Effects of the systemic beta-adrenoceptor antagonist nebivolol on ocular hemodynamics in glaucoma patients

Systemic antihypertensive treatment in glaucoma patients with hypertension carries the potential risk of an additional deterioration in ocular hemodynamics due to the reduction in ocular perfusion pressure. Nebivolol is a beta1-selective adrenoceptor antagonist with known peripheral vasodilatory effects due to NO-releasing properties. The effect of a switch in systemic beta-blocker treatment to nebivolol on retrobulbar hemodynamics in glaucoma patients with arterial hypertension was therefore investigated.

Peak systolic (PSV) and end-diastolic (EDV) velocity in the short and long posterior ciliary arteries (SPCA, LPCA), central retinal artery (CRA), and ophthalmic artery (OA) were recorded by color Doppler imaging (CDI) in 23 glaucoma patients with arterial hypertension using their primary systemic beta-blocker medication and four weeks after a switch to nebivolol.

Compared with the first recording under the primary antihypertensive medication, the CDI measurements after four weeks of nebivolol treatment revealed a significant acceleration of the PSV in the SPCA and LPCA and the EDV in the SPCA and CRA. No significant differences in flow velocities were found for the OA. Intraocular pressure and systemic blood pressure remained unchanged.

Switching blood pressure treatment to nebivolol in glaucoma patients with hypertension leads to accelerated blood flow in the small retrobulbar vessels. A stabilization of ocular perfusion might be of particular importance in this group of co-morbid patients.