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      Observations on Degenerative Changes Within the Optic Nerve in Patients With Primary Open Glaucoma and Arterial Hypertension: 6-Month Follow-Up : Progress of Glaucoma in Hypertensive Patients

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          Most cited references37

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          The impact of ocular blood flow in glaucoma.

          Two principal theories for the pathogenesis of glaucomatous optic neuropathy (GON) have been described--a mechanical and a vascular theory. Both have been defended by various research groups over the past 150 years. According to the mechanical theory, increased intraocular pressure (IOP) causes stretching of the laminar beams and damage to retinal ganglion cell axons. The vascular theory of glaucoma considers GON as a consequence of insufficient blood supply due to either increased IOP or other risk factors reducing ocular blood flow (OBF). A number of conditions such as congenital glaucoma, angle-closure glaucoma or secondary glaucomas clearly show that increased IOP is sufficient to lead to GON. However, a number of observations such as the existence of normal-tension glaucoma cannot be satisfactorily explained by a pressure theory alone. Indeed, the vast majority of published studies dealing with blood flow report a reduced ocular perfusion in glaucoma patients compared with normal subjects. The fact that the reduction of OBF often precedes the damage and blood flow can also be reduced in other parts of the body of glaucoma patients, indicate that the hemodynamic alterations may at least partially be primary. The major cause of this reduction is not atherosclerosis, but rather a vascular dysregulation, leading to both low perfusion pressure and insufficient autoregulation. This in turn may lead to unstable ocular perfusion and thereby to ischemia and reperfusion damage. This review discusses the potential role of OBF in glaucoma and how a disturbance of OBF could increase the optic nerve's sensitivity to IOP.
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            Large diurnal fluctuations in intraocular pressure are an independent risk factor in patients with glaucoma.

            To study the risk associated with diurnal intraocular pressure (IOP) variations in patients with open-angle glaucoma. Sixty-four patients (105 eyes) from the practices of two glaucoma specialists successfully performed home tonometry with a self-tonometer five times a day for 5 days. All patients had open-angle glaucoma and documented IOP below 25 mm Hg over a mean follow-up period of 5 years. Baseline status and time to progression of visual field loss were identified from the clinical charts. The level and variability of diurnal IOP obtained using home tonometry were characterized. Risk of progression was analyzed using a nonparametric time-to-event model, incorporating methods for correlated outcomes. Although mean home IOP and baseline office IOP were similar (16.4 +/- 3.6 mm Hg and 17.6 +/- 3.2 mm Hg, respectively), the average IOP range over the 5 days of home tonometry was 10.0 +/- 2.9 mm Hg. Baseline office IOP had no predictive value (relative hazard, 0.98). The diurnal IOP range and the IOP range over multiple days were significant risk factors for progression, even after adjusting for office IOP, age, race, gender, and visual field damage at baseline (relative hazards [95% confidence intervals], 5.69 [1.86, 17.35] and 5.76 [2.21, 14.98]). Eighty-eight percent of patients in the upper twenty-fifth percentile of IOP and 57% of patients in the lower twenty-fifth percentile progressed within 8 years. In patients with glaucoma with office IOP in the normal range, large fluctuations in diurnal IOP are a significant risk factor, independent of parameters obtained in the office. Fluctuations in IOP may be important in managing patients with glaucoma. Development of methods to control fluctuations in IOP may be warranted.
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              Vascular risk factors for primary open angle glaucoma: the Egna-Neumarkt Study.

              L Bonomi (2000)
              To assess the impact of vascular risk factors on the prevalence of primary open angle glaucoma. Population-based cross-sectional study. Four thousand two hundred ninety-seven patients more than 40 years of age underwent a complete ocular examination in the context of the Egna-Neumarkt Glaucoma Study. Ocular examinations were performed by trained, quality-controlled ophthalmologists according to a predefined standardized protocol including medical interview, blood pressure reading, applanation tonometry, computerized perimetry, and optic nerve head examination. Prevalences of ocular hypertension, primary open-angle glaucoma, normal-tension glaucoma, and other types of glaucoma were determined. Correlation coefficients were calculated for the association between systemic blood pressure and age-adjusted intraocular pressure (IOP) and between age and both intraocular and systemic blood pressures. Odds ratios were computed to assess the risk of primary open-angle glaucoma and normal-tension glaucoma in relation to systemic hypertension or antihypertensive medication, blood pressure levels, diastolic perfusion pressure, and a number of other cardiovascular risk factors. A positive correlation was found between systemic blood pressure and IOP, and an association was found between diagnosis of primary open-angle glaucoma and systemic hypertension. Lower diastolic perfusion pressure is associated with a marked, progressive increase in the frequency of hypertensive glaucoma. No relationship was found between systemic diseases of vascular origin and glaucoma. Our data are in line with those reported in other recent epidemiologic studies and show that reduced diastolic perfusion pressure is an important risk factor for primary open-angle glaucoma.
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                Author and article information

                Journal
                The Journal of Clinical Hypertension
                Wiley-Blackwell
                15246175
                October 2012
                October 2012
                : 14
                : 10
                : 701-710
                Article
                10.1111/j.1751-7176.2012.00694.x
                a9aecdfc-2208-4272-b697-6c8f8d42dfa5
                © 2012

                http://doi.wiley.com/10.1002/tdm_license_1.1

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