Purpose <p>To determine whether the development of incident type I macular neovascularization (MNV) in patients with geographic atrophy (GA) influences the rate of atrophy expansion over time.</p> Methods <p>In a longitudinal matched case-control study, a consecutive series of 28 eyes with GA that developed type I MNV were matched to 28 eyes with GA only, using propensity scores based on baseline atrophic area, duration of follow-up, and presence of subretinal drusenoid deposits (SDD). Atrophic areas were semi-automatically delineated on serial registered fundus autofluorescence (FAF) images. The square root–transformed rate of GA enlargement was calculated and compared between groups for time periods before and after the onset of MNV. The main outcome measure was the GA square root atrophy growth rate before and after MNV development.</p> Results <p>Prior to MNV development, estimates of the square root GA growth rate were similar in both groups (estimate [95% CI]: 0.549 [0.406–0.692] mm/year vs. 0.520 [0.377–0.663] mm/year, <i>p</i> = 0.46). Following the development of MNV, the atrophy expansion rate significantly slowed in the MNV group compared to the GA-only group (0.331 [0.223–0.440] vs. 0.495 [0.387–0.604] mm/year, <i>p</i> = 0.01). Longitudinal modelling indicated that the estimated square root atrophic area began to diverge significantly between groups as early as 72 days prior to MNV diagnosis.</p> Conclusions <p>Eyes affected by GA showed a significant decrease in atrophy expansion rate with the development of type I MNV. The effect on atrophy growth rates appeared to precede the clinical diagnosis of MNV.</p>

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The impact of macular neovascularization development on geographic atrophy progression

  • Mariano Cozzi,
  • Matteo Airaldi,
  • Lucrezia Barbieri,
  • SriniVas R. Sadda,
  • Giovanni Staurenghi,
  • Federico Corvi

摘要

Purpose

To determine whether the development of incident type I macular neovascularization (MNV) in patients with geographic atrophy (GA) influences the rate of atrophy expansion over time.

Methods

In a longitudinal matched case-control study, a consecutive series of 28 eyes with GA that developed type I MNV were matched to 28 eyes with GA only, using propensity scores based on baseline atrophic area, duration of follow-up, and presence of subretinal drusenoid deposits (SDD). Atrophic areas were semi-automatically delineated on serial registered fundus autofluorescence (FAF) images. The square root–transformed rate of GA enlargement was calculated and compared between groups for time periods before and after the onset of MNV. The main outcome measure was the GA square root atrophy growth rate before and after MNV development.

Results

Prior to MNV development, estimates of the square root GA growth rate were similar in both groups (estimate [95% CI]: 0.549 [0.406–0.692] mm/year vs. 0.520 [0.377–0.663] mm/year, p = 0.46). Following the development of MNV, the atrophy expansion rate significantly slowed in the MNV group compared to the GA-only group (0.331 [0.223–0.440] vs. 0.495 [0.387–0.604] mm/year, p = 0.01). Longitudinal modelling indicated that the estimated square root atrophic area began to diverge significantly between groups as early as 72 days prior to MNV diagnosis.

Conclusions

Eyes affected by GA showed a significant decrease in atrophy expansion rate with the development of type I MNV. The effect on atrophy growth rates appeared to precede the clinical diagnosis of MNV.