Investigative ophthalmology & visual science · 2025
Obstructive Sleep Apnea Accelerates Progression of Intermediate Age-Related Macular Degeneration: A Three-Year Prospective Cohort Study.
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Li Qiang, Liu Dongyue, Zhang Min
Аннотация
PURPOSE: Obstructive sleep apnea (OSA) and age-related macular degeneration (AMD) share pathophysiological mechanisms involving oxidative stress and inflammation. We investigated whether OSA accelerates AMD progression in patients with intermediate AMD.
METHODS: This prospective cohort study enrolled 470 patients aged ≥50 years with intermediate AMD and age-matched healthy controls. After baseline polysomnography and multimodal retinal imaging, 470 participants were enrolled and stratified into AMD+OSA (n = 185), AMD-noOSA (n = 185), and healthy controls (n = 100). Of these, 391 completed the 36-month follow-up (AMD+OSA n = 153; AMD-noOSA n = 158; controls n = 80). The primary endpoint was composite AMD progression (central geographic atrophy, neovascular AMD, or ≥15-letter vision loss) over 36 months. Secondary endpoints included changes in visual acuity, drusen volume, and geographic atrophy area.
RESULTS: Of 391 participants completing follow-up (83.2% retention), the AMD+OSA group showed significantly higher progression rates. The primary endpoint occurred in 31.4% (48/153) of AMD+OSA versus 15.2% (24/158) of AMD-noOSA patients (P = 0.002). Visual acuity worsened by 0.15 versus 0.06 logarithm of the minimum angle of resolution (P < 0.001), and drusen volume increased by 0.05 versus 0.02 mm3 (P < 0.001), respectively. Cox regression revealed a dose-dependent relationship: mild OSA (hazard ratio [HR] = 1.45; 95% confidence interval [CI], 0.95-2.20; P = 0.08), moderate OSA (HR = 2.10; 95% CI, 1.35-3.28; P = 0.001), and severe OSA (HR = 2.80; 95% CI, 1.75-4.47; P < 0.001) versus no OSA.
CONCLUSIONS: OSA is an independent, dose-dependent risk factor for accelerated AMD progression. Screening and treating OSA in patients with intermediate AMD may represent a novel strategy to preserve vision.
METHODS: This prospective cohort study enrolled 470 patients aged ≥50 years with intermediate AMD and age-matched healthy controls. After baseline polysomnography and multimodal retinal imaging, 470 participants were enrolled and stratified into AMD+OSA (n = 185), AMD-noOSA (n = 185), and healthy controls (n = 100). Of these, 391 completed the 36-month follow-up (AMD+OSA n = 153; AMD-noOSA n = 158; controls n = 80). The primary endpoint was composite AMD progression (central geographic atrophy, neovascular AMD, or ≥15-letter vision loss) over 36 months. Secondary endpoints included changes in visual acuity, drusen volume, and geographic atrophy area.
RESULTS: Of 391 participants completing follow-up (83.2% retention), the AMD+OSA group showed significantly higher progression rates. The primary endpoint occurred in 31.4% (48/153) of AMD+OSA versus 15.2% (24/158) of AMD-noOSA patients (P = 0.002). Visual acuity worsened by 0.15 versus 0.06 logarithm of the minimum angle of resolution (P < 0.001), and drusen volume increased by 0.05 versus 0.02 mm3 (P < 0.001), respectively. Cox regression revealed a dose-dependent relationship: mild OSA (hazard ratio [HR] = 1.45; 95% confidence interval [CI], 0.95-2.20; P = 0.08), moderate OSA (HR = 2.10; 95% CI, 1.35-3.28; P = 0.001), and severe OSA (HR = 2.80; 95% CI, 1.75-4.47; P < 0.001) versus no OSA.
CONCLUSIONS: OSA is an independent, dose-dependent risk factor for accelerated AMD progression. Screening and treating OSA in patients with intermediate AMD may represent a novel strategy to preserve vision.