Minhee Cho1, Irene A Barbazetto, K Bailey Freund. 1. New York University School of Medicine/Manhattan Eye, Ear & Throat Hospital, Department of Ophthalmology, New York, New York, USA.
Abstract
PURPOSE: To describe a neovascular pattern associated with treatment-refractory neovascular age-related macular degeneration (AMD). DESIGN: A retrospective observational case series. SETTING: Clinical practice. PATIENT POPULATION: Twelve eyes of 12 patients with neovascular AMD in which a poor anatomic response to anti-vascular endothelial growth factor (VEGF) therapy was related to polypoidal choroidal vasculopathy (PCV). OBSERVATION PROCEDURE: Slit-lamp biomicroscopy, optical coherence tomography, fluorescein and indocyanine green angiography. MAIN OUTCOME MEASURES: Snellen visual acuity (VA), anatomic response to therapy including presence or absence of retinal edema, hemorrhage, and lipid exudates. RESULTS: New or persistent PCV was identified in a cohort of patients demonstrating increasing macular exudation despite regular intravitreal ranibizumab (Lucentis; Genentech Inc, South San Francisco, California, USA) or bevacizumab (Avastin; Genentech Inc) injections for a minimum of 6 months. Treatment with verteporfin photodynamic therapy (PDT), PDT/anti-VEGF combination therapy, or continued anti-VEGF monotherapy resulted in complete resolution of exudation in 9 of 12 patients and partial resolution of exudation in the remaining 3 patients. CONCLUSION: Treatment-refractory neovascular AMD may harbor vascular abnormalities such as PCV. Modifications in therapeutic protocols may be indicated in order to improve visual and anatomic outcomes in this population.
PURPOSE: To describe a neovascular pattern associated with treatment-refractory neovascular age-related macular degeneration (AMD). DESIGN: A retrospective observational case series. SETTING: Clinical practice. PATIENT POPULATION: Twelve eyes of 12 patients with neovascular AMD in which a poor anatomic response to anti-vascular endothelial growth factor (VEGF) therapy was related to polypoidal choroidal vasculopathy (PCV). OBSERVATION PROCEDURE: Slit-lamp biomicroscopy, optical coherence tomography, fluorescein and indocyanine green angiography. MAIN OUTCOME MEASURES: Snellen visual acuity (VA), anatomic response to therapy including presence or absence of retinal edema, hemorrhage, and lipid exudates. RESULTS: New or persistent PCV was identified in a cohort of patients demonstrating increasing macular exudation despite regular intravitreal ranibizumab (Lucentis; Genentech Inc, South San Francisco, California, USA) or bevacizumab (Avastin; Genentech Inc) injections for a minimum of 6 months. Treatment with verteporfin photodynamic therapy (PDT), PDT/anti-VEGF combination therapy, or continued anti-VEGF monotherapy resulted in complete resolution of exudation in 9 of 12 patients and partial resolution of exudation in the remaining 3 patients. CONCLUSION: Treatment-refractory neovascular AMD may harbor vascular abnormalities such as PCV. Modifications in therapeutic protocols may be indicated in order to improve visual and anatomic outcomes in this population.