Introduction: Glaucoma is a chronic progressive optic neuropathy in which there is elevated intraocular pressure (IOP), is an important modifiable risk factor. So far, lowering IOP is the mainstay of glaucoma management, with the aim of lowering the rate of progression. Neuroprotection is a promising non-IOP-based approach to the management of glaucoma through increasing the longevity of retinal ganglion cells (RGCs) and increasing their resistance to various stressors. Brimonidine is both an ocular hypotensive and a neuroprotectant of RGCs. However, the exact mechanism through which brimonidine exerts its The neuroprotective effect is not fully understood.
Aim of the study: To investigate the hemodynamic effects of brimonidine on the optic nerve head (ONH) and retinochoroidal circulation, which may add to our understanding of its neuroprotective properties.
Subjects and Methods: This is a prospective longitudinal interventional study where 22 brimonidine-naiive primary open-angle glaucoma (POAG) patients underwent optical coherence tomography angiography (6*6mm macula and 4.5*4.5mm ONH) at baseline and three months after brimonidine. Superficial and deep macular ONH radial peripapillary capillary (RPC) vascular densities as well as subfoveal choroidal thickness (SCT) were compared between baseline and follow-up.
Results: Compared to baseline, there was a statistically significant increase in superficial macular vascular density (SVD) and a decrease in deep macular vascular density (DVD) at three-month follow-up. There was no statistically significant change in either ONH RPC vascular density (RPCPVD) or SCT.
Conclusions: Brimonidine was associated with an increase in SVD, which may constitute a novel mechanism for its neuroprotective properties on RGCs through improved perfusion.