Incidence and Associated Factors of Myopic Maculopathy Progression after Posterior Scleral Contraction in High Myopia.

Abstract

To explore the progression predictors of myopic maculopathy in patients with high myopia after posterior scleral contraction (PSC). Retrospective cohort study from a tertiary hospital. A total of 892 eyes from 892 patients with a spherical equivalent (SE) of -6.00 diopters or less who underwent PSC at the Refractive Surgery Clinical Center, Eye Hospital, Wenzhou Medical University, were included. Myopic maculopathy was classified using the updated Atrophy-Traction-Neovascularization (ATN) system based on fundus photographs and OCT images. Progression, defined as an increase in any ATN component score, was assessed using Kaplan-Meier analysis. Predictors of atrophy, traction, and neovascularization progression were evaluated with Cox regression. Cumulative survival rates and predictors for the progression of myopic maculopathy. Posterior scleral contraction significantly improved best-corrected visual acuity, SE, axial length (AL), intraocular pressure (IOP), and traction scores in those without progression. However, 10.76% of eyes showed ATN progression over a median follow-up of 13.57 months, and the cumulative survival rates for patients with high myopia free of ATN progression were 94.57% at 1 year, 86.44% at 3 years, and 76.22% at 5 years after surgery. For atrophy progression, baseline A1 through A3 components were protective, whereas higher IOP increased risk (hazard ratio [HR], 1.138; P = 0.030). Baseline T2 through T3 were protective for traction progression, whereas steeper baseline steep keratometry (K2) was a risk factor (HR, 1.183; P = 0.026). Baseline T5 and steeper K2 strongly predicted neovascularization progression (HR, 10.773 [P = 0.004] and 1.439 [P = 0.003], respectively). Although PSC significantly improves SE and AL in patients with high myopia, myopic maculopathy inevitably progresses. Baseline steeper K2 and higher IOP are significant associated factors for progression. These findings suggest a mechanobiological mechanism underlying the progression of myopic maculopathy and point to potential preventive strategies. The author(s) have no proprietary or commercial interest in any materials discussed in this article.