Effects of long-term hypotensive therapy with nonselective beta-blockers on ocular hemodynamics in primary open-angle glaucoma

Citation
Dw. Evans et al., Effects of long-term hypotensive therapy with nonselective beta-blockers on ocular hemodynamics in primary open-angle glaucoma, J GLAUCOMA, 8(1), 1999, pp. 12-17
Citations number
24
Categorie Soggetti
Optalmology
Journal title
JOURNAL OF GLAUCOMA
ISSN journal
10570829 → ACNP
Volume
8
Issue
1
Year of publication
1999
Pages
12 - 17
Database
ISI
SICI code
1057-0829(199902)8:1<12:EOLHTW>2.0.ZU;2-X
Abstract
Purpose: Vascular factors have been implicated in the progression of glauco ma, but the impact of long-term beta blocker therapy on ocular circulation remains largely undefined. The purpose of this study was to prospectively e valuate the level of retrobulbar blood flow in patients with primary open-a ngle glaucoma (POAG) before and during long-term treatment with a nonselect ive topical beta blocker, and to compare these measures with those in untre ated control subjects. Methods: Twelve control subjects and 12 patients with POAG were tested for intraocular pressure (IOP), heart rate, blood pressure, contrast sensitivit y, visual field sensitivity, and retrobulbar flow velocity as measured by c olor Doppler imaging (CDI). Patients were evaluated after 4 weeks of drug w ashout and again after 3 and 6 months of treatment with a nonselective beta blocking agent. Control subjects were tested once. Results: At baseline, patients with POAG had significantly higher IOP than normal controls; CDI measures of the central retinal artery (CRA) and short posterior ciliary artery (SPCA) in the patients were significantly differe nt from those in control subjects, in the patients, treatment resulted in a significant reduction in IOP and in CRA and SPCA resistance index. Conclusion: Untreated patients with POAG have altered circulation in the CR A and SPCA compared with subjects of similar age and gender. These measures recover significantly during topical beta blocker therapy. The relationshi p of the pretreatment deficit and posttreatment recovery of CDI blood flow measures to the progression and therapeutic impediment of glaucomatous opti c nerve deterioration remains to be determined.