98th Annual Meeting DOG 2000

K 826

Short posterior ciliary artery, central retinal artery, and choroidal hemodynamics in brimonidine treated primary open angle glaucoma patients

K.-G. Schmidt, V. Klingmüller, A. v. Rückmann

Introduction: Peripapillary hemodynamics is increasingly being discussed in the prognosis of primary open angle glaucomas (PAOG). Current antiglaucomatous drugs - in addition to reducing intraocular pressure
(IOP) - should not impair perfusion to the optic nerve head, the area of primary damage in the glaucomas.

This study was designed to evaluate the influence of brimonidine, a potentially vasoconstrictive alpha-2-receptor agonist, on short posterior ciliary artery (SPCA), central retinal artery (CRA), and choroidal vascular systems in POAG patients.

Methods: The influence of brimonidine (0.2%), in standard dosage (BID, 1 eye) on SPCA, CRA (9 MHz linear and phased array scanners, Elegra Advanced System, Siemens, Germany, transmission energy reduced to 40%, B-, C-, & triplex-modes) and choriodal (ocular pulse amplitude, OPA; OBF-System, OBF Labs UK) hemodynamics, IOP, and systemic perfusion parameters was investigated in 17 POAG patients without clinically relevant extracranial stenosis (< 50% reduction in vessel diameter) as excluded by sonography of common, external and internal carotid arteries. Measurements were taken before and following 4 weeks of brimonidine therapy.

Results (mean ± SD): Following application of brimonidine IOP (mmHg) in drug treated POAG eyes was significantly (sig., p< 0.0001) reduced from 26.4 ± 1.3 to 21.5 ± 1.6. When compared to pretreatment values OPA
(2.1 ± 0.1/2.1 ± 0.1 mmHg), SPCA and CRA perfusion parameters (peak systolic velocity, enddiastolic velocity, pulsatility and resistance indexes and systemic perfusion parameters were not sig. (p> 0.05) altered following application of brimonidine.

Conclusion: Brimonidine reduced IOP by 18.7%, a negative hemodynamic effect on vessels feeding the optic nerve head, the area of primary damage in the glaucomas was excluded by this study.

Department of Ophthalmology, University of Oxford, Walton Street, Oxford, OX2 6 AW, U.K.