All CNV subtypes will respond to anti-VEGF therapy but benefit is only likely in the presence of what?

To understand why the correct response is that benefit from anti-VEGF therapy is most likely present in the context of active disease, it’s essential to recognize the nature of Choroidal Neovascularization (CNV) and the role of vascular endothelial growth factor (VEGF) in this process.

Active CNV is characterized by the presence of new, leaky blood vessels that are contributing to visual deterioration and associated with edema and hemorrhage. Anti-VEGF therapy works by inhibiting the action of VEGF, which is the primary driver of this neovascularization and associated fluid accumulation. When the disease is active, the therapeutic blockade of VEGF can lead to significant improvements in visual acuity and reduction of retinal edema because it targets the active pathological process.

In contrast, conditions like chronic, stable, or non-active disease imply that the CNV is not currently proliferating or causing significant damage to the retinal architecture. In these states, the vasculature may have either stabilized without progression or regressed, rendering anti-VEGF treatment less likely to yield beneficial results. Therefore, clinical outcomes from anti-VEGF therapy are optimal when the disease is actively contributing to the patient's symptoms and visual impairment. This emphasizes the critical nature of disease