Autonomic dysfunction in unselected and untreated primary open angle glaucoma patients: a pilot study

Gherghel, Doina; Hosking, Sarah; Armstrong, Richard; Cunliffe, I A

doi:10.1111/j.1475-1313.2007.00485.x

Cited by 19 publications

(20 citation statements)

References 23 publications

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“…Evaluation of ambulatory BP in patients with glaucoma can provide insight into the presence of associated modifiable vascular risk factors and ischemic risk. In the current study and consistent with previous research, 7,32,41,42 no significant differences in the average diurnal and nocturnal BP variables or the nocturnal dipping status were found between the POAG, NTG, and control groups following 24-hour BP assessment. There is, however, a lack of consistency in results reported by various groups regarding the relationship between systemic BP and glaucoma, with other studies 40,[43][44][45][46][47][48][49][50][51][52][53][54][55] finding associations between abnormal systemic BP and the presence of GON, particularly with regard to hypotension and nocturnal BP dipping.…”

Section: Commentsupporting

confidence: 80%

Primary Open-Angle Glaucoma vs Normal-Tension Glaucoma

et al. 2013

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Section: Commentsupporting

confidence: 80%

Primary Open-Angle Glaucoma vs Normal-Tension Glaucoma

et al. 2013

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“…20 Generally, the sympathetic system affects the vasculature in different ways. First, it may be involved in the process of atherosclerosis through platelet-derived growth factor formation and by inducing mechanical vascular wall injury as a result of increased BP and increased flow velocity.…”

Section: Discussionmentioning

confidence: 99%

“…19 Twenty-four-hour ambulatory BP, ECG monitoring, and frequency domain analysis of HRV reported that untreated POAG patients exhibit abnormal autonomic function. 20 Although there is evidence that autonomic disturbances can have circulatory implications relevant to glaucoma pathogenesis, published results are inconsistent because most of the studies have been performed in selected cases free of systemic vascular diseases such as hypertension. [13][14] Moreover, it is difficult to enroll the patients for 24 hours or 48 hours of ECG or BP measurements.…”

mentioning

confidence: 98%

Autonomic Dysfunction in Normal Tension Glaucoma: The Short-term Heart Rate Variability Analysis

Na¹,

Lee²,

Park

et al. 2010

Journal of Glaucoma

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“…Application of bimatoprost and travoprost resulted in an improvement in the central retinal artery blood flow in newly diagnosed open-angle glaucoma patients (Alagoz et al, 2008). An improved OBF after treatment with latanoprost was also found in patients with POAG, normal tension glaucoma and ocular hypertension (Vetrugno et al, 1998;McKibbin and Menage, 1999;Georgopoulos et al, 2002;Sponsel et al, 2002b;Erkin et al, 2004;Gherghel et al, 2008). Also, unoprostone caused an increase in OBF, a comparison of latanoprost and unoprostone revealed, that latanoprost once daily produced a OBF increase nearly twofold greater than those obtained with unoprostone twice daily (Sponsel et al, 2002a).…”

Section: Improvement Of Ocular Blood Flow By Prostaglandin F Analoguesmentioning

confidence: 94%

Endothelin antagonism as an active principle for glaucoma therapy

Rosenthal

Fromm

2011

British J Pharmacology

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Endothelin, the most potent vasoactive peptide known to date, has been suggested to play a potential role in the pathogenesis of open-angle glaucoma. Open-angle glaucoma is the most common optic nerve head neuropathy and is associated with a loss of retinal ganglion cells and visual field damage. Although an increased intraocular pressure is a major risk factor for glaucomatous optic neuropathy, other factors such as a reduced ocular blood flow play an important role for appearance of the disease. Thus, treatment of glaucoma is focused on lowering of intraocular pressure and preventing the occurrence or progression of glaucomatous optic neuropathy. Endothelin participates in the regulation of intraocular pressure by an effect on trabecular outflow, the main route for aqueous humour outflow from the eye. Trabecular outflow is modulated by trabecular meshwork contractility which is affected by endothelin. In addition to the effects of endothelin in the anterior part of the eye, the vasoconstrictor causes a decrease in ocular blood flow followed by pathological changes in the retina and the optic nerve head which is assumed to contribute to the degeneration of retinal ganglion cells. In sum, inhibition of endothelin signalling leads to lowering of intraocular pressure and exerts neuroprotective effects. Thus, endothelin antagonism in the eye represents a promising approach for pharmacological treatment of glaucoma. AbbreviationsECE, endothelin-converting enzyme; ET-1, endothelin-1; ETA receptor, endothelin receptor A; ETB receptor, endothelin receptor B; FP receptor, prostaglandin F receptor; IOP, intraocular pressure; MLCK, myosin light chain kinase; MMP, matrix-metalloproteinase; OBF, ocular blood flow; PG, prostaglandin; ROCK, Rho kinase; RGC, retinal ganglion cell IntroductionEndothelin-1 (ET-1), the most potent vasoconstrictor known to date, is expressed in many organs and tissues and has been shown to play an important role in vascular homeostasis (Yanagisawa et al., 1988) as well as in a variety of pathological processes (Levin, 1995).In the human eye endothelin is detectable in the posterior part, especially in the choroid, retinal blood vessels, retinal pigment epithelium and optic nerve (Wollensak et al., 1998;Narayan et al., 2004). The precise source of endothelin in the posterior segment of the eye remains unclear. One possible source is the retinal pigment epithelium, which secretes ET-1 towards the basolateral side, suggesting an involvement in the regulation of choroidal blood flow (Narayan et al., , 2004Dibas et al., 2005a). The ET-1 synthesis and release from optic nerve head astrocytes as seen in cultured human cells may contribute to the signal in the optic nerve (Desai et al., 2004).In the anterior part of the eye, ET-1 was found in the iris, non-pigmented ciliary epithelium, ciliary muscle, as well as in the trabecular meshwork, endothelial cells lining Schlemm's canal and corneal epithelium (Wollensak et al., 1998;Fernandez-Durango et al., 2003). Apart from its localization in ocular tissues, ...

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Autonomic dysfunction in unselected and untreated primary open angle glaucoma patients: a pilot study

Abstract: Independent of a history and/or clinical signs of cardiovascular disease, glaucoma patients exhibit abnormal autonomic function.

Cited by 19 publications

References 23 publications

Primary Open-Angle Glaucoma vs Normal-Tension Glaucoma

Primary Open-Angle Glaucoma vs Normal-Tension Glaucoma

Autonomic Dysfunction in Normal Tension Glaucoma: The Short-term Heart Rate Variability Analysis

Endothelin antagonism as an active principle for glaucoma therapy

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