Information for healthcare professionals about CNV.

Choroidal neovascularisation (CNV) occurs when abnormal blood vessels originating from the choroid grow into the retina through the Bruch's membrane. The pathophysiology involves alterations in the normal transport of metabolites, ions and water across Bruch's membrane which alters the nutrition and stability of the retinal pigment epithelium (RPE) and alters the transport of waste out of the retina. VEGF is released by the RPE due to hypoxia, and this starts a series of angiogenic responses. Breaks in Bruch's membrane are required for new vessels to pass from the choroidal vasculature to the retina.¹ CNV can arise in association with a number of eye conditions, including AMD and pathological myopia (a spherical equivalent of −8.0 dioptres or less or a long axial length).²

Symptoms of CNV affecting the central vision include decreased visual acuity, metamorphopsia and scotomas.¹

The aim of CNV treatment is to improve or halt the decline in visual acuity.³ VEGF has been found to play a major role in the pathogenesis of CNV; therefore, treatment can include anti-VEGF agents.²

AMD, age-related macular degeneration; VEGF, vascular endothelial growth factor.

References

1. American Academy of Ophthalmology. Choroidal Neovascularization: OCT Angiography Findings. 2020 Available at: https://eyewiki.aao.org/Choroidal_Neovascularization:_OCT_Angiography_Findings [Accessed July 2020]
2. American Academy of Ophthalmology. Myopic CNVM. 2020. Available at: https://eyewiki.aao.org/Myopic_CNVM [Accessed July 2020].
3. NICE. Single Technology Appraisal: Aflibercept for treating myopic choroidal neovascularisation. 2017. Available at: https://www.nice.org.uk/guidance/ta486/documents/final-scope [Accessed July 2020].