ALTERATIONS OF MACULAR BLOOD FLOW IN SUPERFICIAL AND DEEP CAPILLARY PLEXUSES IN THE FELLOW AND AFFECTED EYES OF PATIENTS WITH UNILATERAL IDIOPATHIC EPIRETINAL MEMBRANE

Andrea M Coppe, Giuliana Lapucci, Marta Gilardi, Francesca Petruzzella, Guido Ripandelli

Research output: Contribution to journalArticle

Abstract

PURPOSE: Previous research suggests that proliferation of the idiopathic epiretinal membrane (IERM) is related to microbreaks in the inner limiting membrane, which are caused by posterior vitreous detachment. In this study, we used optical coherence tomography angiography to determine whether a vascular defect in the inner retina is present before the mechanical damage caused by posterior vitreous detachment.

METHODS: For patients with unilateral IERM (N = 23), optical coherence tomography angiography with blood flow measurement was performed in both eyes at the superficial capillary plexuses (SCP) and deep capillary plexuses (DCP) with 6 mm × 6-mm scans and ETDRS grids centered on the fixation point. These values were then compared with 45 healthy control eyes (CEs).

RESULTS: The optical coherence tomography angiography data showed that blood flow was lower in the fellow eyes of IERM patients than in CEs when the whole enface macula (SCP: P = 0.031, DCP: P = 0.004) and extramacular area (SCP: P = 0.048, DCP: P = 0.026) were compared between groups. The blood flow was also lower in the affected eyes compared with CEs in both whole en face macula (SCP: P < 0.001, DCP: P < 0.001) and extramacular areas (SCP: P = 0.011, DCP: P < 0.001).

CONCLUSION: Data from this study revealed that blood flow is significantly reduced in the fellow eyes of patients with unilateral IERM when compared with CEs. Overall, the data suggest that a vascular retinal defect could produce changes in the inner retina, preceding and influencing the formation of microbreaks occurring at the time of posterior vitreous detachment in the inner limiting membrane. Understanding the upstream mechanism of inner limiting membrane microbreaks may provide a therapeutic target aimed to ultimately prevent Mu[Combining Diaeresis]ller cells, astrocyte, and fibroblast migration, which cause IERM proliferation.

Original languageEnglish
JournalRetina (Philadelphia, Pa.)
DOIs
Publication statusE-pub ahead of print - Jul 10 2019

    Fingerprint

Cite this