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1 General aspects (0)   1.1 Epidemiology (7)   1.2 Population genetics (1)   1.3 Pathogenesis (3)   1.4 Quality of life (5)   1.5 Glaucomas as cause of blindness (1)   1.6 Prevention and screening (1) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (2)   2.2 Cornea (7)   2.3 Sclera (0)   2.4 Anterior chamber angle (0)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (7)     2.5.2 Schlemms canal (0)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (0)     2.6.1 Production (0)     2.6.2 Outflow (0)       2.6.2.1 Trabecular meshwork (1)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (2)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (2)   2.9 Ciliary body (0)   2.10 Lens (0)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (2)   2.13 Retina and retinal nerve fibre layer (16)   2.14 Optic disc (7)   2.15 Optic nerve (2)   2.16 Chiasma and retrochiasmal central nervous system (0)   2.17 Stem cells (0)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (0)   3.2 Electron microscopy (0)   3.3 Immunohistochemistry (7)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (16)     3.4.2 Gene studies (3)   3.5 Molecular biology incl. 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    9.4.1 Steroid-induced glaucoma (8)     9.4.2 Glaucomas associated with disorders of the cornea, conjunctiva, sclera (2)       9.4.2.1 Iridocorneal endothelial syndrome (ICE, incl. irisatrophy) (0)       9.4.2.2 Posterior polymorphous dystrophy (0)       9.4.2.3 Fuchs' endothelial dystrophy (0)       9.4.2.5 Other (0)     9.4.3 Glaucomas associated with disorders of the iris and ciliary body (0)       9.4.3.1 Pigmentary glaucoma (0)       9.4.3.5 Other (0)     9.4.4 Glaucomas associated with disorders of the lens (0)       9.4.4.1 Exfoliation syndrome (9)       9.4.4.2 Glaucomas associated with cataracts (0)       9.4.4.3 Glaucomas associated with lens dislocation (0)       9.4.4.5 Other (0)     9.4.5 Glaucomas associated with disorders of the retina, choroid and vitreous (0)       9.4.5.1 Neovascular glaucoma (1)       9.4.5.5 Other (0)     9.4.6 Glaucomas associated with inflammation, uveitis (2)     9.4.7 Glaucomas associated with ocular trauma (0)     9.4.8 Glaucomas associated 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tube implant (12)     12.8.2 With tube implant or other drainage devices (6)     12.8.3 Non-perforating (8)     12.8.4 Using laser (0)     12.8.5 Other (0)     12.8.10 Woundhealing antifibrosis (9)     12.8.11 Complications, endophthalmitis (6)   12.9 Trabeculotomy, goniotomy (2)   12.10 Cyclodestruction (1)   12.11 Cyclodialysis (1)   12.12 Cataract extraction (2)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (3)   12.14 Combined cataract extraction and glaucoma surgery (0)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (0)     12.14.3 Phacoemulsification (3)   12.15 Capsulotomy (0)   12.16 Vitrectomy (0)   12.17 Anesthesia (3)   12.20 Other (2) 13 Therapeutic prognosis and outcome (0)   13.1 Prognostic factors (0)   13.2 Outcome (0)     13.2.1 IOP (0)     13.2.2 Visual field (0)       13.2.2.1 Progression (0)       13.2.2.2 Improvement (0)     13.2.3 Other (0) 14 Costing studies; pharmacoeconomics (5) 15 Miscellaneous (8)

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Abstract #13956 Published in IGR 8-3

Prevention of visual field defect progression with angiotensin-converting enzyme inhibitor in eyes with normal-tension glaucoma

Hirooka K; Baba T; Fujimura T; Shiraga F
American Journal of Ophthalmology 2006; 142: 523-525

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PURPOSE: To report the effect of angiotensin-converting enzyme (ACE) inhibitor on visual field changes in normal-tension glaucoma (NTG). DESIGN: Retrospective observational case series. METHODS: We retrospectively reviewed a total of 38 patients with NTG. Control subjects had no previous history of hypertension. NTG hypertension patients were divided into two groups, those receiving ACE inhibitor and those receiving other antihypertensive drug treatments. HfaFiles 5, an analytical program for the Humphrey Field Analyzer, was used to calculate the slope for the mean deviation (MD) change per year. RESULTS: In the ACE inhibitor-treated group, the mean MD change per year was 0.48 ± 0.19 dB, in control subjects was -0.38 ± 0.23 dB, and in the other antihypertensive drug-treated group was -0.50 ± 0.39 dB. CONCLUSIONS: Although the present study is retrospective and the sample size is small, ACE inhibitor might have a favorable effect on the visual field in patients with NTG in this small study.

Dr. K. Hirooka, Department of Ophthalmology, Kagawa University Faculty of Medicine, Kagawa, Japan

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Classification:

11.8 Neuroprotection (Part of: 11 Medical treatment)

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