Retinal microvascular morphology versus COVID-19: What to anticipate?
Gobeka, Hamidu Hamisi
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CitationErogul, O., Gobeka, H. H., Dogan, M., Akdogan, M., Balci, A., & Kasikci, M. (2022). Retinal microvascular morphology versus COVID-19: What to anticipate?. Photodiagnosis and Photodynamic Therapy, 102920.
Background To investigate retinal microvascular morphological changes in previously COVID-19 infected patients using optical coherence tomography angiography (OCTA), and compare the findings to age- and gender-matched healthy subjects. Methods In this cross-sectional study, OCTA findings (6.0 × 6.0 mm scan size and scan quality index ≥7/10) from previously COVID-19 infected patients (group 1, 32 patients, 64 eyes) with ≥1 month of complete recovery were compared to healthy subjects (group 2, 33 subjects, 66 eyes) with no history of COVID-19 infection. A positive real-time reverse transcription-polymerase chain reaction test on a naso-pharyngeal swab sample confirmed the diagnosis. The AngioVueAnalytics, RTVue-XR 2017.1.0.155 software measured and recorded OCTA parameters. Results Group 1 had significantly lower superficial capillary plexus vessel densities in all foveal regions than group 2 (P<0.05). Foveal deep capillary plexus vessel density in group 1 was also significantly lower than in group 2 (P=0.009); however, no significant differences were found in other regions (P>0.05). All foveal avascular zone (FAZ) parameters were higher in group 1 than in group 2, with significant differences in FAZ area (P=0.019) and foveal vessel density 300 μm area around FAZ (P=0.035), but not FAZ perimeter (P=0.054). The outer retina and choriocapillaris flows were significantly lower in group 1 than in group 2 (P<0.05). Conclusions Prior COVID-19 infection seems to be associated with significant changes in retinal microvascular density, as well as FAZ and flow parameters, which may be attributed to different pathogenic mechanisms that lead to SARS-CoV-2 infection, such as thrombotic microangiopathy and angiotensin-converting enzyme 2 disruption.