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Development of macular atrophy in neovascular AMD treated with ranibizumab in the HARBOR study

Session Details

Session Title: AMD I

Session Date/Time: Thursday 17/09/2015 | 08:30-10:30

Paper Time: 08:46

Venue: Athena

First Author: : F.Holz GERMANY

Co Author(s): :    L. Tuomi   B. Ding   J. Hopkins        

Abstract Details

PURPOSE:The development of macular atrophy (MA) has been reported in several large clinical trials evaluating anti-vascular endothelial growth factor (VEGF) treatment for neovascular age-related macular degeneration (nAMD). This study evaluated macular atrophy incidence and factors associated with MA development in ranibizumab-treated eyes in HARBOR.


This was a retrospective, post-hoc analysis of the Phase 3 HARBOR study (N=1095), a multi-center, double-masked, randomized controlled clinical trial that evaluated intravitreal ranibizumab 0.5-mg or 2.0-mg administered monthly or as needed (PRN) for nAMD.


MA was assessed on fluorescein angiograms (FA) and color fundus photographs at baseline, month (M)3, M12, and M24, defined as: well-defined areas of depigmentation with increased choroidal vessel visibility, diameter ≥250 µm, corresponding to flat areas of well-demarcated staining on FA; excluding atrophy associated with retinal pigment epithelium tears. All atrophy immediately within, adjacent to and nonadjacent to CNV lesions was included. Outcomes included MA incidence, best-corrected visual acuity (BCVA), and factors associated with MA development.


At baseline, 11.2% of eyes had MA. Among eyes with no detectable MA at baseline, 29% had MA at M24. At M24, mean BCVA gains were +6.7 vs +9.1 letters from baseline in eyes with vs without baseline MA, respectively. Baseline presence of intraretinal cysts (hazard ratio [HR] 2.45; 95% confidence interval [CI], 1.76-3.42) and baseline presence of fellow eye MA (HR, 2.02; 95% CI, 1.42-2.87) were associated with increased incidence of MA. Baseline subretinal fluid (SRF) presence was associated with a decreased incidence of MA (HR, 0.50; 95% CI, 0.33-0.74), and fewer eyes with vs without concurrent SRF developed MA at M24 (8.1% vs 32.9% of eyes, respectively). Ranibizumab dose was not associated with MA development (2.0-mg vs 0.5-mg: HR, 1.09; 95% CI, 0.84-1.41). Monthly vs PRN treatment trended toward a greater association with MA (HR, 1.29; 95% CI, 0.99-1.68); however, injection frequency in the PRN treatment arms did not appear to be associated with MA development (M24 MA rates, 1-6 injections vs more than 18 injections: 0.5-mg, 24% vs 21%; 2.0-mg, 42% vs 19%).


BCVA gains were achieved in the presence of MA over 24 months. Lower MA rates were seen in eyes with SRF present, while fellow eye MA and intraretinal cysts at baseline were associated with increased incidence of MA. In the PRN arms, injection frequency did not appear to be associated with MA incidence. It is unclear whether MA is caused by natural progression of underlying dry AMD, choroidal neovascularization lesion-related collateral damage, or interference with local VEGF levels. Based on existing data, MA development does not appear to outweigh the benefits of ranibizumab therapy for nAMD over 2 years.

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