advertisement
In some patients with open-angle glaucoma (OAG), intraocular pressure (IOP) alone may be responsible for retinal ganglion cell death and corresponding vision loss. In other patients, ocular blood flow deficits may contribute to glaucomatous optic neuropathy. Recent large population based studies have found ocular perfusion pressure (OPP) to be an independent risk factor for the development and progression of glaucoma. In an attempt to understand how changes to perfusion pressure may affect localized ocular blood flow, Boltz et al. (1902) tested the hypothesis that choroidal blood flow (ChBF) regulation may be modified by a latanoprost inducued decrease in IOP during changes in OPP. The authors found that latanoprost significantly reduced IOP (P = 0.008) but that the relative increases in OPP during artificial IOP increases were comparable between placebo and latanoprost. During the squatting-induced elevation of OPP, ChBF increased less after latanoprost than after placebo treatment (P = 0.049). During the suction cup-induced increase in IOP, the decrease in ChBF was less pronounced after latanoprost than after placebo (P = 0.026). The authors suggest that latanoprost improves ChBF regulation during both an increase and a decrease in OPP related to the decrease in IOP. One stregngth of the study is that it was tested in a double-masked, randomized, placebo-controlled environment. One significant limitation is that the experiments were performed in parallel on healthy individuals. The vascular regulation of OAG patients has been reported in many studies to be deficient compared to healthy individuals and this may limit the study findings in terms of applying them to OAG. Another consideration is a possible steal phenomenon from one vascular bed to another which cannot be ruled out due to only one localized vascular bed being measured in the current study. This study by Boltz et al. is an interesting contribution to the growing body of research investigating vascular dysregulation and fluctuation of ocular blood flow during changes in OPP. Confirmation of these findings in a larger sample of OAG patients with multiple measures of blood flow and differing hypotensive treatments is suggested.