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Abstract
Background/aims To investigate the association between longitudinal changes of foveal avascular zone (FAZ) area and the rate of structural and functional progression in glaucoma.
Methods A longitudinal cohort included 115 eyes (46 glaucoma suspect and 66 primary open-angle glaucoma) of 81 patients having ≥2 year follow-up, and ≥4 visits with optical coherence tomography angiography and visual field (VF). Eyes in the longitudinal cohort with a slope greater than that found in 95 percentile of separate healthy test–retest series for FAZ area were categorised into FAZ progressors; all other eyes were defined as FAZ non-progressors. A generalised linear mixed-effect model was used to investigate the association of FAZ progressors with demographic and clinical characteristics.
Results Faster ganglion cell complex (GCC) thinning and faster VF mean deviation (MD) loss were found in eyes with FAZ progressors compared with FAZ non-progressors (mean difference: −0.7 (95% CI, −1.4 to −0.1) µm/y; p=0.026, −0.3 (−0.5 to −0.1) dB/y; p=0.017, respectively), while whole image vessel density was not associated with FAZ progressors (p=0.929). SD of intraocular pressure (IOP) and IOP range were also associated with FAZ progressors in separate multivariable models (OR: 1.54 (1.02 to 2.32) per 1 mm Hg higher, p=0.041; OR: 1.20 (1.01 to 1.41) per 1 mm Hg higher; p=0.035, respectively).
Conclusions Significant FAZ increase was weakly associated with moderately faster rates of both GCC thinning and VF MD loss, but not macular vessel density change in glaucoma eyes. Additional studies are needed to elucidate the pathophysiological associations between macula GCC thinning and FAZ area increases in glaucoma.
- Glaucoma
Data availability statement
Data are available upon request.
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Data availability statement
Data are available upon request.
Footnotes
Contributors Involved in design and conduct of study: TN and RNW. Data collection: TN. Analysis and interpretation of data: TN, SM, LMZ and RNW. Writing: TN and GG. Guarantor: RNW.
Funding National Institutes of Health/National Eye Institute Grants (R01EY034148, R01EY029058, R01EY011008, R01EY019869, R01EY027510, R01EY026574, P30EY022589); University of California Tobacco Related Disease Research Program (T31IP1511), and an unrestricted grant from Research to Prevent Blindness (New York, NY).
Disclaimer The sponsor or funding organisations had no role in the design or conduct of this research.
Competing interests TN: consultant—Topcon; SM: consultant—Topcon; EW: none; GG: none; J-HW: none; AK: Fight for sight, LMZ: consultant—Topcon, Abbvie; financial support—Carl Zeiss Meditec, Heidelberg Engineering, OptoVue. Patent: AISight Health (co-founder), RNW: consultant—Abbvie, Aerie Pharmaceuticals, Allergan, Amydis, Editas, Equinox, Eyenovia, Iantrek, IOPtic, Implandata, iSTAR Medical, Nicox, Santen, Tenpoint and Topcon; financial support—Heidelberg Engineering, Carl Zeiss Meditec, Optovue, Centervue, Zilia and Topcon.
Provenance and peer review Not commissioned; internally peer reviewed.
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