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Updated: Feb 15, 2026

Retinal Vascular Reactivity as Assessed by Optical Coherence Tomography Angiography
Published on: March 26, 2020
Retinal vascular alterations in reticular pseudodrusen with and without outer retinal atrophy assessed by optical
Maria Vittoria Cicinelli1, Alessandro Rabiolo1, Riccardo Sacconi1,2
1Department of Ophthalmology, Scientific Institute San Raffaele, University Vita-Salute, Milan, Italy.
Purpose:
To investigate the intraretinal structural and vascular alterations in patients featuring reticular pseudodrusen (RPD), RPD with outer retinal atrophy (ORA), and drusen.
Design:
Observational cross-sectional study.
Methods:
Clinical practice study including 68 eyes of 57 patients (22 eyes of 17 patients with RPD; 24 eyes of 21 patients with RPD+ORA; 22 eyes of 19 patients with drusen). Each patient underwent spectral-domain optical coherence tomography (OCT) and OCT angiography (OCT-A). Measurement of retinal layers' thickness was obtained by the automated segmentation protocol of the Spectralis OCT (Heidelberg Eye Explorer V.1.9.10.0). The superficial capillary plexus (SCP) and the deep capillary plexus (DCP) vessel density, as well as the size of the foveal avascular zone were calculated on 3×3 OCT-A. Main outcome was to compare vessel density at the SCP and DCP among the groups and controls.
Results:
At the SCP, the vessel density was lower in RPD and RPD+ORA patients with respect to controls (P=0.02 and P=0.003, respectively). At the DCP, meaningful disparity was found between the study groups and the healthy subjects in the vessel density (P<0.001, P=0.04 and P=0.001 for RPD, RDP+ORA and drusen, respectively). The ganglion cell layer (GCL) was thinner in all patients affected either by RPD, RPD+ORA or drusen compared with healthy subjects (P=0.02, P=0.03 and P=0.004, respectively).
Conclusion:
Significant retinal vascular loss is a common feature of patients with non-exudative age-related macular degeneration, more pronounced in those featuring RPD and RPD+ORA. It is associated with retinal thinning, localised particularly at the GCL, compared with controls.
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