Geographic atrophy in patients receiving anti-vascular endothelial growth factor for neovascular age-related macular degeneration.
OBJECTIVE
To examine factors associated with the apparent growth of geographic atrophy (GA) in a consecutive series of eyes with treatment-naive neovascular age-related macular degeneration receiving intravitreal anti-vascular endothelial growth factor therapy on a treat-and-extend regimen.


METHODS
This was a retrospective cohort study. Two independent graders identified areas of GA using near-infrared reflectance imaging and spectral domain optical coherence tomography (SD-OCT). Neovascular lesion subtypes were classified based on fluorescein angiography (FA) as occult choroidal neovascularization, classic choroidal neovascularization, retinal angiomatous proliferation, or mixed choroidal neovascularization, and by the anatomical classification system which utilizes FA and SD-OCT as Types 1 (sub-retinal pigment epithelium), 2 (subretinal), 3 (intraretinal), or mixed neovascularization.


RESULTS
Ninety-one patients (94 eyes) fit the inclusion criteria, of which 52 eyes (55.3%) experienced apparent GA growth. The odds of developing apparent GA were significantly lower in Type 1 neovascularization compared to the other lesion types (P < 0.001). Using both FA and SD-OCT to classify neovascular age-related macular degeneration significantly improves the goodness of fit in the correlation between apparent GA growth and baseline neovascular lesion type (P < 0.001).


CONCLUSIONS
Treatment-naive neovascular age-related macular degeneration eyes with Type 1 neovascularization at baseline were less likely to develop GA than eyes with other types. The correlation between apparent GA growth and subtype of neovascularization is stronger when lesions are classified with an anatomic grading that utilizes both FA and SD-OCT.
*Vitreous Retina Macula Consultants of New York, New York, New York; †Department of Ophthalmology, The New York Eye and Ear Infirmary, New York, New York; ‡Department of Medicine, St. Vincent's Medical Center, Bridgeport, Connecticut; §LuEsther T. Mertz Retinal Research Center, Department of Ophthalmology, Retina Division, Manhattan Eye, Ear, and Throat Hospital, New York, New York; ¶Department of Ophthalmology, New York University School of Medicine, New York, New York; **Department of Ophthalmology, Edward S. Harkness Eye Institute, Columbia College of Physicians and Surgeons, New York, New York; ††Department of Ophthalmology, University and Polytechnic Hospital La Fe, Valencia, Spain; and ‡‡Biostatistical Consultant, Terrytown, New York.
Luna
L
Xu
Sarah
S
Mrejen
Jesse J
JJ
Jung
Roberto
R
Gallego-Pinazo
Desmond
D
Thompson
Marcela
M
Marsiglia
K Bailey
KB
Freund
D000369:Aged, 80 and over; D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D000068258:Bevacizumab; D015331:Cohort Studies; D005260:Female; D005451:Fluorescein Angiography; D005500:Follow-Up Studies; D057092:Geographic Atrophy / Q000175:diagnosis* / Q000503:physiopathology; D006801:Humans; D058449:Intravitreal Injections; D008297:Male; D000069579:Ranibizumab; D040262:Receptors, Vascular Endothelial Growth Factor / Q000627:therapeutic use; D011993:Recombinant Fusion Proteins / Q000627:therapeutic use; D012189:Retrospective Studies; D041623:Tomography, Optical Coherence; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors*; D014792:Visual Acuity / Q000502:physiology; D057135:Wet Macular Degeneration / Q000145:classification / Q000188:drug therapy* / Q000503:physiopathology
D020533:Angiogenesis Inhibitors; D061067:Antibodies, Monoclonal, Humanized; D011993:Recombinant Fusion Proteins; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; C533178:aflibercept; D000068258:Bevacizumab; D040262:Receptors, Vascular Endothelial Growth Factor; D000069579:Ranibizumab