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Baek, Jiwon, PhD, MD*; Dansingani, Kunal K., MA, FRCOphth†,‡; Lee, Jae Hyung, PhD, MD§; Lee, Won Ki, MD, PhD§; Freund, K. Bailey, MD¶,**

doi: 10.1097/IAE.0000000000002188
Original Study: PDF Only

Purpose: This study analyzes a subset of patients with peripapillary polypoidal choroidal vasculopathy (PCV) to determine whether quantifiable pachychoroid features colocalize with disease foci.

Methods: Patients with PCV diagnosed by indocyanine green angiography were identified for the analysis of medical records and multimodal imaging and classified as having peripapillary or macular PCV. The ratio of Haller layer thickness to total choroidal thickness was calculated at the fovea and at the site of dilated Haller vessels that showed spatial correlation with the origin of neovascularization. Choroidal thickness was measured horizontally across the fovea and circumferentially around the temporal side of the disk to study its relationship to neovascularization.

Results: Three hundred and fourteen eyes of 299 patients with PCV were identified, of which 17 eyes (5%) had peripapillary disease. Although eyes with peripapillary PCV exhibited thinner subfoveal choroids than those with macular PCV, at the extrafoveal disease foci, choroidal thickness, Haller’s layer thickness, and its ratio to total choroidal thickness were relatively high.

Conclusion: Quantitative indices of choroidal structure previously identified in macular PCV performed consistently when applied to a peripapillary PCV cohort, thus supporting the hypothesis that inner choroidal thinning and Haller vessel enlargement are mechanistically relevant to these related entities.

Choroidal thickness was measured at the fovea and at extrafoveal disease foci in eyes with peripapillary polypoidal choroidal vasculopathy. Focal choroidal thickening, which was attributable to Haller vessel enlargement and attenuation of choriocapillaris/Sattler’s layer at sites of manifest disease, was observed in peripapillary polypoidal choroidal vasculopathy as seen in macular polypoidal choroidal vasculopathy.

*Department of Ophthalmology and Visual Science, Bucheon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Kyung-gi, Republic of Korea;

Department of Ophthalmology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania;

Moorfields Eye Hospital, London, United Kingdom;

§Department of Ophthalmology and Visual Science, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea;

Vitreous Retina Macula Consultants of New York, New York, New York; and

**Department of Ophthalmology, New York University School of Medicine, New York, New York.

Reprint requests: Won Ki Lee, MD, PhD, Department of Ophthalmology, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 222 Banpo-daero, Seocho-gu, Seoul 06591, Republic of Korea; e-mail:

W.K.L. has served on advisory boards for Novartis, Bayer, Allergan, Alcon, and Santen and has received consultancy fees from these companies. He has received payments for lectures from Novartis, Bayer, Allergan, and Alcon. K.B.F. is a consultant for Optovue, Optos, Heidelberg Engineering, Genentech, and Spark Therapeutics. He receives research support from Genentech/Roche. The remaining authors have any financial/conflicting interests to disclose.

© 2019 by Ophthalmic Communications Society, Inc.