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Vascular dysfunction in glaucoma has been well documented in a generalized sense, but consensus regarding the specificity of biomarkers and their ability to predict glaucoma status remains elusive. Distinguishing a primary perfusion deficit from a secondary reduction of blood flow due to intraocular pressure (IOP) and/or localized tissue loss is a critical consideration in determining the influence of vascular dysfunction on a person's overall risk for the development and progression of glaucoma.
A significant strength of the current study is the identification of altered hemodynamics in glaucomatous optic neuropathy that was independent of covariates such as IOP, blood pressure, pulse and/or ocular tissue loss
Cousins et al. present evidence of systemic vascular dysfunction as a predictor for glaucomatous status. Utilizing a modality originating over 25 years ago as presented by Gasser and Flammer, the authors identified reduced resting nailfold capillary blood flow in persons with primary openangle glaucoma compared to healthy controls. Specifically they found that every picolitre per second increase in resting nailfold blood flow was associated with a 6% (95% CI 0.92 to 0.96) reduced odds of POAG (p < 0.0001). A significant strength of the current study is the identification of altered hemodynamics in glaucomatous optic neuropathy that was independent of covariates such as IOP, blood pressure, pulse and/or ocular tissue loss. The author's data builds upon the previous findings of Gasser and Flammer who identified reduced blood flow velocity in normal tension glaucoma patients that was especially evident following a cold provocation. However, a weakness of the current, as well as historical, studies is the cross sectional design which limits the ability to determine the influence on glaucoma progression. Another limitation is the lack of a modality to directly measure ocular blood flow, such as optical coherence tomography angiography, which might help confirm if nailfold flow reductions correspond to optic nerve perfusion reductions in glaucoma subjects. In summary, the authors present important novel data confirming systemic vascular dysfunction in glaucoma independent of traditional clinical covariates. However, it is important to stress the need for large sample longitudinal studies to confirm the utility of vascular biomarkers in determining not only glaucoma disease status, but also predicting disease progression.