Purpose: To use projection-resolved optical coherence tomographic angiography (PR-OCTA) to characterize the microvascular changes in 3 distinct retinal plexuses in retinitis pigmentosa (RP) patients. Design: Prospective cross-sectional study. Methods: A commercial 70-kHz spectral-domain optical coherence tomography (OCT) system was used to acquire 6-mm macular scans from RP patients and age-matched healthy participants at a tertiary academic center. Blood flow was detected using a commercial version of split-spectrum amplitude-decorrelation angiography (SSADA) algorithm. The PR-OCTA algorithm was used to suppress projection artifacts and resolve microvasculature in 3 plexuses around the macula. Vessel density was calculated from en face OCTA of the parafoveal and perifoveal regions in each of the 3 plexuses, as well as the all-plexus inner retinal slab. Inner and outer retinal thicknesses were measured form structural OCT scans. Generalized estimating equations and Spearman's rank correlation statistical methods were used. Results: Forty-four eyes from 26 RP patients and 34 eyes from 26 healthy subjects were included. Significant reduction in vessel density was detected in the perifovea but not the parafovea of inner retinal slab of RP patients (P = .001 and P = .56, respectively) compared to controls. We also found deeper retinal plexuses (intermediate and deep capillary plexuses, ICP and DCP) were primarily damaged by RP, compared to superficial vascular complex (SVC). Significant thickening of the inner retina and thinning of the outer retina were also observed. Strong correlation was found between the vessel density in the perifoveal ICP and DCP and outer retinal thickness in RP patients with no history of cystoid macular edema. Conclusions: PR-OCTA enables the detection of microvascular changes in the perifoveal regions of the ICP and DCP in RP, with relative sparing of the SVC. OCT and OCTA parameters might be able to provide better understanding of the pathophysiology of the disease, as well as monitoring disease progression and the response to experimental treatments.
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