Effect of nifedipine on ocular pulse amplitude in normal pressure glaucoma

Abstract

Ocular pulse amplitude (OPA) is reduced in normal tension glaucoma (NTG) patients when compared to non-glaucomatous, healthy control subjects. This might be related to a vasospastic reaction. The objective of this study was to determine if low OPA in NTG is associated with a vasospastic reaction and its response to vasodilation. Nifedipine, a calcium channel blocker, vasodilator and systemic antihypertensive agent improves visual fields in NTG patients following acute and chronic dosing. The effect of 60 mg of daily orally administered nifedipine on OPA, intraocular pressure (IOP, German abbreviation: IOD), blood pressure (BP, German abbreviation: RR) and pulse rate (PR, German abbreviation: HF) were measured prior to and for 3 months after initiating nifedipine therapy in 32 NTG patients with and without a vasospastic reaction as manifested by a local cold exposure test. Before treatment, all patients had reduced OPA evaluated with the Langham Ocular Blood Flow System. During nifedipine treatment NTG patients with a vasospastic reaction showed a significant (p < 0.001) increase in OPA, whereas NTG patients without a vasospastic reaction showed no sig. (p > 0.05) change in OPA. There may be two different subgroups of NTG patients, those who have a vasospastic reaction and react to nifedipine, while others lack the ability to react to nifedipine or might have a different, non-vasospastic pathology. Calcium channel blockers and other vasodilators may be useful in the treatment of vasospastic NTG patients.