One-third of patients with primary OAG have normal intraocular pressures (IOPs) at the time of glaucoma diagnosis. This suggests that other risk factors, such as vascular changes, contribute to the pathogenesis of glaucomatous optic neuropathy [1, 2]. Recent population-based studies, including the Barbados Eye Study, Proyecto VER (vision evaluation and research), Baltimore Eye Survey, and Egna-Neumarkt Glaucoma Study, have shown that reduced ocular perfusion pressure, and most often diastolic perfusion pressure, is a significant risk factor for the prevalence and incidence of OAG [3-6]. The Early Manifest Glaucoma Trial (EMGT) recently found that lower systolic perfusion pressure, lower systolic blood pressure, and cardiovascular disease history are new predictors for glaucoma progression, strengthening the evidence for the role of vasculopathy in glaucoma . Nevertheless, the role of ocular blood flow in glaucoma is controversial. A debate remains regarding whether blood flow abnormalities can lead to OAG primarily, if elevated IOP can secondarily damage the vasculature, or if the combination of vascular dysregulation and increased IOP causes OAG.
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