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Over the past two decades the evidence for a vascular contribution to glaucomatous optic neuropathy has increased exponentially. The breadth of accumulating ocular blood flow data was the focus of the recent 2009 World Glaucoma Association meeting1 where a consensus was reached that ocular perfusion pressure and vascular dys - regulation are likely involved in glaucoma pathology. Martinez and Sanchez-Salorio (1223) contribute to this growing body of evidence with a prospective study of predictors for visual field progression and the effects of treatment with dorzolamide 2% or brinzolamide 1% (both carbonic anhydrase inhibitors (CAI)) each added to timolol 0.5% in primary open-angle glaucoma over a sixty- month period. This article is the second in a series2 from the authors which found predictive baseline factors for glaucoma progression were: lower diastolic blood pressure, lower mean arterial pressure, anti-hypertensive treatment, lower end-diastolic velocity in the ophthalmic and short posterior ciliary arteries, and a higher vascular resistivity in both blood vessels. The risk for progression in patients treated with dorzolamide was reported to be half that of patients treated with brinzolamide. Describing vascular risk factors for glaucoma progression over longer time periods represents an important next step and is a strength of the current article. The authors present longitudinal evidence that suggests ocular blood flow as assessed with color Doppler imaging may indeed be predictive of glaucoma progression. In comparison of CAI treatments, however, great caution must be applied to any study describing differing progression in which small sample sizes are used: n = 50 (dorzolamide) and only n = 35 (brinzolamide) at the endpoint. Further, insufficiently described non-uniform treatment groups, unequal bilaterally assessed eyes (which can influence progression),3 use of vasoactive systemic medications, presence of systemic hypertension and cardiovascular disease all may have influenced ocular blood flow measurements and glaucoma progression, with a majority of these patients in the brinzolamide treatment group.
Martinez and Sanchez-Salorio present interesting data that strengthens the call for more research to be conducted elucidating ocular blood flow and glaucoma progression. The authors should be commended for these efforts. Larger multi-center prospective trials with uniform study groups are needed to confirm the long term effects of these CAI treatments on glaucoma progression.