May 2004
Volume 45, Issue 13
ARVO Annual Meeting Abstract  |   May 2004
A proposed mechanism for the pathogenesis of Retinal Angiomatous Proliferation
Author Affiliations & Notes
  • V.R. Patel
    Ophthalmology, McGill University, Montreal, PQ, Canada
  • S. Conti
    Ophthalmology, McGill University, Montreal, PQ, Canada
  • J.C. Chen
    Ophthalmology, McGill University, Montreal, PQ, Canada
  • Footnotes
    Commercial Relationships  V.R. Patel, None; S. Conti, None; J.C. Chen, None.
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 3103. doi:
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      V.R. Patel, S. Conti, J.C. Chen; A proposed mechanism for the pathogenesis of Retinal Angiomatous Proliferation . Invest. Ophthalmol. Vis. Sci. 2004;45(13):3103.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: To propose a theory for the pathogenesis of retinal angiomatous proliferation (RAP). Methods: We reviewed the clinical, fluorescein angiographic, and OCT features of 16 eyes of 13 consecutive patients with a diagnosis of RAP. Results: Clinical examination revealed a retinal pigment epithelial detachment (PED) with overlying intraretinal hemorrhages in the majority of patients. Fluorescein angiography (FA) demonstrated findings consistent with a fibrovascular PED and areas of early leakage with progressive hyperfluorescence ("hot spots") corresponding to the observed intraretinal hemorrhages on clinical examination and fundus photography. Typical OCT features included evidence of irregular, tented PEDs associated with an overlying, thickened zone of hyperreflectivity within the fluid–filled subretinal space. The hyperreflective bands extend intraretinally, with cystoid accumulations within the surrounding intraretinal space. Conclusions: Understanding the origin of intraretinal neovascularization within exudative ARMD, a pathological process presumably localizing to Bruch’s membrane, poses an interesting challenge. Similarly, a PED created by a pathological retinal process is also inconsistent with the conventional understanding of its etiology. We propose a pathogenetic theory which reconciles these findings in a way that still implicates Bruch’s membrane as the primary site of dysfunction. We suggest that the presence of a diffusely thickened hydrophobic Bruch’s membrane creates an anatomic barrier to effective diffusion of soluble nutrients essential to the metabolic activities of the avascular outer retina; this in turn produces a relatively ischemic state resulting in the formation of incompetent new intraretinal vessels. Furthermore, the same hydrophobic Bruch’s membrane likely impedes the flow of fluid from the retina to the choroid; leakage from neovascular retinal proliferations may then overwhelm the RPE’s ability to extrude the excess retinal fluid into the choroid across this diffusion barrier, leading to the formation of a PED within the zone of compromised Bruch’s–RPE adhesion as described by Bird (Eye. 1991;5 ( Pt 1):1–12).

Keywords: age–related macular degeneration • clinical (human) or epidemiologic studies: prevalence/incidence 

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