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Bosnian journal of basic medical sciences

The role of lipid dysregulation and vascular risk factors in glaucomatous retrobulbar circulation.


PMID 26042513

Abstract

The aim of this study was to evaluate selected lipid-related and vascular factors and their effect on retrobulbar hemodynamics in glaucoma. Fifty-six patients with primary open angle glaucoma (POAG) [POAG group; mean age 68.32 years (SD±0.21)] and 54 patients in control group [CG, mean age 68.1 years (SD±5.34)] were examined. Peak systolic velocity, end-diastolic velocity, mean velocity, pulsatility index, and resistive index of the ophthalmic artery, the central retinal artery and the posterior ciliary arteries were measured by Color Doppler Imaging. Selected lipid-related, systemic and local vascular parameters were evaluated. Statistical methods included Shapiro-Wilk, Student-t and Mann-Whitney U tests, and Spearman rank correlations. In POAG group systolic arterial blood pressure, diastolic arterial blood pressure, total cholesterol, low density lipoprotein cholesterol (LDL-ch), and intraocular pressure were significantly higher; while ocular perfusion pressure, high density lipoprotein cholesterol (HDL-ch) and diastolic ocular perfusion pressure were significantly lower (p≤0.05). Color Doppler Imaging confirmed blood flow abnormalities in all investigated arteries. In addition, significant correlations of HDL-ch, LDL-ch and triglycerides (TG) with peak systolic velocity, end-diastolic velocity and mean velocity were found in individual arteries (p≤0.05). Also, significant associations of systolic arterial blood pressure, ocular perfusion pressure, systolic oclular perfusion pressure and diastolic ocular perfusion pressure with peak systolic velocity, end-diastolic velocity, mean velocity and resistive index were revealed in the posterior ciliary arteries (p≤0.05). Dysregulation of lipid-related and vascular factors, as well as statistical correlation between the above and retrobulbar blood flow indices, might imply their role in vasoconstrictive processes during glaucomatous endotheliopathy.