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Nocturnal hypotension associated with visual field damage in normal tension glaucoma
Low nocturnal diastolic blood pressure and nocturnal diastolic blood pressure dip significantly increase the risk of visual field progression in patients with normal tension glaucoma, according to a study.
At the Glaucoma Clinic of Asan Medical Center of Seoul, Korea, 119 patients (119 eyes) with normal tension glaucoma (NTG) underwent 24-hour automated blood pressure monitoring (ABPM) at baseline.
IOP was measured every 2 hours during the day in the sitting position and three times during the night in the supine position. Visual field examinations were performed every 6 months over an average follow-up of about 3.4 years.
Forty-one eyes (34%) showed visual field progression during the follow-up. Patients in this group had significantly lower nocturnal DBP (less than 60 mm Hg) and greater magnitude and duration of night-time diastolic blood pressure (DBP) dip of more than the established cutoff point (greater than 10 mm Hg) at baseline. Systolic blood pressure parameters were not significantly associated with visual field progression.
In NTG, optic nerve damage is partly caused by perfusion insufficiency, which is linked to low DBP, the authors explained. Hypotension, particularly occurring at night, might therefore explain progressive visual field damage occurring despite well-controlled IOP.
“In this context, 24-hour ABPM would be of great value in monitoring and planning for patients with NTG,” they suggested.
Adjusting the therapy to less aggressive blood pressure targets may also be necessary for patients on antihypertensive medications, while others may benefit from methods to maintain proper nighttime DBP, such as aerobic exercises, nocturnal salt-loading or sufficient water drinking.
“Spontaneous or drug-induced excessive nocturnal DBP dip should be avoided, because it is a potential risk factor for visual field progression in NTG,” they wrote. – by Michela Cimberle
Disclosure: The authors reported no relevant financial disclosures.
Perspective
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The landmark clinical trials have proven that elevated IOP is a strong risk factor for the onset and progression of glaucomatous optic neuropathy. Not having been studied prospectively, IOP fluctuation is more contentious but may increase the risk of disease progression, particularly when pressures are low.
Kwon and colleagues now suggest that blood pressure variability, specifically significant and extended dips in nocturnal DBP, exacerbate visual field loss in normal tension glaucoma. Nocturnal IOP spikes in concert with physiologic or iatrogenic DBP troughs may compromise ocular perfusion pressure. Aggravated by impaired autoregulation of blood flow, repeated episodes of optic nerve ischemia and reperfusion lead to retinal ganglion cell dysfunction and death.
These investigators go on to suggest that modification of DBP (and, by extension, ocular perfusion pressure) may ultimately join IOP as a modifiable risk factor in the treatment of glaucoma.
At present, particularly in patients progressing at low in-office IOP, clinicians would be wise to consider management strategies that both lower IOP and dampen nocturnal IOP and blood pressure fluctuation. These strategies would include: topical prostaglandin analog and carbonic anhydrase inhibitor (rather than beta-blocker and alpha agonist), selective laser trabeculoplasty, minimally invasive glaucoma surgery or incisional surgery, and consulting with primary care providers about morning rather than evening dosing of blood pressure medication.