Sehnaz Ozcaliskan1, Ozgur Artunay2, Sevcan Balci3, Irfan Perente2, Nursal Melda Yenerel3. 1. University of Health Sciences, Beyoglu Eye Training and Research Hospital, Istanbul, Turkey. Electronic address: drsehnaz@yahoo.com. 2. University of Health Sciences, Beyoglu Eye Training and Research Hospital, Istanbul, Turkey. 3. University of Health Sciences, Haydarpasa Numune Training ad Research Hospital, Istanbul, Turkey.
Abstract
PURPOSE: To investigate the structural and microvascular alterations of the inner retinal layers in patients with intermediate age-related macular degeneration (iAMD), and determine an association between structural and microvascular parameters. METHODS: In this prospective study, 58 eyes of iAMD patients and 64 age and sex-matched control eyes were enrolled. Participants underwent spectral-domain optical coherence tomography (OCT) and swept-source OCT angiography (OCTA) imaging. Retinal layer segmentation was performed automatically using the built-in software of the OCT device. Retinal nerve fiber layer (RNFL), ganglion cell layer (GCL), inner plexiform layer (IPL), inner nuclear layer (INL), and outer plexiform layer (OPL) thicknesses were analyzed in the central and parafoveal region. Foveal avascular zone (FAZ) area and vessel density of the superficial and deep capillary plexuses (SCP and DCP) in the fovea and parafoveal region were obtained. RESULTS: In iAMD eyes, the RNFL, GCL, and IPL were significantly thinner compared to control eyes in the parafovea (p < 0.05 all). The overall parafoveal SCP vessel density significantly decreased in iAMD eyes compared to the controls (p = 0.022). There was also a non-significant reduction in DCP vessel density measurements in iAMD eyes compared to controls (p > 0.05 all). The ganglion cell complex was significantly correlated with SCP vessel density measurements in iAMD eyes (r = 0.224, p = 0.043). CONCLUSION: This study demonstrates that the inner retina is effected in iAMD in terms of structural and microvascular components. Inner retinal thinning is significantly correlated with vessel density reduction, suggesting a cause and effect relationship between these parameters. Further longitudinal studies may aid in characterizing these alterations to better understand AMD pathogenesis.
PURPOSE: To investigate the structural and microvascular alterations of the inner retinal layers in patients with intermediate age-related macular degeneration (iAMD), and determine an association between structural and microvascular parameters. METHODS: In this prospective study, 58 eyes of iAMD patients and 64 age and sex-matched control eyes were enrolled. Participants underwent spectral-domain optical coherence tomography (OCT) and swept-source OCT angiography (OCTA) imaging. Retinal layer segmentation was performed automatically using the built-in software of the OCT device. Retinal nerve fiber layer (RNFL), ganglion cell layer (GCL), inner plexiform layer (IPL), inner nuclear layer (INL), and outer plexiform layer (OPL) thicknesses were analyzed in the central and parafoveal region. Foveal avascular zone (FAZ) area and vessel density of the superficial and deep capillary plexuses (SCP and DCP) in the fovea and parafoveal region were obtained. RESULTS: In iAMD eyes, the RNFL, GCL, and IPL were significantly thinner compared to control eyes in the parafovea (p < 0.05 all). The overall parafoveal SCP vessel density significantly decreased in iAMD eyes compared to the controls (p = 0.022). There was also a non-significant reduction in DCP vessel density measurements in iAMD eyes compared to controls (p > 0.05 all). The ganglion cell complex was significantly correlated with SCP vessel density measurements in iAMD eyes (r = 0.224, p = 0.043). CONCLUSION: This study demonstrates that the inner retina is effected in iAMD in terms of structural and microvascular components. Inner retinal thinning is significantly correlated with vessel density reduction, suggesting a cause and effect relationship between these parameters. Further longitudinal studies may aid in characterizing these alterations to better understand AMD pathogenesis.