PMC10020832_01
Macular atrophy corresponding to previous area of choroidal neovascularization in a patient with neovascular age-related macular degeneration treated with frequent injections of a vascular endothelial growth factor-neutralizing protein. Top row shows a fundus photograph and late frame of a fluorescein angiogram (FA) at initial visit for patient 1 when visual acuity (VA) was 20/80 and antivascular endothelial growth factor (VEGF) treatment was initiated. Fundus photograph shows hypopigmented areas, and FA shows a large area of minimally classic choroidal neovascularization throughout the entire macula. The bottom row shows a fundus photograph and a late frame of an FA after 5 years and 45 injections of a VEGF-neutralizing protein. VA was 20/32, and fundus photograph and FA showed atrophy that corresponds to the area of choroidal neovascularization that was present 5 years earlier, except there is less atrophy in the fovea, where there is still active choroidal neovascularization.
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F2
Figure 2 shows images from a patient who developed atrophy throughout a region of the macula previously occupied by a large CNV lesion. The patient is an 84-year-old female with neovascular AMD who presented with distortion and a VA of 20/80 in the left eye due to poorly defined CNV throughout the entire macula (Figure 2, top row). Over a 5-year period, she received 45 injections of a VEGF-neutralizing protein in the left eye, after which VA was stable at 20/32 and fundus photographs showed atrophy that corresponded to the area of prior CNV, except that there was less atrophy in the fovea than in the surrounding areas (Figure 2, bottom row).
Correspondence of macular atrophy and pre-existent choroidal neovascularization in a patient with neovascular age-related macular degeneration treated with a vascular endothelial growth factor-neutralizing protein. Top row shows a fundus photograph and a late frame of a fluorescein angiogram (FA) from the initial visit of patient 2 at the initiation of antivascular endothelial growth factor (VEGF) treatment when visual acuity (VA) was 20/50. There were subretinal hemorrhage and a few hypopigmented spots, and FA showed poorly defined choroidal neovascularization (CNV) superior-temporal and inferior-temporal to the fovea. Roughly 7 years after the initial visit, VA was 20/125 and fundus photograph and FA showed atrophy throughout the area previously occupied by CNV (bottom row). During the 7-year follow-up period, the patient received 23 intravitreous injections of a VEGF-neutralizing protein.
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F3
Figure 3 shows another patient who developed atrophy that corresponded to an area of prior ill-defined CNV. Fundus photograph and FA in the left eye showed a large area of occult CNV superior to the fovea that appeared to extend under the fovea to a region of CNV inferior to the fovea (Figure 3, top row). FA showed atrophy that corresponded to the prior area of CNV (Figure 3, bottom row). Figure 4 shows images from a patient who presented with predominantly classic CNV unlike the ill-defined occult CNV seen in the 2 patients discussed above.
Incomplete correspondence of predominantly classic choroidal neovascularization and subsequent atrophy after treatment with a vascular endothelial growth factor (VEGF)-neutralizing protein in a patient with age-related macular degeneration. Fundus photograph shows subretinal hemorrhage and fluid (top left) overlying predominantly classic choroidal neovascularization (CNV) seen in a late frame of a fluorescein angiogram (FA) (top right) from the initial visit of patient 8, when visual acuity (VA) was 20/40 and antivascular endothelial growth factor treatment was initiated. Five years after the initial visit, during which time the patient received 24 injections of a VEGF-neutralizing protein, VA was 20/200 and fundus photograph (bottom left) and FA (bottom right) showed an area of atrophy with the greatest window defect on FA within the boundaries of the classic component of the CNV and less profound atrophy beyond the temporal border of the classic CNV. Close inspection of the previous FA (top right) shows subtle abnormalities temporal to the classic CNV that may represent occult CNV.
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F4
FA showed atrophy that corresponded to the prior area of CNV (Figure 3, bottom row). Figure 4 shows images from a patient who presented with predominantly classic CNV unlike the ill-defined occult CNV seen in the 2 patients discussed above. The most profound atrophy as seen by the greatest area of window defect seen on FA (Figure 4, bottom right) was within the boundaries of the classic component of the CNV seen 5 years earlier (Figure 4, top right), but there was also atrophy temporal to the border of the prior classic CNV. On the initial FA, there were subtle abnormalities temporal to the classic CNV that may represent occult CNV (Figure 4, top right).