PubMed2002
PURPOSE: The main purpose of this study was to assess the improvement in visual function in patients with glaucomatous neuropathy treated with Ramipril (angiotensin-converting enzyme inhibitor); we were thus able to link ischemia and visual deterioration in glaucoma. Ramipril increases endothelium-dependent relaxation and vasodilatation to bradykinin via B2 receptors linked to the formation of nitric oxide (NO). On the other hand, Ramipril could have an influence on retinal neurotransmission modulation. MATERIALS AND METHODS: Ramipril was administered to 22 patients suffering from chronic glaucoma in whom intraocular pressure (IOP) was controlled by classic treatment, combining Ramipril with this treatment. It was given orally (1.25mg daily) for 3 months in order to improve visual function. In addition to the standard follow-up (visual acuity, intraocular pressure, automatic perimetry, optic disk), this study focused on the systemic tolerance to Ramipril. RESULTS: Thirty eyes in 22 patients were evaluated. Mean intraocular pressure did not change, but the mean visual acuity improved from 0.53 to 0.74. After 3 months of treatment, the perimetric test (Octopus) showed an improvement in the mean defect (MD) (48%) and the corrected loss variance (CLV) (54%). No complications in terms of arterial pressure were observed. CONCLUSION: This study has shown that Ramipril was an effective agent in glaucomatous neuropathy. It improved visual function without changing IOP and had a satisfactory general tolerance in all patients. This could be explained in part by a higher production of NO by endothelial cells. This gas is a powerful vasodilator. It is formed from L-arginine by constitutive nitric oxide synthetase. This would provide an improvement in local blood flow autoregulation altered in glaucoma by an endothelial dysfunction.