Study finds additive hypotensive effect when combining dorzolamide with bimatoprost

The authors evaluated the effects of adding dorzolamide hydrochloride 2% (Trusopt) to morning-dosed bimatopost 0.03% on the diurnal IOP curve and retrobulbar hemodynamics of primary open-angle glaucoma patients. The results of this interesting study demonstrate that the addition of the topical carbonic anhydrase inhibitor dorzolamide reduced vascular resistance overnight in these patients. It would be helpful to see a study evaluate whether this reduced vascular resistance helps control glaucoma.

Twenty-five patients with primary open-angle glaucoma were subjects in the current study. After a one-week run-in period with bimatoprost, they were treated with bimatoprost dosed once in the morning for one month, after which dorzolamide was added twice daily for two months. Goldmann applanation IOP, arterial blood pressure and heart rate were measured every two hours for 24 hours and diurnal ocular perfusion pressure was calculated. Color Doppler imaging of the ophthalmic artery and the central retinal artery was recorded five times daily.

Mean baseline IOP was 14.8 mmHg. Mean IOP following bimatoprost monotherapy (12.8 mmHg) and after two months of dorzolamide adjunctive therapy (12.2 mmHg) were not statistically significantly different (P = 0.544). IOP was significantly reduced using the combined treatment at the 4:00 h time point only (P = 0.013). Twenty-four hour IOP fluctuations were lower when dorzolamide was added (6.0 mmHg vs. 4.6 mmHg, P = 0.0016). Repeated analysis of variance detected a significant decrease in vascular resistance in the ophthalmic artery (P = 0.0167) with adjunctive dorzolamide treatment.

The authors conclude that the addition of dorzolamide to morning-dosed bimatoprost had a significant additive hypotensive effect on the night-time but not the daytime IOP curve and lead to a lower 24-hour IOP fluctuation. They say the results suggest that dorzolamide may improve ocular blood flow independently of IOP reduction but the mechanism by which topical carbonic anhydrase inhibitors influence the vascular bed remains unknown.