Abstract
Vascular endothelial growth factor (VEGF) is produced by the retina as a response to ischemia. In lower concentrations, VEGF induces retinal vascular hyperpermeability; in higher concentrations, intraocular neovascularization. Intraocular concentrations of VEGF after retinal vein occlusion (RVO) fall along a continuum. Therefore, most RVOs are, to some degree, ischemic, a revision of the dichotomous ischemic/ nonischemic classification commonly used from 1970- 2000. Anti-VEGF therapy is useful in treating RVOs with macular edema and intraocular neovascularization. The four drugs in use are pegaptanib, bevacizumab, ranibizumab, and aflibercept. For ranibizumab, there is level I evidence supporting effectiveness in treating macular edema following BRVO and CRVO. For aflibercept, there is level I evidence supporting effectiveness in treating macular edema following CRVO. For bevacizumab and pegaptanib, there is level II evidence for macular edema following BRVO and CRVO. For all four drugs, there is level I and II evidence of effectiveness against varieties of intraocular neovascularization. Durations of effectiveness depend on intraocular half lives and binding affinities of the different drugs for VEGF. In general, the durations of effectiveness of a single injection vary from one to three months with aflibercept seeming to have the longest duration of action. Concerns of potential adverse effects of these drugs on retinal capillary perfusion have not been validated.
Keywords: Aflibercept, bevacizumab, branch retinal vein occlusion, BRAVO, central retinal vein occlusion, COPERNICUS, CRUISE, GALILEO, macular edema, neovascularization, nonischemic, pegaptanib, ranibizumab, Vascular endothelial growth factor, ischemia
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