The results of the BRAVO and CRUISE studies leave some unanswered questions. Will visual acuity gains be maintained after 6 months? How many patients will need ongoing VEGF suppression? Will other anti- VEGF agents be equivalent or superior to ranibizumab? Currently, a phase 3 study, COPERNICUS (Controlled Phase III Evaluation of Repeated Intravitreal Administration of VEGF Trap-Eye In Central Retinal Vein Occlusion: Utility and Safety) is recruiting patients, and the results of this study may answer this last question. Anti-VEGF agents (specifically ranibizumab in the BRAVO and CRUISE trials) are shown to decrease macular edema secondary to BRVO and CRVO and these decreases are associated with significant visual acuity gains. The results of the BRAVO and CRUISE trials imply several points regarding the pathophysiology of RVO. First is the implication that edema is VEGF-mediated, which is surprising to me because I had previously believed that Starling's law or osmotic forces would have more of an effect on edema because of the increased venous pressure. Second is the implication that anti-VEGF treatment may decrease retinal hemorrhage, a theory for which we are currently performing more data analysis. Third, these results also imply that all RVOs must be ischemic to some extent. Further, patients with RVO who have significant nonperfusion must be closely monitored if anti-VEGF is not administered indefinitely because unchecked, these patients are likely to develop neovascularization at some point.
|Original language||English (US)|
|Number of pages||5|
|Issue number||APRIL SUPPL.|
|State||Published - Apr 1 2010|
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