To evaluate the association between macula vascular density assessed by optical coherence tomography angiography (OCT-A) and central visual field (VF) threshold sensitivities in healthy, glaucoma suspect, and glaucoma patients.
A total of 185 eyes from 38 healthy participants, 31 glaucoma suspects, 72 mild glaucoma patients, and 44 moderate/severe glaucoma patients from the Diagnostic Innovations in Glaucoma Study who underwent OCT-A images of the macula and 10-2 VF testing were enrolled in this observational cross-sectional study. The relationship between central VF mean sensitivity (MS) and superficial macula whole-image vessel density (wiVD), and the relationship between the MS of the 4 central points of the 10-2 VF (MS4) and parafoveal vessel density (pfVD), were assessed using linear regression models.
Mean wiVD (52.5%, 49.8%, 49.4% and 45.2%, respectively) and mean pfVD (54.9%, 52.1%, 51.8% and 47.7%, respectively) were found to be significantly higher in healthy eyes and glaucoma suspect eyes compared with glaucoma eyes with mild and moderate/severe disease [analysis of covariance (ANCOVA) P<0.001]. The univariate associations between 10-2 MS and wiVD (R 2=26.9%) and between 10-2 MS4 and pfVD (R 2=16.8%) were statistically significant (P<0.001 for both). After adjusting for scan quality, age, sex and intraocular pressure, superficial macula wiVD and pfVD were still independently associated with central VF loss. Macula wiVD performed better [area under the receiver operator characteristic (AUROC)=0.70] than ganglion cell complex thickness (AUROC=0.50) for differentiating between glaucoma suspect and healthy eyes (P=0.010).
Loss of OCT-A macula vessel density is associated with central 10-2 VF defects. Macula vessel density is a clinically relevant parameter that may enhance monitoring of glaucoma suspects and patients.
*Department of Ophthalmology, Hamilton Glaucoma Center, Shiley Eye Institute, University of California, San Diego, La Jolla, CA
†Department of Ophthalmology, Saitama Medical University, Saitama
‡Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan
Supported in part by National Institutes of Health/National Eye Institute grants EY011008 (L.M.Z.), EY14267 (L.M.Z.), EY019869 (L.M.Z.), EY027510 (L.M.Z.), core grant P30EY022589; an unrestricted grant from Research to Prevent Blindness (New York, NY); grants for participants’ glaucoma medications from Alcon, Allergan, Pfizer, Merck, and Santen.
Disclosure: L.M.Z.: research support—Carl Zeiss Meditec, Heidelberg Engineering, National Eye Institute, Topcon Inc. T.S.: research support—Pfizer, Senju, Alcon, Santen, Kowa, Otsuka. T.A.: research support—Santen, Pfizer, Senju, Alcon, Kowa. R.N.W.: research support—Carl Zeiss Meditec, Genentech, Heidelberg Engineering, National Eye Institute, Optovue, Optos and Topcon; consultant—Aerie Phamaceuticals, Alcon, Allergan, Bausch & Lomb, Novartis, Sensimed, Valeant. The remaining authors declare no conflict of interest.
Reprints: Robert N. Weinreb, MD, Department of Ophthalmology, Hamilton Glaucoma Center, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0946 (e-mail: email@example.com).
Received December 21, 2017
Accepted April 8, 2018