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Vascular contributions to glaucomatous pathophysiology have been identified in retinal, choroidal and retrobulbar blood supplies, while reduced ocular perfusion pressure continues to be confirmed as a risk factor for glaucoma incidence, prevalence and progression. Contributing to this body of evidence, Portmann et al. (1361) present data on choroidal blood flow response to isometric exercise in ocular hypertension (OHT), glaucoma (OAG) and healthy control subjects. The authors found healthy eyes demonstrated higher laser Doppler flowmetry blood flow at baseline than both other groups (ANOVA p = 0.003). Following isometric hand-grip test (bulb dynamometer) OAG patients exhibited a two-fold increase in choroidal flow compared to controls (+8.1 ± 8.0% vs. +3.7 ± 6.7%, p = 0.007) with non-significant differences between OAG OHT subjects. The authors conclude the increase in choroidal measurements in OAG patients in the face of exercise-induced blood pressure rise indicates inhibited vascular regulatory capacity in OAG patients. This data complements various existing data that has previously shown inhibited vascular autoregulation in OAG subjects following posture manipulations; hypercapnia and other provocation tests.
Many patients with OAG have reduced ocular blood flow and inefficient vascular regulation during periods of fluctuation in ocular perfusion pressure
The author's inclusion of OHT, OAG and healthy controls with 45 subjects in each group is a strength of the current study design. In addition, the similar age across groups and use of ocular hypotensive washout was beneficial to the study. One significant limitation was that intraocular pressures were not measured during the exercise period eliminating the possibility to examine ocular perfusion pressure relationships during the provocation. Since measurements were limited to a choroidal analysis only, other vasogenic effects and possible steal phenomenon from retinal and other vascular beds were also unexamined. Acknowledging these limitations, the data presented affirm that many patients with OAG have reduced ocular blood flow and inefficient vascular regulation during periods of fluctuation in ocular perfusion pressure. Studies which are specifically designed to assess vascular deficits in relation to glaucoma progression, remain the next vital step in advancing our understanding of the vascular risk for glaucomatous optic neuropathy.