Association Between Parapapillary Microvasculature Dropout and Central Retinal Vessel Trunk in Primary Open Angle Glaucoma.

PRCIS: Central retinal vessel trunk displacement is an important factor in the generation and development of deep-layer microvasculature dropout in primary open angle glaucoma. PURPOSE: To investigate the association between the microvasculature dropout and the central retinal vessel trunk in primary open angle glaucoma eyes. METHODS: In total, 112 eyes from 112 patients with primary open-angle glaucoma were included. Matched 26 no microvasculature dropout eyes and 26 microvasculature dropout eyes, they had similar axial length and global retinal nerve fiber layer thickness. Central retinal vessel trunk shift index was calculated as the distance of the central retinal vessel trunk from the Bruch membrane opening center relative to that of the Bruch membrane opening border. The correlation of the presence, extent, and location of microvasculature dropout and the displacement extent and location of the central retina vessel trunk was analyzed. RESULTS: The central retinal vessel trunk shift index differed significantly between the 2 matched groups. Multivariate logistic analyses showed that in 112 eyes from 112 patients, eyes with microvasculature dropout was significantly associated with larger shift index than eyes without microvasculature dropout. The angular circumference of microvasculature dropout was significantly associated with adjusted shift index (a linear mixed model was constructed, exclude the influence of axial length and global retinal nerve fiber layer thickness on shift index). The location of the microvasculature dropout and central retinal vessel trunk contralateral were significantly correlated. CONCLUSIONS: In primary open angle glaucoma eyes, microvasculature dropout and the central retinal vessel trunk were significantly correlated. Because the central retinal vessel trunk represents the structural stability of the lamina cribrosa, microvasculature dropout seems to correlate with lamina cribrosa's structural stability.

Clinical Utility of Bruch Membrane Opening-Minimum Rim Width for Detecting Early Glaucoma in Myopic Eyes.

PRCIS: Bruch membrane opening-minimum rim width (BMO-MRW) is overall a useful parameter for diagnosing early glaucoma in myopic eyes. PURPOSE: The aim of this study was to determine the diagnostic value of BMO-MRW compared with peripapillary retinal nerve fiber layer (pRNFL) thickness for detecting early glaucoma in patients with moderate to severe myopia. METHODS: One eye was randomly selected from each of the 253 subjects (127 normal controls, 82 with glaucoma suspect, and 44 with early glaucoma). All patients underwent visual acuity testing, refractive error assessment, slit-lamp inspection, intraocular pressure measurement, fundus photography, perimetry. BMO-MRW and pRNFL thickness data were obtained using spectral-domain optical coherence tomography. Area under the receiver operating characteristic curves (AUC) for global and sectoral thickness parameters were calculated. RESULTS: Global analyses for the discrimination of early glaucoma in all myopic subjects showed comparable AUCs between BMO-MRW and pRNFL thickness [AUC 0.952 (95% confidence interval, 0.918-0.975) and 0.934 (95% confidence interval, 0.896-0.961), respectively, P=0.345]. However, in sectoral analysis, BMO-MRW showed significantly better diagnostic performance than pRNFL thickness except for the superotemporal sector. The AUC for discriminating early glaucoma from glaucoma suspect, BMO-MRW showed statistically better diagnostic performance in the inferotemporal, inferonasal, superonasal, and nasal sectors. When dividing the subject based on a threshold Bruch membrane opening (BMO) area of 2.5 mm2, the diagnostic power of BMO-MRW was generally lower except for the inferonasal sector in the subgroup with a large BMO area. CONCLUSIONS: BMO-MRW was overall a useful parameter for diagnosing early glaucoma in myopic eyes. However, its diagnostic performance was decreased in myopic eyes with large BMO and there were no significant differences from pRNFL thickness.

Acircularity and circularity indexes of the foveal avascular zone in high myopia.

This study explored the association between foveal avascular zone (FAZ) parameters and high myopia using optical coherence tomography angiography. We divided 106 eyes of 106 patients into quartiles based on the axial length. The upper quartile was then defined as the high myopia group (n = 27), while the lower quartile was the non-high myopia group (n = 26). The areas and minor axis lengths of superficial and deep FAZ, the perimeters and major axis lengths of deep FAZ were significantly larger in eyes with high myopia than in eyes with non-high myopia (P < 0.05). Inversely, the subfoveal choroidal thickness was significantly thinner in eyes with high myopia than in those with non-high myopia. Linear regression analyses showed that no significant correlation was observed between FAZ areas and acircularity and circularity indexes of FAZ in non-high myopia group. Conversely, FAZ areas strongly correlated with acircularity and circularity indexes of FAZ in high myopia group. We found that an increase in the FAZ area in highly myopic eyes was accompanied by a significant variation in FAZ acircularity and circularity indexes. Further research should address whether these findings are associated with future disease development in highly myopic eyes.

Parapapillary atrophy and changes in the optic nerve head and posterior pole in high myopia.

