Ranibizumab for Retinal Angiomatous Proliferation in Age-related Macular Degeneration

K Atmani; M Voigt; V Le Tien; G Querques; G Coscas; G Soubrane; E H Souied


Eye. 2010;24(7):1193-1198. 

In This Article

Abstract and Introduction


Purpose To assess the 1-year functional outcome and to evaluate the morphological changes after intravitreal injections of ranibizumab in eyes affected with retinal angiomatous proliferation (RAP) due to age-related macular degeneration (AMD).
Methods A prospective, non-randomized, interventional study was conducted on 26 consecutive patients with newly diagnosed RAP. All eyes were treatment naive and were randomized to receive intravitreal injections of ranibizumab for a 12-month period. After the first three monthly injections, re-treatment was performed in case of best-corrected visual acuity (BCVA) loss of at least five letters associated with fluid within the macula, central macular thickness (CMT) increase of at least 100 μm, and/or persistence of fluid within the macula as evaluated by optical coherence tomography, new onset macular haemorrhages, persistence of leakage from the lesions on fluorescein angiography.
Results All patients completed the 12-month follow-up: 25 of the 29 treated eyes (86.2%) were stabilized, with a loss of less than 15 letters. Nineteen eyes (65.5%) maintained or improved their BCVA, and three eyes (10.3%) gained three lines or more. Overall, mean BCVA remained stable at the 12-month follow-up (−0.07 letters; P>0.05). Mean CMT significantly decreased from 386±147 to 216±74μm at the 12-month follow-up. No significant adverse events were observed during the study. The mean number of injections was 5.8±1.7 during the follow-up period.
Conclusion The 1-year follow-up outcomes in our series suggest that ranibizumab is an effective treatment for RAP in AMD, allowing stabilization of BCVA and reduction of CMT.


Retinal angiomatous proliferation (RAP), also known as a retinal choroidal anastomosis (RCA) or type 3 neovascularization, is a distinct form of exudative age-related macular degeneration (AMD) characterized by an abnormal communication between the choroidal and the retinal vasculatures. The pathogenesis of this peculiar entity, which was first described in 1992 as a retinal angiomatous lesion associated with drusen, causing retinal pigment epithelium detachments (PEDs),[1] and in 1995 as an RCA causing PEDs,[2,3] still remains controversial. In 2001, Yannuzzi et al suggested that an angiomatous proliferation originating from the deep retinal layers extends posteriorly to anastomose with a sub-retinal pigment epithelium (RPE) neovascularization (type 1).[4] In 2003, on the basis of clinical and angiographic observations, Gass et al[5] postulated that the initial neovascular event for RAP is an occult type 1 neovascularization extending anteriorly to form a sub-retinal (type 2) 'piggyback' neovascularization, resulting ultimately in an RCA. The term 'type 3 neovascularization' proposed by Freund et al[6] makes no reference to pathogenesis and could be helpful to distinguish this lesion from the two other types of neovascularization, the well-defined type 2 choroidal neovascularization (CNV) and the occult type 1 (CNV).[7,8] Until the anti-VEGF era, treatment of RAP has been disappointing, with poor anatomical and functional outcomes. Direct laser photocoagulation of the vascular lesion, laser photocoagulation of the feeder vessel, photodynamic therapy, and transpupillary thermotherapy rarely allow the anatomical closure of the lesion, especially once the vascular complex is well established.[9] Promising outcomes are expected from the use of anti-VEGF drugs, as shown by the short-term results of intravitreal pegaptanib sodium,[10] ranibizumab,[11,12] and bevacizumab[13] in the treatment of these lesions.

The purpose of this study was to evaluate prospectively the effectiveness of ranibizumab in eyes affected with RAP because of AMD.


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