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Retina Anti–vascular Endothelial Growth Factor Therapy for Myopic Choroidal Neovascularisation Josep Badal, Luis Amselem, Ricardo Aleman and Frederic Huste Retinal and Vitreous Surgery, Ophthalmology Department, Moises Broggi Hospital, Barcelona, Spain Abstract Pathological myopia represents the most common cause of choroidal neovascularisation in young patients. Its natural course has a devastating prognosis. Several treatments have been assessed, but photodynamic therapy is currently the only approved treatment for subfoveal choroidal neovascularisation related to pathological myopia. Anti-vascular endothelial growth factor therapy has demonstrated promising results in any form and localisation of choroidal neovascularisation, although there is an absence of data obtained from randomised clinical trials. The aim of this article is to compare different treatment options, combinations and retreatment criteria for the management of choroidal neovascularisation in eyes with high myopia. Keywords Choroidal neovascularisation, pathological myopia, photodynamic therapy, anti-vascular endothelial growth factor, ranibizumab, bevacizumab, pegaptanib Disclosure: The authors have no conflicts of interest to declare. Received: 18 June 2013 Accepted: 17 July 2013 Citation: European Ophthalmic Review, 2013;7(2):84–6 Correspondence: Josep Badal, Department of Ophthalmology, Moises Broggi Hospital, Jacint Verdaguer s/n, Sant Joan Despí 08970, Barcelona, Spain. E: High myopia affects approximately 2 % of the general population, and represents an important cause of visual impairment in many developed countries. Choroidal neovascularisation (CNV) is one of the most vision-threatening complications of myopia. 1–3 Nearly 10  % of eyes with pathological myopia (PM) develop CNV, 4 and represents the most common cause of CNV in young patients, accounting for almost 60 % of CNV in patients under the age of 50. 5 It is also known that more than 30 % of myopic patients with pre-existing CNV will develop CNV in the fellow eye within 8 years. The natural course of this disease has a devastating prognosis, accounting for low visual acuity (VA) (20/200) in 44–60 % of the patients after 24 months. 6 Current Targets and Treatments Current treatment of CNV in PM is still not well defined. Laser photocoagulation is the standard treatment for extrafoveal CNV, 7 while photodynamic therapy (PDT) with verteporfin (Visudyne®, Novartis AG, Basel, Switzerland) is the only approved treatment by the European Agency for the Evaluation of Medicinal Products (EMEA) and the US Food and Drug Administration (FDA) for subfoveal CNV related to PM. Several other treatments have been assessed, such as macular translocation, 8–9 surgical removal of CNV, 10 radiotherapy 11 and indocyanine green mediated photothrombosis. 12,13 Recently, anti-vascular endothelial growth factor (anti-VEGF) therapy has become the most widespread treatment throughout he scientific community. Photodynamic Therapy The only evidence derived from randomised controlled trials is provided by the Verteporfin in Photodynamic Therapy (VIP) Study. 14,15 This study showed a significant benefit in eyes treated with verteporfin compared with placebo at 12-month follow-up (86 % of the verteporfin- treated patients lost fewer than 15 letters of best-corrected VA [BCVA], 84 in comparison with 67  % of the placebo-treated patients). However, the effect of PDT was not sustained by the end of the second year. As PDT monotherapy showed limited VA improvement, subretinal fibrosis and chorioretinal atrophy were observed, and the need to find an association with other therapies increased. An attempt to improve the efficacy of PDT by enhancing the fluence 16 or combining PDT with intravitreal triamcinolone acetonide injection 17,18 showed inconsistent results. However, Rishi et al. 19 described good results in combining PDT with anti-VEGF injection in a retrospective study of 26 patients. Coutinho et al. 20 also had interesting results, describing a VA gain of ≥3 lines in 32.6 % of the eyes treated with PDT in a retrospective study of 43 eyes at 5-year follow-up. Anti-vascular Endothelial Growth Factor Therapy The factors that stimulate pathological neovascularisation are not completely understood, but VEGF has been found to be one of the main elements in angiogenesis, and several reports have provided evidence that VEGF-A plays an important role in promoting CNV in PM. 21–26 Moreover, studies carried out by Tong et al. showed increased VEGF concentrations in aqueous humour of patients with CNV secondary to PM when compared to controls. 27 So far, ranibizumab (Lucentis®, Novartis, Basel, Switzerland) and bevacizumab (Avastin®, Genentech, South San Francisco, CA, US) are the most diffuse anti-VEGF drugs, giving a pan-VEGF blocking. 28–30 Ranibizumab is a specific, affinity-mature fragment of a recombinant, humanised immunoglobulin G1 (IgG1) monoclonal antibody that neutralises all active forms of VEGF-A, which was approved by the FDA for the treatment of exudative age-related macular degeneration (AMD) in June 2006. Bevacizumab is a full-length humanised antibody © Touc h ME d ic a l ME d ia 2013