Swept source OCT-A of retinal vascular features in patients with naïve CNV: Advanced qualitative and quantitative analysis

Session Details

Session Title: Free Paper Session 21: Imaging III

Session Date/Time: Sunday 10/09/2017 | 08:00-09:30

Paper Time: 08:06

Venue: Room 113

First Author: : A.Arrigo ITALY

Co Author(s): :    L. Pierro   M. Gagliardi   F. Bandello                       

Abstract Details

Purpose:

Choroidal Neovascularization (CNV) is a condition affecting a large number of patients with macular disorders. The current etiopathological hypothesis includes both inflammatory and ischaemic origin; these phenomena determine a strong stimulus for VEGF production, thus causing the onset of new vessels formation. The main purpose of this study is to describe qualitative and quantitative changes of retinal vascular structures both at macular and optic nerve head levels.

Setting:

Department of Ophthalmology, IRCCS Ospedale San Raffaele, University “Vita-Salute” San Raffaele, Milan - Italy.

Methods:

Forty patients with naïve CNV on age-related macular degeneration (AMD) were recruited. The diagnosis was made by slit lamp fundus examination and OCT-A analysis; it was confirmed by FAG/ICGA examination. OCT and OCT-A scans were performed by means of DRI OCT Triton (Topcon Medical Systems Inc., Oakland, NJ, USA). Both macular and optic nerve head structures were evaluated by means of qualitative and quantitative analyses. Qualitative analysis included OCT and OCT-A based description of retinal structural and vascular features, both in b-scans and en-face analyses. Quantitative analysis was performed considering a number of parameters, including vessel density, vessel tortuosity and foveal avascular zone (FAZ) area. One-way Anova was used to test statistical significance of the following measurements: CNV eye (CE) vs healthy contralateral eye (HH) vs control group (CG). Bonferroni’s correction was applied to correct for multiple comparisons. Statistical significance was set to p<0.05.

Results:

Six patients were excluded from the analysis because of the contralateral eye involvement by ophthalmologic disorders; four were excluded because of poor quality OCT-A examination. Thirty patients with one CNV affected eye and the contralateral healthy eye (18 males, mean age 62.6) and thirty healthy eyes of thirty control subjects (16 males, mean age 61.4) were included. The qualitative analysis on en-face images revealed the presence of both hyperreflective and hyporeflective regions at different retinal levels in CE. Sparse signal changes were also detected in HH. The quantitative analysis revealed statistically significant changes of parameters considered (p<0.05) both in CE and HH if compared with CG. Interestingly, significant changes were strongly detected at the level of peripapillary capillary plexus of patients with CNV (p<0.05). With regards to the FAZ area, it resulted significantly increased in patients with CNV (p<0.05).

Conclusions:

Our data confirmed structural alterations previously described by other studies and showed new interesting features of both CNV affected and contralateral healthy eye. Reported findings suggest that the initial inflammatory/ischaemic stimulus as well as the increased production of VEGF may cause widespread changes of the structural setting of the retina. Moreover, based on previous studies, we advance the hypothesis that peripapillary alterations might occur earlier if compared to macular ones, thus providing the basis of a possible future predictive marker of CNV onset. Our analysis confirmed the important role of OCT-A for the study of macular disorders in a non-invasive way. Further studies should be conducted in order to confirm our findings as well as to apply similar study protocols for other causes of CNV, e.g. diabetic retinopathy and elevated myopic macular degeneration.

Back to previous
EURETINA, Temple House, Temple Road, Blackrock, Co Dublin. | Phone: 00353 1 2100092 | Fax: 00353 1 2091112 | Email: euretina@euretina.org

Privacy policyHotel Terms and Conditions Cancellation policy