ABSTRACT.Purpose: To determine whether retinal vessel oxygen saturation in patients with glaucoma is associated with structural optic disc and retinal nerve fibre layer (RNFL) changes and visual field (VF) defects. Methods: Fifty-nine patients with confirmed glaucoma were recruited at University Hospitals Leuven. Retinal oxygen saturation in patients with glaucoma was measured with a noninvasive spectrophotometric retinal oximeter (Oxymap ehf, Reykjavik, Iceland). VF and Heidelberg retinal tomographies (HRTs) were performed on the same day. Statistical analysis was performed using Student's t-test and Pearson's or Spearman correlation coefficient. Results: The mean oxygen saturation in venules was higher in patients with severe VF defects compared to those patients with mild VF defects (69 ± 3% versus 65 ± 6% respectively; p = 0.0003; n = 59). Accordingly, the arteriovenous (AV) difference in oxygen saturation was lower in patients with worse VF compared to those with better VF (29 ± 3% versus 33 ± 6% respectively; p = 0.002). The oxygen saturation in venules correlated with the VF mean defects (r = )0.42; p = 0.001; n = 59) as well as with the structural HRT parameters rim area and RNFL thickness (r = )0.39; p = 0.008 and r = )0.26; p = 0.05 respectively; n = 53). The AV difference decreased significantly as the VF defect worsened (r = 0.38; p = 0.003), as the rim area diminished (r = 0.29; p = 0.03) and as the RNFL thickness decreased (r = 0.27; p = 0.05). No correlation was found between the oxygen saturation in retinal arterioles and either of these parameters. Conclusion: Severe glaucomatous damage is associated with increased oxygen saturation in retinal venules and decreased AV difference in oxygen saturation. These data suggest that in eyes with severe glaucomatous damage, reduced retinal oxygen consumption is consistent with tissue loss.
Glaucoma patients with advanced glaucoma have higher oxygen saturation in venules and lower arteriovenous difference in oxygen saturation compared with healthy individuals. The decreased arteriovenous difference in severe glaucoma may be related to lower oxygen consumption secondary to neuropathy.
Proliferative diabetic retinopathy (PDR) the sequel of diabetic retinopathy (DR), a frequent complication of diabetes mellitus (DM), is the leading cause of blindness in the working-age population. The current screening process for the DR risk is not sufficiently effective such that often the disease is undetected until irreversible damage occurs. Diabetes-associated small vessel disease and neuroretinal changes create a vicious cycle resulting in the conversion of DR into PDR with characteristic ocular attributes including excessive mitochondrial and retinal cell damage, chronic inflammation, neovascularisation, and reduced visual field. PDR is considered an independent predictor of other severe diabetic complications such as ischemic stroke. A “domino effect” is highly characteristic for the cascading DM complications in which DR is an early indicator of impaired molecular and visual signaling. Mitochondrial health control is clinically relevant in DR management, and multi-omic tear fluid analysis can be instrumental for DR prognosis and PDR prediction. Altered metabolic pathways and bioenergetics, microvascular deficits and small vessel disease, chronic inflammation, and excessive tissue remodelling are in focus of this article as evidence-based targets for a predictive approach to develop diagnosis and treatment algorithms tailored to the individual for a cost-effective early prevention by implementing the paradigm shift from reactive medicine to predictive, preventive, and personalized medicine (PPPM) in primary and secondary DR care management.
The pattern of blood flow velocities in the OA throughout the cardiac cycle seems to be altered in glaucoma patients. Further studies on how systemic blood pressure affects waveform variables in glaucoma patients may provide a better understanding of an underlying vascular dysfunction.
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