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Retinal Venous Vulnerability in Primary Open Angle Glaucoma: The Combined Effects of Intraocular Pressure and Blood Pressure with Application to the Thessaloniki Eye Study.

Created on 17 Jul 2025

Authors

Rajat Rai, Giovanna Guidoboni, Christopher K Wikle, Fotis Topouzis, Brent Siesky, Alice Verticchio Vercellin, Gal Antman, Alon Harris

Published in

La matematica. Volume 4. Issue 1. Pages 66-83. Epub Dec 23, 2024.

Abstract

Primary open angle glaucoma (POAG) is a leading cause of irreversible blindness with risk factors including elevated intraocular pressure (IOP), and both high and low blood pressure (BP). This study investigates the joint influence of IOP and BP on retinal hemodynamics, emphasizing venous circulation. A synthetic dataset comprising 2500 eyes with varied IOP [5-45] mmHg, systolic BP (SBP) [90-200] mmHg and diastolic BP (DBP) [40-120] mmHg was created. Mean pressure ( P ) , mean flow ( Q ) , and mean resistance ( R ) , were estimated using a validated mathematical model. The values of these hemodynamic output variables were then analyzed in relation to different values of IOP and mean arterial pressure (MAP; MAP = 1/3 SBP + 2/3 DBP). Clinical data from a population-based Greek study were similarly analyzed. Differences in the simulated hemodynamic output variables and clinical markers between healthy and POAG eyes were then measured. Synthetic dataset analysis revealed that R and P vary significantly depending on different IOP-MAP combinations. Notably, eyes with low MAP and high IOP demonstrated a drastic increase in R in the venules accompanied with a dramatic decrease in P in the central retinal vein (CRV). Clinical data indicated that venules in POAG eyes had significantly higher R than healthy eyes (p < 0.01), along with decreased P in the CRV of POAG eyes compared to healthy eyes (p = 0.01). The study highlights the increased susceptibility to venous collapse in POAG eyes and the importance of considering the venous side of retinal circulation in the combined impact of risk factors in POAG.

PMID:
40673059
Bibliographic data and abstract were imported from PubMed on 17 Jul 2025.

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