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REDUCED CHORIOCAPILLARIS FLOW IN EYES WITH TYPE 3 NEOVASCULARIZATION AND AGE-RELATED MACULAR DEGENERATION

Borrelli, Enrico, MD*,†,‡; Souied, Eric, H., MD, PhD§; Freund, K., Bailey, MD¶,**,††; Querques, Giuseppe, MD, PhD‡‡; Miere, Alexandra, MD§; Gal-Or, Orly, MD¶,**,§§; Sacconi, Riccardo, MD‡‡,¶¶; Sadda, SriniVas, R., MD*,†; Sarraf, David, MD*,***,†††

doi: 10.1097/IAE.0000000000002198
Original Study: PDF Only

Purpose: To study choriocapillaris (CC) flow in eyes with Type 3 neovascularization (NV) and age-related macular degeneration, using optical coherence tomography angiography analysis.

Methods: In this multicenter, retrospective, observational study, we collected data from 21 patients with unilateral Type 3 NV and age-related macular degeneration, based on clinical examination, structural optical coherence tomography, and fluorescein angiography when available. An additional group of 20 nonneovascular age-related macular degeneration eyes with unilateral Type 1 or Type 2 NV due to age-related macular degeneration was included for comparison. En face optical coherence tomography angiography imaging (3 × 3 mm scans) with quantitative microvascular analysis of the CC was performed. Main outcome measures were: 1) the percent nonperfused choriocapillaris area; and 2) the average CC signal void size.

Results: We included 21 patients with unilateral Type 3 NV (15 female, 71.5%) and 20 patients with unilateral Type 1 or 2 NV (9 female, 45.0% P = 0.118). Mean ± SD age was 82.1 ± 7.4 years in the unilateral Type 3 patients and 78.3 ± 8.1 in unilateral Type 1/2 NV subjects (P = 0.392). The percent nonperfused choriocapillaris area was 56.3 ± 8.1% in eyes with Type 3 NV and 51.9 ± 4.3% in the fellow eyes (P = 0.016). The average signal void size was also increased in those eyes with Type 3 NV (939.9 ± 680.9 μm2), compared with the fellow eyes (616.3 ± 304.2 μm2, P = 0.039). The number of signal voids was reduced in the Type 3 NV eyes (604.5 ± 282.9 vs. 747.3 ± 195.8, P = 0.046). The subfoveal choroidal thickness was 135.9 ± 54.2 μm in eyes with Type 3 NV and 167.2 ± 65.4 μm in the fellow eyes (P = 0.003). In addition, the fellow eyes of patients with unilateral Type 3 NV displayed more significant CC flow abnormalities versus the fellow eyes with unilateral Type 1/2 NV (percent nonperfused choriocapillaris area = 51.9 ± 4.3% vs. 46.0 ± 2.1%, respectively, P < 0.0001; and average signal void size 616.3 ± 304.2 μm2 versus 351.4 ± 65.5 μm2, respectively, P < 0.0001; and number of signal voids 747.3 ± 195.8 vs. 998.5 ± 147.3, respectively, P < 0.0001).

Conclusion: Eyes with unilateral Type 3 NV illustrated increased CC nonperfusion versus fellow nonneovascular eyes. These results suggest that choroidal ischemia may play an important role in the development of Type 3 NV.

Alterations of the choriocapillaris characterize eyes with Type 3 neovascularization and their fellow unaffected eyes.

*Department of Ophthalmology, Stein Eye Institute, David Geffen School of Medicine at UCLA, Los Angeles, California;

Doheny Image Reading Center, Doheny Eye Institute, Los Angeles, California;

Ophthalmology Clinic, Department of Medicine and Science of Ageing, University G. D'Annunzio Chieti-Pescara, Chieti, Italy;

§Department of Ophthalmology, University Paris XII, Center Intercommunal de Creteil, Creteil, France;

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

**LuEsther T. Mertz Retinal Research Center, Manhattan Eye, Ear and Throat Hospital, New York, New York;

††Department of Ophthalmology, New York University School of Medicine, New York, New York;

‡‡Department of Opthalmology, San Raffaele University Hospital, Milan, Italy;

§§Department of Ophthalmology, Rabin Medical Center, Petach-Tikva, Israel;

¶¶Eye Clinic, Department of Neurological, Biomedical and Movement Sciences, University of Verona, Verona, Italy;

***Retinal Disorders and Ophthalmic Genetics Division, Stein Eye Institute, David Geffen School of Medicine at UCLA, Los Angeles, California; and

†††Greater Los Angeles VA Healthcare Center, Los Angeles, California.

Reprint requests: David Sarraf, MD, Retinal Disorders and Ophthalmic Genetics Division, Stein Eye Institute, UCLA Geffen School of Medicine, Los Angeles, CA 90095; e-mail: dsarraf@ucla.edu

Supported by an Unrestricted Grant from Research to Prevent Blindness, Inc to the Department of Ophthalmology, Stein Eye Institute, UCLA (D.S.) and the Macula Foundation Inc, New York, NY.

E. H. Souied: Novartis (C), Bayer (C), Thea (C), and Roche (C). K. B. Freund: Optovue (C), Heidelberg Engineering (C), Zeiss (C), Novartis (C), and Genentech/Roche (F); G. Querques: Allergan (C, S), Bayer (C, S), Novartis (C, S), Zeiss (C, S), Alimera (C), Bausch & Lomb (C), and Heidelberg (C); S. R. Sadda: Allergan (C, F), Carl Zeiss Meditec (F), Genentech (C, F), Iconic (C), Novartis (C), Optos (C, F), Optovue (C, F), Regeneron (F), and Thrombogenics (C); D. Sarraf: Amgen (C), Allergan (F), Bayer (C), Genentech (C, F), Novartis (C), Regeneron (F), and Optovue (C, F). The remaining authors have no conflicting interests to disclose.

© 2018 by Ophthalmic Communications Society, Inc.