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      Comparison of ophthalmic artery blood flow between open-angle glaucoma and nonglaucomatous eyes of Indian patients

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          Abstract

          This study was undertaken to compare ophthalmic artery blood flow in eyes having primary open angle glaucoma (POAG) with age matched non glaucomatous eyes using the technique of Color Doppler imaging in Indian patients. One hundred patients of either sex over 40 years of age were divided into two groups of 50 patients each. Group 1 included 50 patients diagnosed with POAG whereas group 2 included patients who did not have POAG. Tests like visual fields and OCT RNFL were conducted and a radiologist assessed the ophthalmic artery blood flow using Color Doppler imaging. Hemodynamic calculations of ocular blood flow were done using the parameters of resistivity index (RI) and pulsatility index (PI). Statistically significant increase in the values of RI and PI were noted in patients with POAG as compared to those who did not have POAG.

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          The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma.

          Primary open-angle glaucoma (POAG) is one of the leading causes of blindness in the United States and worldwide. Three to 6 million people in the United States are at increased risk for developing POAG because of elevated intraocular pressure (IOP), or ocular hypertension. There is no consensus on the efficacy of medical treatment in delaying or preventing the onset of POAG in individuals with elevated IOP. Therefore, we designed a randomized clinical trial, the Ocular Hypertension Treatment Study. To determine the safety and efficacy of topical ocular hypotensive medication in delaying or preventing the onset of POAG. A total of 1636 participants with no evidence of glaucomatous damage, aged 40 to 80 years, and with an IOP between 24 mm Hg and 32 mm Hg in one eye and between 21 mm Hg and 32 mm Hg in the other eye were randomized to either observation or treatment with commercially available topical ocular hypotensive medication. The goal in the medication group was to reduce the IOP by 20% or more and to reach an IOP of 24 mm Hg or less. The primary outcome was the development of reproducible visual field abnormality or reproducible optic disc deterioration attributed to POAG. Abnormalities were determined by masked certified readers at the reading centers, and attribution to POAG was decided by the masked Endpoint Committee. During the course of the study, the mean +/- SD reduction in IOP in the medication group was 22.5% +/- 9.9%. The IOP declined by 4.0% +/- 11.6% in the observation group. At 60 months, the cumulative probability of developing POAG was 4.4% in the medication group and 9.5% in the observation group (hazard ratio, 0.40; 95% confidence interval, 0.27-0.59; P<.0001). There was little evidence of increased systemic or ocular risk associated with ocular hypotensive medication. Topical ocular hypotensive medication was effective in delaying or preventing the onset of POAG in individuals with elevated IOP. Although this does not imply that all patients with borderline or elevated IOP should receive medication, clinicians should consider initiating treatment for individuals with ocular hypertension who are at moderate or high risk for developing POAG.
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            Current concepts in the pathophysiology of glaucoma

            Glaucoma, the second leading cause of blindness, is characterized by changes in the optic disc and visual field defects. The elevated intraocular pressure was considered the prime factor responsible for the glaucomatous optic neuropathy involving death of retinal ganglion cells and their axons. Extensive investigations into the pathophysiology of glaucoma now reveal the role of multiple factors in the development of retinal ganglion cell death. A better understanding of the pathophysiological mechanisms involved in the onset and progression of glaucomatous optic neuropathy is crucial in the development of better therapeutic options. This review is an effort to summarize the current concepts in the pathophysiology of glaucoma so that newer therapeutic targets can be recognized. The literature available in the National Medical Library and online Pubmed search engine was used for literature review.
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              Color Doppler analysis of ocular vessel blood velocity in normal-tension glaucoma.

              The pathogenesis of normal-tension glaucoma remains unknown. Because ocular vasospasm has been proposed as a possible mechanism, we investigated ocular vessel flow velocity in normal-tension glaucoma patients at rest and under treatment with a cerebral vasodilator. Ten normal-tension glaucoma patients and nine age- and gender-matched controls had flow velocity measured in three vessels (ophthalmic artery, central retinal artery, and temporal short posterior ciliary artery) by using color Doppler imaging, under baseline conditions and during carbon dioxide supplementation sufficient to increase end-tidal PCO2 by 15%. Peak systolic and end-diastolic velocities were measured, and the resistance index (peak systolic velocity minus end-diastolic velocity, divided by peak systolic velocity) was calculated. Compared with controls, these normal-tension glaucoma patients had significantly lower end-diastolic velocities (P = .002) and higher resistance indices (P = .007) in the ophthalmic artery at baseline. When PCO2 was increased, control subjects remained unchanged, whereas it increased end-diastolic velocity in patients (P = .003) and abolished the difference in resistance index between the two groups. Patients and control subjects differed little in their baseline or carbon dioxide response velocities or in resistance in the other two vessels. These results indicate that at baseline these normal-tension glaucoma patients may have increased vascular resistance distal to the ophthalmic artery, although this increased resistance cannot be specifically ascribed to the central retinal arterial or to temporal short posterior ciliary arterial vascular beds. The responsiveness of these patients to a cerebral vasodilator (increased PCO2) indicates further that the increased resistance distal to the ophthalmic artery may be the reversible result of vasospasm.
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                Author and article information

                Journal
                Oman J Ophthalmol
                Oman J Ophthalmol
                OJO
                Oman Journal of Ophthalmology
                Wolters Kluwer - Medknow (India )
                0974-620X
                0974-7842
                Sep-Dec 2020
                02 November 2020
                : 13
                : 3
                : 112-116
                Affiliations
                [1] Department of Ophthalmology, Command Hospital, Chandimandir, Haryana, India
                Author notes
                Address for correspondence: Dr. Hiteshi Saini, HCMS MO, Panchkula - 134 109, Haryana, India. E-mail: hiteshi.saini@ 123456yahoo.co.in
                Article
                OJO-13-112
                10.4103/ojo.OJO_16_2018
                7852412
                33542597
                06c88aa0-a0b9-4f22-b752-09abcf9cc17c
                Copyright: © 2020 Oman Ophthalmic Society

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                : 12 February 2018
                : 02 May 2020
                : 02 August 2020
                Categories
                Original Article

                Ophthalmology & Optometry
                optical coherence tomography retinal nerve fiber layer,primary open-angle glaucoma,pulsatility index,resistivity index

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