To evaluate the size and location of macular atrophy in eyes with Type-1 neovascularization (NV) and age-related macular degeneration receiving chronic intravitreal anti–vascular endothelial growth factor therapy.
A retrospective review of a case series of 27 eyes with Type-1 NV and retinal pigment epithelial detachment (PED) having a minimum of 12 months follow-up was performed. Demographic information and visual acuity at baseline and the final follow-up were collected. Spectral-domain optical coherence tomography (OCT) and near-infrared reflectance were analyzed at 6-month intervals to detect and measure macular atrophy. Location and area (in square millimeter) of macular atrophy were measured using Heidelberg software tools. Also, OCT angiography was used to colocalize the area of Type-1 NV flow versus the location of atrophy.
Twenty-seven eyes of 27 patients were included in this analysis. The median visual acuity was 20/50, mean age was 82.7 years, and mean number of injections was 29.5. A larger percentage of eyes (59.3%) developed atrophy predominantly eccentric to the PED versus predominantly overlying the PED (11.1%) when measured with spectral-domain OCT and near-infrared imaging. At the final follow-up, there was a larger area of atrophy surrounding the fibrovascular PED (mean, 3.326 mm2) than overlying it (mean, 0.542 mm2), and this was statistically significant (P = 0.0118). En-face OCT images were overlaid with OCT angiography in 11 eyes, and a predominantly eccentric pattern of atrophy was identified in 9 of 11 eyes. Using this method, the mean area of atrophy predominantly overlying the Type-1 NV was 1.652 mm2 (range of 0–10.464 mm2), whereas the area of atrophy predominantly eccentric to the neovascular complex was 4.345 mm2 (range of 0.705–13.758 mm2), and this was statistically significant (P = 0.0465). The average rate of atrophy progression was 1.04 mm2/year (SD 0.938).
With long-term anti–vascular endothelial growth factor therapy for eyes with Type-1 NV secondary to age-related macular degeneration, macular atrophy tends to develop predominantly eccentric to the PED and the neovascular flow imaged on OCT angiography. With chronic vascular endothelial growth factor suppression, Type-1 NV may evolve into a multilayered PED that may confer a protective effect to the overlying retinal pigment epithelium and outer retina.
Long-term anti–vascular endothelial growth factor therapy in the setting of a Type-1 neovascularization lesion with a pigment epithelial detachment appears to contribute to atrophy in a pattern predominantly eccentric to the pigment epithelial detachment.
*Retinal Disorders and Ophthalmic Genetics Division, Stein Eye Institute, UCLA, Los Angeles, California;
†Vitreous Macula Retina Consultants, New York, New York;
‡Department of Ophthalmology, New York University School of Medicine, New York, New York;
§Retina and Macular Diseases Division, Doheny Eye Institute, UCLA, Los Angeles, California; and
¶Greater Los Angeles VA Healthcare Center, Los Angeles California.
Reprint requests: David Sarraf, MD, UCLA Stein Eye Institute, 100 Stein Plaza, UCLA, Los Angeles, CA 90095; e-mail: firstname.lastname@example.org
Supported in part by The Macula Foundation, Inc, New York, NY.
K. B. Freund is a consultant to Genentech, Optos, Optovue, Heidelberg Engineering, and Bayer HealthCare. D. Sarraf is a consultant to Bayer, Genentech, Novartis, and Optovue and receives research grants from Allergan, Heidelberg, Genentech, Optovue and Regeneron. The remaining authors have no conflicting interests to disclose.