High Pulse Wave Velocity Is Associated With Decreased Macular Vessel Density in Normal-Tension Glaucoma

PURPOSE. To investigate the relationship between pulse wave velocity (PWV) and retinal vessel density (VD) measured by optical coherence tomography angiography (OCTA) in patients with normal-tension glaucoma (NTG). METHODS. This retrospective study included 103 patients with NTG and 109 healthy controls who underwent glaucoma examination and PWV measurements. Each group was classified into two subgroups according to a brachial-ankle PWV of 1400 cm/s. NTG was diagnosed when the maximum untreated intraocular pressure was < 21 mmHg on three repeated measurements obtained at different times in the presence of glaucomatous optic discs (neuroretinal rim thinning and excavation), peripapillary retinal nerve fiber layer defects, and glaucomatous visual field defects. Healthy controls did not have glaucomatous optic discs or visual field defects and exhibited normal retinal nerve fiber layer thickness. The interval between glaucoma examination and PWV measurements did not exceed six months. Univariate and multivariate logistic regression analyses were performed to identify factors associated with high PWV. RESULTS. PWV was higher in the NTG group than in the control group, while peripapillary VD and macular VD (mVD) were lower (all P < 0.05). Stepwise logistic regression analysis revealed that high PWV was significantly associated with age, mean arterial pressure (MAP), and mVD in the NTG group. Meanwhile, high PWV was significantly associated with age, MAP, and low-density lipoprotein cholesterol levels in healthy controls. CONCLUSIONS. High PWV is associated with decreased mVD in NTG patients, suggesting that systemic arterial stiffness might be involved in the pathogenesis of NTG.

Automated summary

The study found that PWV was higher in NTG patients, with lower retinal vessel density, and high PWV was significantly associated with age, mean arterial pressure, and mVD. This suggests that systemic arterial stiffness may play a role in the pathogenesis of NTG.