Impaired ocular blood flow regulation in patients with open-angle glaucoma and diabetes.

Background:   To elucidate the potential impact of diabetes mellitus on primary open-angle glaucoma pathology through vascular deficiency.

Design:   Cross-section analysis from a longitudinal, prospective study.

Participants:   Eighty-four open-angle glaucoma patients (20 diabetic open-angle glaucoma patients and 64 non-diabetic open-angle glaucoma patients)

Methods:   Patients were analyzed for ocular structure, ocular perfusion pressure (OPP), retrobulbar blood flow and retinal capillary perfusion. Statistical analysis was performed by SPSS version 18.0. Comparisons between groups were made as well as multivariate linear regression analysis.

Main Outcome Measure:   Retrobulbar blood flow and the retinal microcirculation.

Results:   Central retinal artery peak systolic velocity was 13.5% lower in diabetic patients (P = 0.007). In diabetic open-angle glaucoma patients, ocular perfusion pressure positively correlated with central retinal artery and temporal posterior ciliary artery peak systolic velocity (R = 0.476, P = 0.039 and R = 0.529, P = 0.02, respectively), and with central retinal artery and nasal posterior ciliary artery resistance index (R = 0.537, P = 0.018 and R = 0.566, P = 0.012 respectively). Average retinal nerve fibre layer positively correlated with central retinal artery peak systolic velocity and temporal posterior ciliary artery end diastolic velocity (R = 0.501, P = 0.029 and R = 0.553, P = 0.019, respectively), and negatively correlated with superior and inferior retinal avascular space in the diabetic group (R = -0.498, P = 0.030 and R = -0.700, P = 0.001, respectively); no correlations were found in the non-diabetic group. Negative correlations between retrobulbar and retinal circulations were only found in the diabetic open-angle glaucoma patients, whereas positive correlations between retinal flow and non-flow were only found in non-diabetic open-angle glaucoma patients.

Conclusion:   Diabetes may interfere with normal vascular regulation and contribute to glaucoma progression.