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Purpose a) to determine subfoveal choroidal hemodynamics in patients with primary open angle glaucoma (POAG) and patients with ocular hypertension (OH); b) to assess the effects of diabetes (DM), systemic hypertension (SHT) and myopia on subfoveal choroidal hemodynamics Methods Laser Doppler flowmetry (LDF) was used to determine the subfoveal choroidal blood velocity (ChBVel), volume (ChBVol), and flow (ChBF) in 1) patients with POAG (n=85) and patients with OHT (n=25); 2) patients with glaucoma risk factors which were further subdivided into three subgroups; DM (n=93), SHT (n=57) and myopia (n=29) respectively. Subjects with each risk factor were further subdivided into two subgroups (without and with POAG), 3) age matched healthy controls (n=100). Results All LDF parameters were significantly reduced in all groups of patients compared with age matched controls. No statistically significant differences in the LDF parameters among HTG, NTG and OHT subgroups were detected. No significant difference in the LDF parameters between the two subgroup of each risk factor (without and with POAG) was noted.The LDF data of glaucomatous patients with risk factors demonstrated a significant reduction of ChBF and an increase in resistance in comparison to glaucomatous patients without risk factors Conclusion Subfoveal choroidal LDF parameters are reduced in subjects with POAG, OHT and patients with glaucoma risk factors, such as DM, SHT (under antihypertensive therapy) and myopia when compared with age matched healthy controls. However, the role of these choroidal circulatory alterations in the development or progression of the glaucomatous optic neuropathy remains to be clarified.

The maintenance of normal retinal structure and function depends on a tightly regulated environment. This requires intact blood‐retinal barriers as well as an efficient regulation of blood flow and delivery of oxygen and metabolic substrates to the retinal tissue. Thanks to the development of noninvasive techniques allowing the quantitative assessment of retinal hemodynamics in the human eye, much progress has been achieved in recent years in the understanding of retinal blood flow regulation and the mechanisms involved in this physiological process. Retinal blood flow is regulated by the interaction of myogenic and metabolic mechanisms through the release of vasoactive substances by the vascular endothelium and retinal tissue surrounding the arteriolar wall. This regulation is achieved by adaptation of the vascular tone of the resistance vessels to changes in the perfusion pressure or metabolic needs of the tissue. This adaptation occurs through the interaction of multiple mechanisms affecting mainly the arteriolar smooth muscle cells. These mechanisms, which involve the close interaction between nitric oxide, lactate and arachidonic acid metabolites released by the neuronal and glial cells, optimize blood flow according to the metabolic needs of the tissue. Impairments of structure and function of the retinal neural tissue and endothelium during the evolution of ischemic microangiopathies affect the interaction of the retinal metabolic pathways and alter blood flow regulation. Assessing retinal blood flow and its response to various physiological stimuli and the mechanisms mediating and modulating these responses has provided important insight into these pathological processes, which lead to severe losses of vision.

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