Second Eye Myopic Macular Neovascularization Risk Increases in Younger Patients

The risk of second eye myopic macular neovascularization is significantly elevated in individuals with the disease in one eye who are younger than 40 years, according to research published in Ophthalmology Retina. This increased risk should warrant more education and closer monitoring in this patient population, the report suggests.

Researchers retrospectively reviewed data from 88 patients with high myopia (mean age, 57 years; 58% women) and an active myopic macular neovascular lesion in only one eye between 2005 and 2018. The team obtained spherical equivalent and axial length data, noted the presence of diffuse or patchy chorioretinal atrophy and lacquer cracks, and examined the incidence rate and risk factors for second eye involvement among the cohort.

Overall, 27% of fellow eyes developed myopic macular neovascularization during the follow-up period. The mean time until disease development in the second eye was 48 months, the incidence rate of second eye involvement was 4.6 (95% CI, 2.9 – 6.7) per 100 person-years, and cumulative incidence was 8% at 2 years, 21% at 5 years, and 38% at 10 years, according to the report.

Individuals younger than 40 years experienced a significantly higher risk of second eye involvement compared with individuals older than 40 years (hazard ratio [HR], 3.8; 95% CI, 1.65-8.69; P =.002). While the presence of lacquer cracks also appeared to increase myopic macular neovascularization risk, this risk was not statistically significant (HR, 2.25; 95% CI, 0.94-5.39; P =.07). 

“Older patients in our study population had a lower risk of myopic [macular neovascularization] development in the second eye, and impaired [vascular endothelial growth factor] upregulation with age may be an explanation,” according to the study authors. “The structural changes that occur in the retina and choroid of high myopes is known to result from excessive axial elongation, and hypoxia in the retinal pigment epithelial cells and glia cells are hypothesized to trigger [vascular endothelial growth factor] upregulation and angiogenesis.”

Study limitations include a retrospective nature and variability in follow-up duration.