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Characterisation of the vascular anterior surface of type 1 macular neovascularisation after anti-VEGF therapy
  1. Federico Corvi1,2,
  2. Tommaso Bacci3,
  3. Giulia Corradetti1,2,
  4. Giovanni Staurenghi4,
  5. David Sarraf2,5,6,
  6. K. Bailey Freund7,8,
  7. SriniVas Sadda1,2
  1. 1Department of Ophthalmology, Doheny Eye Institute, Los Angeles, California, USA
  2. 2David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA
  3. 3Dipartimento di Scienze Mediche Chirurgiche e Neuroscienze, Universita degli Studi di Siena, Siena, Italy
  4. 4Eye Clinic, Department of Biomedical and Clinical Science, Luigi Sacco Hospital, University of Milan, Milan, Italy
  5. 5Department of Ophthalmology, Jules Stein Eye Institute, Los Angeles, California, USA
  6. 6Greater Los Angeles VA Healthcare Center, Los Angeles, California, USA
  7. 7Vitreous Retina Macula Consultants of New York, New York, New York, USA
  8. 8Department of Ophthalmology, NYU Grossman School of Medicine, New York, New York, USA
  1. Correspondence to Dr SriniVas Sadda, Doheny Image Reading Center, Doheny Eye Institute Doheny Image Reading Center, Los Angeles, California, USA; ssadda{at}doheny.org

Abstract

Background To evaluate whether the status of vasculature at the top of type 1 macular neovascularisation (MNV) could function as mediator of the observed protective effect against the development of complete retinal pigment epithelial and outer retinal atrophy (cRORA).

Methods In consecutive treatment-naïve patients, the vasculature at the anterior surface of the MNV was isolated using a slab designed to extract the most superficial vascular portion of the MNV lesion showing a choriocapillaris (CC)-like structure which we termed the ‘neo-CC’. The ratio between the neo-CC area (isolated using this custom slab) and the MNV area (isolated using the standard outer retina-CC slab) at baseline and at last follow-up was evaluated.

Results Forty-four eyes from 44 patients were included. 20 showed cRORA by the final follow-up (median 23 months), whereas 24 did not progress to atrophy (median 23.5 months). The proportion of MNV with neo-CC at the anterior surface was significantly lower in eyes which progressed to cRORA compared with those which did not. The multivariate regression showed that a lower proportion of neo-CC coverage over the MNV was associated with an increased odds for cRORA development.

Conclusions More extensive coverage of neo-CC is associated with a lower likelihood of development of macular atrophy in eyes receiving antivascular endothelial growth factor therapy, suggesting the protective effect of a type 1 MNV may be mediated by the development of a neo-CC and may provide insights into the biological significance of MNV as a response mechanism in eyes with age-related macular degeneration.

  • Imaging
  • Macula
  • Neovascularisation
  • Retina

Data availability statement

All data relevant to the study are included in the article or uploaded as supplementary information.

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Data availability statement

All data relevant to the study are included in the article or uploaded as supplementary information.

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Footnotes

  • Contributors FC: study conception, design, analysis, data acquisition, interpretation of data, drafting and revision final approval and overall content. TB, and GC: data acquisition and data analysis, revision and final approval. GS and DS: interpretation of data, drafting and revision, and final approval. KBF and SS: study conception, design, interpretation of data, drafting and revision, and final approval.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests GS reports personal fees from Heidelberg Engineering; grants, personal fees and others from Zeiss Meditec; grants from Optovue; grants and others from Optos; grants, personal fees and others from Centervue; grants from Nidek; grants, personal fees and others from Novartis; personal fees and others from Bayer; others from Boeheringer, Allergan, Alcon, outside the submitted work. DS reports consulting fees from Amgen, Bayer, Genetech and Optovue and has received grant support from Heidelberg, Regeneron, Topcon. KBF reports consulting fees from Heidelberg Engineering, Zeiss, Allergan, Bayer, Genentech, Regeneron and Novartis; and research support from Genentech/Roche outside the submitted work. SRS reports consulting fees from Amgen, Allergan, Regeneron, Roche/Genentech, Novartis, Merck, 4DMT, Optos, Heidelberg and Centervue; and also receiving research instruments from Topcon, Nidek, Heidelberg, Centervue, Optos and Carl Zeiss Meditec, outside the submitted work.

  • Provenance and peer review Not commissioned; externally peer reviewed.