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  • Relationship of macular ganglion cell complex thickness to choroidal microvasculature drop-out in primary open-angle glaucoma

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Clinical science
Relationship of macular ganglion cell complex thickness to choroidal microvasculature drop-out in primary open-angle glaucoma
  1. Eleonora Micheletti1,
  2. Sasan Moghimi2,
  3. Nevin El-Nimri1,
  4. Takashi Nishida2,
  5. Min Hee Suh3,
  6. James A Proudfoot4,
  7. Alireza Kamalipour1,
  8. Linda M Zangwill5,
  9. Robert N Weinreb5
  1. 1 Viterbi Family Department of Ophthalmology, University of California San Diego, La Jolla, California, USA
  2. 2 Viterbi Family Department of Ophthalmology, University of California at San Diego Department of Ophthalmology at the Shiley Eye Institute, La Jolla, California, USA
  3. 3 Ophthalmology, Inje University College of Medicine, Busan, Korea (the Republic of)
  4. 4 Hamilton Glaucoma Center, University of California San Diego, La Jolla, California, USA
  5. 5 Hamilton Glaucoma Center, Shiley Eye Institute, Viterbi Family Department of Ophthalmology, University of California San Diego, La Jolla, California, USA
  1. Correspondence to Dr Robert N Weinreb, Hamilton Glaucoma Center, Shiley Eye Institute, Viterbi Family Department of Ophthalmology, University of California San Diego, La Jolla, California, USA; rweinreb{at}ucsd.edu

Abstract

Background/aims To investigate the rate of ganglion cell complex (GCC) thinning in primary open-angle glaucoma (POAG) patients with and without deep-layer microvasculature drop-out (MvD).

Methods POAG patients who had at least 1.5 years of follow-up and a minimum of three visits were included from the Diagnostic Innovations in Glaucoma Study. MvD was detected at baseline by optical coherence tomography angiography (OCT-A). Area and angular circumference of MvD were evaluated on en face choroidal vessel density images and horizontal B-scans. Rates of global and hemisphere GCC thinning were compared in MvD and non-MvD eyes using linear mixed-effects models.

Results Thirty-six eyes with MvD and 37 eyes without MvD of 63 patients were followed for a mean of 3.3 years. In 30 out of 36 eyes, MvD was localised in the inferotemporal region. While mean baseline visual field mean deviation was similar between the two groups (p=0.128), global GCC thinning was significantly faster in eyes with MvD than in those without MvD (mean differences: −0.50 (95% CI −0.83 to –0.17) µm/year; p=0.003)). Presence of MvD, area and angular circumference of MvD were independently associated with a faster rate of thinning (p=0.002, p=0.031 and p=0.013, respectively).

Conclusion In POAG eyes, GCC thinning is faster in eyes with MvD. Detection of MvD in OCT-A images can assist clinicians to identify patients who are at higher risk for central macula thinning and glaucomatous progression and may require more intensive management.

  • glaucoma

Data availability statement

Data are available on reasonable request.

http://dx.doi.org/10.1136/bjophthalmol-2021-320621

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    Data availability statement

    Data are available on reasonable request.

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    Footnotes

    • EM and SM are joint first authors.

    • Contributors Concept design: EM, SM and RNW; acquisition and reviewing data: TN, SM, NE-N, MHS and AK; analysis or interpretation of data: EM, SM, TN, JAP, LMZ, RNW; drafting of the manuscript: EM, SM, NE-N and RNW; critical revision of the manuscript: all authors; obtained funding: SM, LMZ and RNW; supervision: SM, LMZ and RNW; guarantor: RNW.

    • Funding National Institutes of Health/National Eye Institute Grants R01EY029058, R01EY011008, R01EY026574, R01EY019869 and R01EY027510; Core Grant P30EY022589; by the donors of the National Glaucoma Research Program (no grant number); a programme of the BrightFocus Foundation Grant (G2017122); an Unrestricted Grant from Research to Prevent Blindness (New York, NY); UC Tobacco Related Disease Research Program (T31IP1511); and grants for participants’ glaucoma medications from Alcon, Allergan, Pfizer, Merck and Santen.

    • Disclaimer The sponsor or funding organisations had no role in the design or conduct of this research.

    • Competing interests Acknowledgment/financial support: National Institutes of Health/National Eye Institute Grants R01EY029058, R01EY011008, R01EY026574, R01EY019869 and R01EY027510; Core Grant P30EY022589; by the donors of the National Glaucoma Research Program (no grant number); a programme of the BrightFocus Foundation Grant (G2017122); an Unrestricted Grant from Research to Prevent Blindness (New York, NY); UC Tobacco Related Disease Research Program (T31IP1511); and grants for participants’ glaucoma medications from Alcon, Allergan, Pfizer, Merck, and Santen. Financial Disclosures: Eleonora Micheletti: none; SM: none; TN: none; NE-N: none; MHS: none ; JAP: none ; AK: none; LMZ: National Eye Institute (F), Carl Zeiss Meditec (F), Heidelberg Engineering(F), OptoVue (F, R), Topcon Medical Systems Inc. (F, R) Merck (C); Robert N. Weinreb: Allergan (C), Eyenovia (C), Topcon (C), Heidelberg Engineering (F), Carl Zeiss Meditec (F), Konan (F), OptoVue (F), Topcon (F), Centervue (F).

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

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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