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Original Research

Quantifying choriocapillaris hypoperfusion in patients with choroidal neovascularization using swept-source OCT angiography

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Pages 1613-1620 | Published online: 26 Aug 2019
 

Abstract

Purpose

To compare choriocapillaris flow voids (FV) in patients with neovascular age-related macular degeneration (AMD) with age-matched normal controls using swept-source optical coherence tomography angiography (SS-OCTA).

Patients and methods

Eleven eyes of 11 subjects with neovascular AMD and 11 eyes of 11 age-similar normal subjects were imaged using SS-OCTA with a 6x6mm scanning pattern. Choriocapillaris FV, defined as a percentage of regions determined to have flow deficits divided by the total scanned region, was measured using a one standard deviation thresholding algorithm developed from a database of age-similar normal subjects.

Results

Choriocapillaris FV was more extensive in patients with choroidal neovascularization (CNV) compared to age-similar normal subjects (FV: 20.56±4.95, 95% CI: 17.64–23.49 vs FV: 10.95±2.08, 95% CI: 9.73–12.18, respectively; P=0.0001). FV within a two-degree margin surrounding CNV in wet AMD subjects (FV: 35.04±9.34; 95% CI: 29.52–40.56) was increased compared to normal subjects (P<0.001). FV of the region outside the two-degree margin surrounding CNV (FV: 19.61±6.08, 95% CI: 16.02–23.20) was increased compared to age-similar controls (P=0.0002). In neovascular AMD eyes, FV was greater within two degrees of the margin of CNV than in the remainder of the macula (margin: 35.04±9.34; outside: 19.61±6.08; P=0.002), and CNV lesion area was positively correlated with FV (correlation coefficient =0.84; 95% CI: 0.49–0.96; P=0.001).

Conclusion

Choriocapillaris flow deficits were significantly greater in wet AMD subjects than age-similar normal subjects, suggesting that choroidal hypo-perfusion likely plays a role in the pathogenesis of neovascular AMD. Recognition of choriocapillaris flow deficits in patients with AMD may facilitate earlier diagnosis and identify alternative therapeutic targets for this multifactorial disease.

Acknowledgments

This work was supported by the National Institutes of Health (EY002162, EY024239, EY24158), Food and Drug Administration (R01-41001), L.L. Hillblom Foundation Research Network Grant, That Man May See, Inc., Foundation Fighting Blindness, Research to Prevent Blindness, Bernard A. Newcomb Macular Degeneration Fund, Hope for Vision, Beckman Initiative for Macular Research (1201), Claire Giannini Fund, Hedco Foundation, Pritzker Foundation, and Advanced Retina Imaging Network.

Disclosure

Qinqin Zang: University of Washington (Patent). Ruikang K Wang: University of Washington (Patent), Oregon Health & Science University (Patent). Ruikang K Wang reports grants, non-financial support from Carl Zeiss Meditec Inc., and National Eye Institute, during the conduct of the study. Ruikang K Wang also reports grants, non-financial support from Moptim Inc, outside the submitted work. Ruikang K Wang has a patent OCTA licensed to Moptim Inc, a patent OCTA licensed to Carl Zeiss Meditec and a patent OCTA with royalties paid to Kowa Inc. Jacque L Duncan reports personal fees from AGTC, Spark Therapeutics, SparingVision, Editas, Okustim, Ocucyte, Ionis, Novelion, jCyte and ProQR Therapeutics, outside the submitted work. Jacque L Duncan also reports grants from Second Sight Medical Products, Allergan, NightstaRx and non-financial support from Neurotech, Inc. Daniel M Schwartz is a stockholder in Varocto, Inc. Daniel M Schwartz has a patent US 7,995,814 issued and a patent US 8,369,594 issued. The authors report no other conflicts of interest in this work.