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Aaron Nagiel, K Bailey Freund, Jesse J Jung, Kavita Bhavsar, Richard F Spaide, David Sarraf; Origin and behavior of Type 3 neovascularization revealed by spectral-domain optical coherence tomography. Invest. Ophthalmol. Vis. Sci. 2014;55(13):3938.
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To demonstrate the origin, maturation, and treatment response of Type 3 neovascularization in eyes with age-related macular degeneration (AMD) using high-resolution spectral-domain optical coherence tomography (OCT).
We retrospectively analyzed 21 eyes with Type 3 neovascularization and AMD for which spectral-domain OCT images were obtained over multiple clinic visits. Images were evaluated for site of origin, associated retinal pigment epithelium detachment (PED), intraretinal edema, sub-retinal pigment epithelium (RPE) fluid, reticular pseudodrusen, and progression to geographic atrophy.
18/21 (86%) Type 3 lesions were associated with an underlying PED, of which 16 (89%) were drusenoid and 2 (11%) were serous. In 7 eyes, serial OCT imaging captured the development of Type 3 neovascularization from an early precursor lesion that appeared to originate above the external limiting membrane (ELM) without evidence of underlying Type 1 or 2 choroidal neovascularization. In every case, the mature Type 3 lesions were associated with outer retinal and RPE disruption as well as adjacent cystoid edema of the retina. In 7/21 (33%) eyes, the vascular complex was associated with sub-RPE fluid. Treatment with intravitreal anti-vascular endothelial growth factor (VEGF) agents resulted in complete resolution of the intraretinal and sub-RPE fluid as well as involution of the lesion in every case. Following treatment, most cases (57%) progressed to geographic atrophy (GA) at the former site of the Type 3 vessels.
Type 3 neovascularization in AMD appears to originate above the ELM from the deep retinal capillary plexus and matures into a larger vascular complex that usually forms over a drusenoid PED. The mature vascular plexus appears to exude fluid into the retina and beneath the RPE through a focal RPE defect. Regression of these lesions following treatment with intravitreal anti-VEGF therapy is often associated with the development of GA.
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