Macular neovascularization changes persist in AMD, even with long-term anti-VEGF therapy
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Key takeaways:
- Macular neovascularization size increased at 1.24 mm2 per year.
- Outer retina atrophy lesions grew at a rate of 1.22 mm2 per year.
Continuous growth of macular neovascularization size, as well as development of outer retina atrophy, was observed in neovascular age-related macular degeneration, even with frequent anti-VEGF treatment, according to research in PLoS One.
“Despite frequent long-term anti-VEGF therapy, we observed ongoing [macular neovascularization (MNV)] growth,” Daniel Pauleikhoff, MD, chair of the department of ophthalmology at St. Franziskus-Hospital Münster, and colleagues wrote. “This is consistent with the concept that the development of MNV may be a physiological biological repair mechanism to preserve [retinal pigment epithelium] and photoreceptor function, provided hyperpermeability and fluid exudation are controlled.”
In a single-center, retrospective cohort study, researchers evaluated 143 eyes with neovascular AMD from 94 patients who began anti-VGEF therapy between 2009 and 2018. Therapy was continued until the last recorded visit, which ranged from 1 to 14 years (mean follow-up, 5.3 years), with a mean 33.3 injections overall, or approximately seven per year.
Researchers assessed MNV size, as well as complete retinal pigment epithelium (RPE) and outer retina atrophy (cRORA), via OCT volume scans at baseline and annual follow-ups.
According to results, MNV growth was continuous at a mean rate of 1.24 mm2 per year, with no significant correlation to baseline MNV size, age, gender or number of injections per year.
In addition, cRORA developed in association with increasing MNV size and was present in 60% of eyes after 6 years and all eyes after 10 years. Researchers reported “continuous, linear” growth of mean cRORA at a rate of 1.22 mm2 per year, similar to that of MNV size.
“This supports the concept that MNV may be part of a physiological biological repair mechanism and could support RPE and photoreceptor function, if permeability can be controlled effectively by anti-VEGF therapy,” Pauleikhoff and colleagues wrote. “Whether remaining low anti-VEGF levels or other factors independent of VEGF are responsible for MNV growth under therapy must be investigated in future studies.”
Perspective
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With a population living longer and more active lives, AMD remains a concern among patients at risk for vision loss from the disease. Anti-VEGF injections are considered first-line treatment for exudative neovascular AMD. However, exact mechanisms behind many morphological changes in AMD remain unknown.
This retrospective study, spanning 14 years, looks at changes in MNV and complete RPE and cRORA under long-term anti-VEGF therapy. Despite following OCT-based retreatment criteria and excluding patients with treatment interruptions, investigators found both MNV size and the development and size of cRORA increased over time.
One hypothesis is that MNV plays a nourishing role to the RPE and photoreceptors up to a point, but larger complexes lose this ability as they mature. Permeability and suppression of fluid exudation appear to be a greater concern with respect to visual function.
This study was limited in its analysis, as the type of anti-VEGF agents for patients varied. With newer anti-VEGF agents having longer-acting mechanisms, further investigation is needed to see if these changes hold true on individualized treatments.
While we work towards future treatments that address both morphological and visual function, it’s important that clinicians discuss current treatment options and limitations with patients.
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