Structural–hemodynamic choroidal alterations in diabetic macular edema assessed by Doppler and SD-OCT

Abstract Background Diabetic macular edema (DME) is associated with retinal microvascular dysfunction, but the relationship between retrobulbar hemodynamics and choroidal structure remains incompletely understood. This study evaluated retrobulbar arterial hemodynamics and choroidal thickness in treatment-naïve eyes with DME and explored potential structural–hemodynamic associations. Methods This analytical observational cross-sectional study with prospective data collection included 56 eyes of 28 treatment-naïve patients with bilateral DME and 56 eyes of 28 healthy controls. Color Doppler imaging was used to assess peak systolic velocity (PSV), end-diastolic velocity (EDV), and resistive index (RI) in the central retinal artery (CRA), short posterior ciliary arteries (SPCA), and ophthalmic artery (OA). Enhanced-depth imaging spectral-domain optical coherence tomography was used to measure subfoveal and mean choroidal thickness. Linear mixed-effects models accounting for inter-eye correlation and adjusted for age were used to evaluate between-group differences and structural–hemodynamic associations. Results Patients with DME were significantly older than controls (62.6 ± 7.6 vs. 40.6 ± 12.4 years, P < 0.0001). DME eyes showed significantly higher RI in the CRA, SPCA, and OA compared with controls. After adjustment for age, mean and subfoveal choroidal thickness did not differ significantly between groups. No significant group-by-hemodynamic parameter interactions were identified for mean or subfoveal choroidal thickness in the primary analyses. An exploratory post-hoc sensitivity analysis excluding one participant with extreme choroidal thinning yielded a significant interaction between SPCA PSV and mean choroidal thickness ( P = 0.045). Conclusions Treatment-naïve eyes with DME exhibited altered retrobulbar hemodynamics, characterized by higher resistive indices in the CRA, SPCA, and OA, whereas choroidal thickness did not differ significantly from controls after adjustment for age. Structural–hemodynamic interactions were not statistically significant in the primary analysis. These findings should be considered exploratory and warrant further investigation in larger, appropriately matched cohorts.