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Purpose: Niacin, a treatment for dyslipidemia, is known to induce vasodilation as a secondary effect. Previous instances of patients with chronic central retinal vein occlusion (CRVO) and cystoid macular edema (CME) have been observed to spontaneously improve when placed on systemic niacin for hypercholesterolemia. The purpose of this study was to evaluate the effects of niacin on CRVO and associated ocular complications., Methods: A prospective, single-center, non-randomized, interventional case series of niacin for CRVO was conducted. Best-correct visual acuity (BCVA), central macular thickness (CMT), and ocular complications were analyzed in 50 patients over 1 year. Eight patients were controls., Results: The mean initial logMAR BCVA was 0.915, and improved with niacin to 0.745 (P = 0.12), 0.665 (P = 0.02) and 0.658 (P = 0.03) after 3, 6, and 12 months of follow-up, respectively. At baseline, mean CMT was 678.9 μm, and improved to 478.1 μm (P = 0.001), 388.6 μm (P < 0.001), and 317.4 μm (P < 0.001) for the same time points. The control group had a mean initial logMAR BCVA of 1.023, which gradually deteriorated to 1.162 (P = 0.36) after 12 months, and baseline CMT of 700.0 μm at baseline, which gradually improved to 490.9 μm (P = 0.06) after 12 months. Panretinal photocoagulation for neovascularization was required in 5 patients (13.2%) receiving niacin and 3 (37.5%) controls., Conclusions: These data suggest that niacin may be associated with functional and anatomic improvements in eyes with CRVO. Future investigations will help ascertain whether there is a role for niacin as an adjunct therapy to intravitreal injections in the management of CRVO.

Timolol is widely used in glaucoma treatment without sufficient knowledge of its vascular retinal effects. In this study, we measured the retinal vessel diameters before and after instillation of 0.5% timolol twice daily in one eye for 1 week, using photographic enlargements (x44). A total of 12 normal, caucasian subjects aged 25-39 years (average, 30.6 +/- 4.2 years) participated in this study. In all, 75% of the subjects had a diminution of retinal arterial size in the treated eye. The mean arterial diametric decrease was 4.1% in treated eyes compared with both untreated eyes and pretreatment values of treated eyes. These diminutions were statistically significant according to Student's paired t-test (P less than 0.05). No statistical difference was found in venous diameters (t = -0.065). Results showed that 0.5% timolol may have a vasoconstrictive effect on the retinal arteries of normal human subjects after 1 week of unilateral instillation twice daily. We suggest that this arterial vasoconstriction could be caused by the effect of timolol on the vascular beta-2 receptors. Further investigations are warranted to determine whether timolol also acts on ciliary arteries and whether arterial vasoconstriction participates in lowering intraocular pressure.