To evaluate the response to aflibercept therapy for Type 1 and Type 3 neovascularization in pigment epithelial detachments associated with treatment-naive, neovascular age-related macular degeneration.
In this multicentered, prospective study, eligible eyes underwent an intravitreal aflibercept injection protocol for 12 months. Visual acuity and morphologic features of the pigment epithelial detachments were compared at baseline and follow-up intervals between eyes with Type 1 versus Type 3 neovascularization.
Thirty-six eyes were analyzed. At 12 months, Type 1 lesions showed a 4.5 ± 23 Early Treatment of Diabetic Retinopathy Study letter improvement (P = 0.1665) versus a 14 ± 11 (P = 0.0072) letter improvement with Type 3 lesions. Both Type 1 and 3 eyes showed a significant decrease in pigment epithelial detachment size, subretinal fluid, and subretinal hyperreflective material; however, Type 3 eyes had a greater reduction in pigment epithelial detachment size and subretinal hyperreflective material, as well as a reduction in central retinal thickness. Type 1 eyes required an average of 1.636 (range, 1–4) injections to resolve fluid, which was greater than Type 3 eyes, which required an average of 1.143 (range, 1–2) injections (P = 0.0251).
Intravitreal aflibercept injections were efficacious for pigment epithelial detachments, but baseline and follow-up anatomical and functional outcomes differed in Type 1 versus Type 3 neovascularization. The better response of Type 3 eyes with fewer injections suggests that differentiation of the neovascularization subtype at the initial diagnosis may allow for a more tailored, optimal therapy.
A 1-year multicentered, prospective study of aflibercept therapy for Type 1 and Type 3 neovascularization in pigment epithelial detachments associated with treatment-naive, neovascular age-related macular degeneration was performed. Aflibercept monotherapy was efficacious for pigment epithelial detachments, but baseline and follow-up anatomical and functional outcomes differed between Type 1 and Type 3 neovascularization.
*Department of Ophthalmology, David Geffen School of Medicine, Stein Eye Institute, University of California Los Angeles, Los Angeles, California;
†Department of Ophthalmology, David Geffen School of Medicine, Doheny Eye Institute, University of California Los Angeles, Los Angeles, California;
‡Southern California Desert Retina Consultants, Palm Desert, California;
§Department of Ophthalmology, Loma Linda University Eye Institute, Loma Linda, California;
¶Black Hills Regional Eye Institute, Rapid City, South Dakota; and
**Department of Ophthalmology, Greater Los Angeles Veterans Affairs Healthcare System, Los Angeles, CA.
Reprint requests: David Sarraf, MD, Retinal Disorders and Ophthalmic Genetics Division, Stein Eye Institute, University of California Los Angeles, 100 Stein Plaza, Los Angeles, CA 90095; e-mail: dsarraf@ucla.edu
Supported by a research grant from Regeneron. No support was received from the NIH, Wellcome Trust, or HHMI. C. K. Chan receives research support from Genentech, NEI, Acucela, Ophthotech, Sequenom, Regeneron, Allergan, and Theratechnologies. P. Abraham receives research support from Allergan, Genentech, NEI, Juvenile Diabetes Research Foundation, Ophthotech, Pfizer, Schering-Plough, and Thrombogenics. M. Lalezary and S. G. Lin receive research support from Allergan, Acucela, Regeneron, Genentech, Ophthotect, and NEI. D. Sarraf has research grants from Regeneron, Genentech, and Optovue. S. Sadda is a consultant for Optos, Carl Zeiss Meditec, Allergan, Genentech, Regeneron, Bayer, Novartis, and Iconic and receives research support from Optos, Carl Zeiss Meditec, Allergan, and Genentech. X. Chen, M. Al-Sheikh, and A. H. Hariri have no financial disclosures.
The preliminary results of this article were presented at the International Retinal Imaging Symposium IV, March 19, 2016, Los Angeles, CA.
None of the authors have any conflicting interests to disclose.
