ArticleGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2026
Myopic macular neovascularization as an inducing factor of atrophy in high myopia.
Article in Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundChorioretinal atrophy is a leading cause of vision loss in highly myopic eyes. Myopic macular neovascularization (mMNV) may accelerate atrophy, but progression determinants remain unclear.
methodsIn this retrospective study, atrophy area and perimeter were quantified at three time points: pre-MNV, at mMNV diagnosis, and final follow-up using ImageJ. Variables analyzed included macular staphyloma, membrane-atrophy contact, intravitreal injections, and best-corrected visual acuity (BCVA). Accelerated progression rate was defined as an annual increase exceeding twice the pre-mMNV atrophy. Univariate and multivariate analyses identified predictors of final atrophy.
resultsOf 225 eyes with high myopia (axial length ≥ 26 mm) and confirmed mMNV, 168 met inclusion criteria; mean follow-up was 4.96 ± 2.5 years. Atrophy area increased from 0.77 ± 1.92 mm² pre-MNV to 3.95 ± 7.41 mm² at diagnosis and 6.95 ± 9.76 mm² at final visit (p < 0.001). Area-based atrophy progression increased significantly after mMNV onset (0.25 ± 0.62 vs. 0.92 ± 1.96 mm²/year; p = 0.023), indicating greater absolute lesion enlargement over time. However, perimeter-adjusted progression rates, which normalize lesion growth for lesion size, did not differ significantly (0.50 ± 0.44 vs. 0.82 ± 0.43 mm²/mm/year; p = 0.40), suggesting that the increase in area mainly reflects larger lesion size rather than faster boundary expansion. Membrane-atrophy contact was associated with larger atrophy in univariate analysis (p < 0.001) but was not independent. Independent determinants were pre-MNV atrophy (β = 0.92; p < 0.001) and macular posterior staphyloma (β = 0.15; p = 0.009). Finally, final BCVA showed a moderate positive correlation with final atrophy area (r = 0.41; p < 0.001) and with foveal involvement (r = 0.326; p < 0.001).
conclusionsAtrophy progresses continuously in eyes with mMNV and accelerates after neovascular development, independent of anti-VEGF therapy. Pre-existing atrophy and macular posterior staphyloma determine final lesion size, while membrane-atrophy contact contributes to rapid progression.
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