Myopic macular neovascularization as an inducing factor of atrophy in high myopia.

BACKGROUND: Chorioretinal atrophy is a leading cause of vision loss in highly myopic eyes. Myopic macular neovascularization (mMNV) may accelerate atrophy, but progression determinants remain unclear. METHODS: In 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. RESULTS: Of 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). CONCLUSIONS: Atrophy 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.