPOSE: To identify the prevalence and progression of macular atrophy (MA) in neovascular age-related macular degeneration (AMD) patients under long-term anti-vascular endothelial growth factor (VEGF) therapy and to determine risk factors. METHOD: This retrospective study included patients with neovascular AMD and ≥30 anti-VEGF injections. Macular atrophy (MA) was measured using near infrared and spectral-domain optical coherence tomography (SD-OCT). Yearly growth rate was estimated using square-root transformation to adjust for baseline area and allow for linearization of growth rate. Multiple regression with Akaike information criterion (AIC) as model selection criterion was used to estimate the influence of various parameters on MA area. RESULTS: Forty-nine eyes (47 patients, mean age 77 ± 14) were included with a mean of 48 ± 13 intravitreal anti-VEGF injections (ranibizumab:37 ± 11, aflibercept:11 ± 6, mean number of injections/year 8 ± 2.1) over a mean treatment period of 6.2 ± 1.3 years (range 4-8.5). Mean best-corrected visual acuity improved from 57 ± 17 letters at baseline (= treatment start) to 60 ± 16 letters at last follow-up. The MA prevalence within and outside the choroidal neovascularization (CNV) border at initial measurement was 45% and increased to 74%. Mean MA area increased from 1.8 ± 2.7 mm2 within and 0.5 ± 0.98 mm2 outside the CNV boundary to 2.7 ± 3.4 mm2 and 1.7 ± 1.8 mm2 , respectively. Multivariate regression determined posterior vitreous detachment (PVD) and presence/development of intraretinal cysts (IRCs) as significant factors for total MA size (R2 = 0.16, p = 0.02). Macular atrophy (MA) area outside the CNV border was best explained by the presence of reticular pseudodrusen (RPD) and IRC (R2 = 0.24, p = 0.02). CONCLUSION: A majority of patients show MA after long-term anti-VEGF treatment. Reticular pseudodrusen (RPD), IRC and PVD but not number of injections or treatment duration seem to be associated with the MA size.
Authors: Ebenezer Daniel; Wei Pan; Gui-Shuang Ying; Benjamin J Kim; Juan E Grunwald; Frederick L Ferris; Glenn J Jaffe; Cynthia A Toth; Daniel F Martin; Stuart L Fine; Maureen G Maguire Journal: Ophthalmology Date: 2018-02-14 Impact factor: 12.079
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