Transorbital ultrasonography reveals persistent decrease in retinal artery flow and optic nerve diameter in treated giant cell arteritis

Objectives To longitudinally assess ocular involvement in newly diagnosed giant cell arteritis (GCA) patients by evaluating changes in transorbital ultrasonography (TOS) parameters and their association with systemic vascular inflammation and treatment response. Methods In this prospective cohort study, newly diagnosed GCA patients underwent serial TOS assessments of the central retinal artery flow velocity [peak systolic velocity (PSV), end-diastolic velocity (EDV), resistance index (RI)] and optic nerve diameter (OND) at three-monthly intervals for 12-months. Vascular ultrasonography and calculation of OMERACT Giant Cell Arteritis Ultrasonography (OGUS) Score was conducted. Longitudinal changes and associations were analyzed using linear mixed-effects models, accounting for repeated measurements within patients. Results Thirty-six GCA patients were enrolled. At baseline, 17 (47.2%) patients reported visual symptoms. Compared to baseline, PSV significantly decreased at three (β=-0.81 cm/s, p = 0.046) and nine months (β=-0.93 cm/s, p = 0.029). OND decreased at three (β=-0.30 mm, p = 0.020) and twelve months (β=-0.35 mm, p = 0.008), with a consistent trend over follow-up (β = −0.07, p = 0.024). Symptomatic eyes displayed significantly higher PSV (β = 0.96, p = 0.017) and EDV (β = 0.34, p = 0.037) over disease course. Baseline pathological vessel count and OGUS Score were negatively associated with PSV (β=-0.43, p = 0.031; β=-3.15, p = 0.055) and EDV (β=-0.15, p = 0.022; β=-1.45, p = 0.007), and positively associated with OND (β = 0.15, p = 0.006; β = 0.94, p = 0.040). During disease course, significant associations with pathological vessel count and OGUS Score were noted for EDV (β=-0.04, p = 0.024; β=-0.77, p = 0.005) and OND (β = 0.05, p < 0.001; β = 0.72, p < 0.001). Conclusions Utilizing TOS, we demonstrated progressive decrease in retinal artery flow and OND, indicating ongoing impairment in retinal vascular supply and potential optic nerve atrophy despite clinical improvement post-treatment. Our findings suggest that intracranial vascular changes in GCA may respond less effectively to treatment than extracranial vessels and support a shared pathophysiological mechanism in GCA.