Topical Brimonidine is a well-established topical antigalucoma, ocular hypotensive therapeutic that has been in use since 1996. Brimonidine stands out among other topical ocular hypotensives in that it has a neuroprotective effect that is independent of IOP reduction. This has been demonstrated in multiple animal and human controlled studies both in vivo and in vitro. The mechanisms proposed so far to account for this neuroprotection focus mainly on molecular level antiapoptotic effects and modulation of some excitatory stimuli like glutamate. In this study we try to test the hypothesis that a positive hemodynamic profile of Brimonidine on ocular blood flow may be responsible at least in part for its unique neuroprotective effects.
* Study Design: A prospective, longitudinal, interventional, uncontrolled study * Participants: primary open angle glaucoma patients recruited during the period of study from the fayoum university hospital ophthalmic outpatient clinic. * Methods: Primary open angle glaucoma patients that are Brimonidine naiive and at the same time either medication naiive or have been on a fixed antiglaucoma medication for at least a month prior will be commenced on Brimonidine 0.2% bid with prior baseline imaging by OCT angiography (Optovue) of macula 6\*6 mm and ONH 4.5\*4.5 mm. After commencing Brimonidine patients will be followed up by OCT angiography at three visits assigned for 1,2,3 months after commencing Brimonidine. Every time the patient is imaged by OCT, imaging is done twice, once in a seated position at presentation and another- also in a seated position-, but after a protocol of right recumbency for 30 minutes in order to produce a postural position change as a vascular stress test to assess autoregulatory capacity of ocular and systemic circulation. At each visit, IOP and arterial blood pressure are measured both in the seated position and after the 30-minute recumbency protocol in order to mathematically calculate the mean ocular perfusion pressure that will be correlated with OCT angiography data including vascular density, as well as indirect parameters of blood flow. Data will be statistically analysed using the SPSS software.
Study Type
INTERVENTIONAL
Allocation
NA
Purpose
TREATMENT
Masking
NONE
Enrollment
41
Topical Brimonidine tartrate 0.2% bid ophthalmic solution. A selective alpha 2 adrenergic agonist with ocular hypotensive and neuroprotective properties used in glaucoma and ocular hypertension.
Fayoum University Hospitals
Al Fayyum, Egypt
Change in macular and peripapillary vascular densities
The vascular density measured by optical coherence tomography angiography represents the percentage area of flow-positive regions compared to the whole imaged area. Measured densities include (superficial and deep vascular densities) both of the macular area as well as radial peripapillary capillary density of the parapapillary area.
Time frame: At baseline before Brimonidine and 1,2,3 months thereafter.
Change in macular and peripapillary flow indices
An arbitrary flow index will be indirectly calculated using the density data of optical coherence tomography angiography, intraocular pressure and arterial blood pressure measurements.
Time frame: At baseline before Brimonidine and 1,2,3 months thereafter.
Change in intraocular pressure
Comparing intraocular pressure measurements at baseline with those on subsequent visits.
Time frame: At baseline before Brimonidine and 1,2,3 months thereafter.
Change in vascular autoregulatory capacity
Assessing both systemic as well as ocular vascular autoregulatory capacity making use of the 30-minute recumbency protocol as a vascular stress test.
Time frame: At baseline before Brimonidine and 1,2,3 months thereafter.
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