We investigated the relationship between microstructure of ß-parapapillary atrophy (ß-PPA) and morphologic features of optic nerve head (ONH) and posterior pole in highly myopic eyes. Eighty-nine highly myopic eyes were included in this study. Bruch's membrane opening (BMO) area, lamina cribrosa (LC) thickness, anterior laminar depth, peripapillary and subfoveal choroidal thickness (CT), macular Bruch's membrane (BM) length, and width of ß-PPA with and without Bruch's membrane (PPA+BM and PPA-BM) were evaluated. The mean age and axial length of the included subjects were 26.88 ± 2.44 years and 27.03 ± 0.88 mm, respectively. The width of PPA-BM was larger with increasing BMO area (P = 0.001), whereas the BMO area was not associated with the width of PPA+BM. The large PPA+BM was significantly related to a thinner LC (P = 0.003), deeper anterior lamina surface (P < 0.001), longer macular BM length (P = 0.008), and thinner temporal peripapillary CT (P = 0.034). We found that the morphologic features of the ONH and posterior pole in highly myopic eyes were different based on the microstructure of ß-PPA. Whether these features are linked to the development of glaucoma in myopic eyes should be investigated in future studies.

Association of macular thickness with parapapillary atrophy in myopic eyes.

BACKGROUND: To investigate whether macular structure could be affected by axial elongation and to determine the association between macular intraretinal thickness and the microstructure of ß-zone parapapillary atrophy (PPA) in myopic eyes. METHODS: The study recruited 113 healthy myopic subjects (113 eyes). Images of the macula, subfoveal choroid, and optic nerve head were acquired using spectral-domain optical coherence tomography (SD-OCT). An automatic segmentation algorithm was used to segment the macular images into 7 intraretinal layers. PPA widths with and without Bruch's membrane (PPA+BM and PPA-BM, respectively) were evaluated. Linear regression analysis was performed to evaluate the association between macular intraretinal thickness and axial length and the microstructure of PPA. RESULTS: An increase in axial length was associated with a decrease in whole macular thickness of the peripheral region and an increase in whole macular thickness of the central region. Thickness alterations of the macular intraretinal layers were most apparent in the peripheral region. A significant correlation was found between PPA-BM width and macular intraretinal layer thickness, whereas no significant correlation was found between PPA+BM width and macular intraretinal layer thickness. Moreover, both PPA+BM and PPA-BM widths significantly correlated with subfoveal choroidal thickness. CONCLUSIONS: Macular intraretinal layer thickness may be affected by PPA-BM width. These findings indicate that the microstructure of PPA should be considered when evaluating the macula in patient with myopia and glaucoma.

Neuroprotective Effect of Brazilian Green Propolis on Retinal Ganglion Cells in Ischemic Mouse Retina.

PURPOSE: The current study was undertaken to investigate whether Brazilian green propolis (BGP) can increase the viability of retinal ganglion cells (RGCs) in ischemic mouse retina, and examined the possible mechanisms underlying this neuroprotection. MATERIALS AND METHODS: C57BL/6J mice were subjected to constant elevation of intraocular pressure for 60 min to establish retinal ischemia-reperfusion injury. Mice then received saline or BGP (200 mg/kg) intraperitoneally once daily until sacrifice. The expression of hypoxia-inducing factor (HIF)-1α and glial fibrillary acidic protein (GFAP) and the level of histone acetylation were assessed at 1, 3, and 7 days after injury. The expression of Bax, Bcl-2, p53, NF-κB, Nrf2, and HO-1 were also analyzed at 3 days after injury. The neuroprotective effect of BGP treatment on RGC survival was evaluated using Brn3a immunohistochemical staining. RESULTS: The expression of HIF-1α and GFAP was increased and the level of histone acetylation decreased in saline-treated ischemic retinas within 7 days. BGP treatment effectively attenuated the elevated expression of HIF-1α, GFAP, Bax, NF-κB and p53. The expression of Bcl-2, Nrf2, HO-1 and the level of histone acetylation increased by BGP treatment, resulting in a significant difference between BGP-treated and saline-treated retinas. Immunohistochemical staining for Brn3a also revealed that BGP treatment protected against RGC loss in ischemic retina. CONCLUSIONS: Our results suggest that BGP has a neuroprotective effect on RGCs through the upregulation of histone acetylation, downregulation of apoptotic stimuli, and suppression of NF-κB mediated inflammatory pathway in ischemic retina. These findings suggest that BGP is a potential neuroprotective agent against RGC loss under oxidative stress.

HDAC2 Regulates Glial Cell Activation in Ischemic Mouse Retina.

The current study was undertaken to investigate whether histone deacetylases (HDACs) can modulate the viability of retinal ganglion cells (RGCs) and the activity of glial cells in a mouse model of retinal ischemia-reperfusion (IR) injury. C57BL/6J mice were subjected to constant elevation of intraocular pressure for 60 min to induce retinal IR injury. Expression of macroglial and microglial cell markers (GFAP and Iba1), hypoxia inducing factor (HIF)-1α, and histone acetylation was analyzed after IR injury. To investigate the role of HDACs in the activation of glial cells, overexpression of HDAC1 and HDAC2 isoforms was performed. To determine the effect of HDAC inhibition on RGC survival, trichostatin-A (TSA, 2.5 mg/kg) was injected intraperitoneally. After IR injury, retinal GFAP, Iba1, and HIF-1α were upregulated. Conversely, retinal histone acetylation was downregulated. Notably, adenoviral-induced overexpression of HDAC2 enhanced glial activation following IR injury, whereas overexpression of HDAC1 did not significantly affect glial activation. TSA treatment significantly increased RGC survival after IR injury. Our results suggest that increased activity of HDAC2 is closely related to glial activation in a mouse model of retinal IR injury and inhibition of HDACs by TSA showed neuroprotective potential in retinas with IR injuries.