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Gisela Velez; A study of geographic atrophy as the footprint of choroidal neovascularization in age-related macular degeneration. Invest. Ophthalmol. Vis. Sci. 2017;58(8):2331.
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Progressive geographic atrophy (GA) in patients treated for exudative macular degeneration with anti-vegf therapy represents a challenge. Visual acuity loss continues in many of these patients despite apparent regression of the choroidal neovascular membrane (CNVM) with resolution of leakage. We hypothesize that areas of the retina affected by CNVM are at highest risk of developing GA. We present a retrospective case series of patients with photographic and angiographic documentation of GA progression in the context of management of CNVM,
Records of patients diagnosed with exudative macular degeneration from 2007 to 2016 were reviewed. Patients included in our series had the following characteristics: (1) consistent documentation of funduscopic findings with photography and angiograpy no less than every 6 months for at least 24 months, (2) uninterrupted management with anti-vegf therapy during the study period without missed follow-up or treatment appointments. Six eyes (six patients) were identified with documentation of their disease that showed progression of the atrophic component. Photos and angiograms from the initial diagnosis were compared with those from the most recent visit to assess extent, location and progression of GA.
All six eyes were treated with anti-vegf intraocular injections. Eyes were managed for 28 to 132 months, with a mean of 71 months. Three eyes were treated with bevacizumab only, three with bevacizumab followed by aflibercept. Number of total injections ranged from 18 to 77, with a mean of 44 injections. Visuall acuity at the time of diagnosis ranged from 20/20 to 20/50, with final visual acuities in the range of 20/20 to 20/400. In all 6 eyes, fundus photography and angiography comparisions showed progression of atrophy which corresponded to areas of neovascularization.
We can demonstrate in carefully documented cases that GA develops preferentially in areas of active choroidal neovascularization, therefore representing a damage “footprint”. This suggests that aggressive management of CNVM leakage and size may play an important role in containing the damage that can later result in GA and subsequent loss of vision.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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