Purpose <p>To investigate the long-term incidence and progression of macular atrophy (MA) in patients with type 3 macular neovascularization (MNV) undergoing anti-vascular endothelial growth factor (VEGF) therapy and to identify associated clinical factors.</p> Methods <p>This retrospective observational study included 23 eyes from 19 Japanese patients diagnosed with treatment-naïve type 3 MNV. Patients received anti-VEGF therapy and were followed for a mean duration of 8.9 ± 1.7 years (median 8.8 years, range 7.0–13.2 years). MA was assessed at baseline, 1–2 years, and the final visit using fundus autofluorescence (FAF), near-infrared reflectance (NIR), and spectral-domain optical coherence tomography (SD-OCT). MA size, progression rate, subretinal drusenoid deposits (SDD) regression, and subfoveal choroidal thickness (SCT) were evaluated.</p> Results <p>MA developed in 87% of eyes, with a significant increase in lesion size from 0.78 ± 1.50&#xa0;mm² at year 1–2 to 9.62 ± 11.1&#xa0;mm² at the final visit (<i>p</i> &lt; 0.001). MA progression accelerated after year 2. A significant negative correlation was observed between baseline SCT and final MA size (<i>r</i> = -0.42, <i>p</i> &lt; 0.05). SDD regression was associated with faster MA growth. No significant association was found between MA progression and anti-VEGF injection number, recurrence frequency, or PDT history. Visual acuity declined significantly over time and correlated with final MA size (<i>r</i> = 0.59, <i>p</i> &lt; 0.01).</p> Conclusion <p>MA in type 3 MNV continued to enlarge over nearly 9 years of anti-VEGF treatment. Atrophy progression was linked to choroidal thinning and SDD regression, rather than treatment burden, highlighting the need for phenotype-based risk stratification and alternative therapeutic strategies.</p>

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Analysis of macular atrophy in type 3 macular neovascularization cases: a follow-up of over 7 years

  • Junichiro Honjo,
  • Ryo Mukai,
  • Kanako Itagaki,
  • Keiichiro Tanaka,
  • Koki Norikawa,
  • Yutaka Kato,
  • Akihito Kasai,
  • Tetsuju Sekiryu

摘要

Purpose

To investigate the long-term incidence and progression of macular atrophy (MA) in patients with type 3 macular neovascularization (MNV) undergoing anti-vascular endothelial growth factor (VEGF) therapy and to identify associated clinical factors.

Methods

This retrospective observational study included 23 eyes from 19 Japanese patients diagnosed with treatment-naïve type 3 MNV. Patients received anti-VEGF therapy and were followed for a mean duration of 8.9 ± 1.7 years (median 8.8 years, range 7.0–13.2 years). MA was assessed at baseline, 1–2 years, and the final visit using fundus autofluorescence (FAF), near-infrared reflectance (NIR), and spectral-domain optical coherence tomography (SD-OCT). MA size, progression rate, subretinal drusenoid deposits (SDD) regression, and subfoveal choroidal thickness (SCT) were evaluated.

Results

MA developed in 87% of eyes, with a significant increase in lesion size from 0.78 ± 1.50 mm² at year 1–2 to 9.62 ± 11.1 mm² at the final visit (p < 0.001). MA progression accelerated after year 2. A significant negative correlation was observed between baseline SCT and final MA size (r = -0.42, p < 0.05). SDD regression was associated with faster MA growth. No significant association was found between MA progression and anti-VEGF injection number, recurrence frequency, or PDT history. Visual acuity declined significantly over time and correlated with final MA size (r = 0.59, p < 0.01).

Conclusion

MA in type 3 MNV continued to enlarge over nearly 9 years of anti-VEGF treatment. Atrophy progression was linked to choroidal thinning and SDD regression, rather than treatment burden, highlighting the need for phenotype-based risk stratification and alternative therapeutic strategies.