Abstract
Objective
Evidence suggests that ocular blood flow dysregulation in patients with vasospasticity
could occur in response to biomechanical stimuli, contributing to optic nerve head
susceptibility in glaucoma. We evaluate the role of vasospasticity in the association
between ocular rigidity (OR) and neuroretinal damage, hypothesizing that low OR correlates
with greater glaucoma damage in patients with vasospasticity.
Design
Cross-sectional study.
Participants
Patients with open-angle glaucoma (OAG), suspect discs, or no glaucoma.
Methods
OR was measured using a noninvasive, validated method developed by our group. Retinal
nerve fibre layer (RNFL) and ganglion cell complex thicknesses were acquired using
spectral domain optical coherence tomography. Vasospasticity was assessed by a standardized
questionnaire that was based on existing validated questionnaires and adapted to our
requirements. Atherosclerosis was evaluated based on Broadway and Drance's (1998)
cardiovascular disease score. Correlations between OR and structural parameters were
assessed in patients with vasospasticity and those with atherosclerosis.
Results
Of 118 patients with either OAG (n = 67), suspect discs (n = 26), or no glaucoma (n = 25)
who were recruited consecutively, 10 were classified as having vasospasticity, and
37 as having atherosclerosis. In the vasospastic group, significant correlations were
found between OR and the minimum ganglion cell complex thickness (rs = 0.681, p = 0.030), the average RNFL thickness (rs = 0.745, p = 0.013), and the RNFL in the temporal quadrant (rs = 0.772, p = 0.009), indicating more damage with lower OR. Similar trends were maintained when
applying multiple testing correction; however, only the eighth RNFL clock hour corresponding
to the inferior-temporal peripapillary region remained significantly correlated with
OR in the vasospastic group (p = 0.015). In contrast, no correlation was found in the atherosclerotic group (p > 0.05).
Conclusions
The findings of the current pilot study indicate a trend for more neuronal structural
damage in less-rigid eyes of patients with vasospasticity, meaning that OR may play
a greater role in glaucoma in vasospastic patients than in patients with atherosclerosis.
Although these results provide interesting insight into the pathophysiology of OAG,
further investigation is needed to confirm our observations.
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Article Info
Publication History
Published online: March 28, 2022
Accepted:
February 12,
2022
Received in revised form:
February 8,
2022
Received:
June 7,
2021
Publication stage
In Press Corrected ProofIdentification
Copyright
© 2022 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved.
