Association of the optic disc structure with the use of antihypertensive medications: the thessaloniki eye study.

PURPOSE: To investigate the association of antihypertensive medications with optic disc structure by blood pressure (BP) level, in nonglaucoma subjects. DESIGN: Cross-sectional, population-based study. METHODS: A subset of Thessaloniki Eye Study participants was included in this study. Subjects were interviewed for medical history and underwent extensive ophthalmic examination, BP measurement, and optic disc imaging with the Heidelberg retinal tomograph. Subjects treated for hypertension were grouped in the following groups: (1) angiotensin-converting enzyme inhibitors and/or angiotensin-receptor blockers; (2) beta blockers and/or calcium-channel blockers; (3) diuretics alone or combined with others; and (4) other combinations. Cup size and cup-to-disc (C/D) ratio in the above groups were compared with the untreated group, using regression models. Analyses were rerun for subjects with systolic BP (SBP)<140 mm Hg, SBP≥140 mm Hg, diastolic BP (DBP)<90 mm Hg, and DBP≥90 mm Hg. RESULTS: Among 232 subjects, 131 were receiving antihypertensive medications. In subjects with DBP<90 mm Hg, all medications groups were associated with larger cup size and higher C/D ratio compared with the untreated group. Results were similar in subjects with SBP<140 mm Hg, with the exception of the beta blockers and/or calcium-channel blockers group. None of the medications groups were associated with the Heidelberg retinal tomograph parameters in those with DBP≥90 mm Hg or SBP≥140 mm Hg. CONCLUSIONS: All classes of antihypertensive medications were associated with larger cup size and higher C/D ratio in subjects with either DBP<90 mm Hg or SBP<140 mm Hg. These results suggest that there is no specific medication-related effect on optic disc structure, and the associations found are mediated through the hypotensive effect of antihypertensive medications.

Diabetic macular oedema: physical, physiological and molecular factors contribute to this pathological process.

Diabetic macular oedema (DMO) is an important cause of vision loss in patients with diabetes mellitus. The underlying mechanisms of DMO, on both macrocellular and microcellular levels, are discussed in this review. The pathophysiology of DMO can be described as a process whereby hyperglycaemia leads to overlapping and inter-related pathways that play a role not only in the initial vascular events, but also in the continued tissue insult that leads to chronic DMO. On a macrocellular level, DMO is believed to be in part caused by alterations in hydrostatic pressure, oxygen tension, oncotic pressure and shear stress. Three key components of the microvascular pathways include angiogenic factor expression, inflammation and oxidative stress. These molecular mediators, acting in conjunction with macrocellular factors, which are all stimulated in part by the hyperglycaemia and hypoxia, can have a direct endothelial effect leading to hyperpermeability, disruption of vascular endothelial cell junctions, and leukostasis. The interactions, signalling events and feedback loops between the various molecules are complicated and are not completely understood. However, by attempting to understand the pathways involved in DMO, we can help guide new treatment options targeted towards specific factors or mediators.

Intravitreal bevacizumab for choroidal neovascularization secondary to presumed ocular histoplasmosis syndrome.

PURPOSE: The purpose of this study was to assess the efficacy of intravitreal bevacizumab for choroidal neovascularization resulting from presumed ocular histoplasmosis syndrome. METHODS: This is a chart review of retrospective consecutive case series in which intravitreal bevacizumab (1.25 mg) was injected into 24 eyes with choroidal neovascularization resulting from presumed ocular histoplasmosis syndrome. Visual acuity was measured in all patients. Optical coherence tomography and/or fluorescein angiography was performed before and after treatment. The minimum follow-up time was 3 months. Retreatment criteria included failure to improve visual acuity and/or persistent leakage as determined by optical coherence tomography or fluorescein angiography. RESULTS: Patients' mean age was 43.08 years (standard deviation, 13.58 years) and mean follow-up was 31.8 weeks (standard deviation, 20.79 weeks). The average number of bevacizumab injections was 6.8 injections/year. After 3 months, visual acuity improved from mean logMAR 0.76 +/- 0.48 (Snellen equivalent of 20/114) to mean logMAR 0.45 +/- 0.47 (Snellen equivalent of 20/55) (P < 0.001, paired t test; n = 24). After 12 months, visual acuity improved from mean logMAR 0.86 +/- 0.35 (Snellen equivalent of 20/150) to mean logMAR 0.34 +/- 0.33 (Snellen equivalent of 20/45) (P = 0.006, paired t test; n = 9). Fourteen (58.3%) eyes had final visual acuity of 20/40 or better compared with 5 (20.8%) eyes at baseline (P = 0.003, McNemar test). Ten patients (41.6%) had visual acuity of 20/200 or worse at baseline compared with 5 (20.8%) eyes at the final visit (P = 0.059, McNemar test). CONCLUSION: Intravitreal injection of bevacizumab seems to be an effective treatment for choroidal neovascularization resulting from presumed ocular histoplasmosis syndrome.

Effects of exercise on intraocular pressure and ocular blood flow: a review.

Glaucoma is a disease characterized by progressive optic neuropathy resulting in retinal ganglion cell death, which affects approximately 68 million people worldwide. Risk factors include intraocular pressure (IOP), genetics, race, age, and vascular factors. Exercise is known to affect IOP and systemic cardiovascular factors and, therefore, may affect glaucoma pathophysiology. This review discusses the results of articles relevant to glaucoma, IOP, ocular blood flow (OBF), and exercise. Isometric and dynamic exercises have been studied with respect to effects on IOP and OBF. Isometric exercise results in an acute decrease in IOP, which correlates with hypocapnia. Dynamic exercise results in a more pronounced but also short duration decrease in IOP. Physical fitness is associated with lower baseline IOP but diminished acute IOP-lowering response to exercise. Upon cessation of exercise, values return to pretrained levels within 1 month. In glaucoma patients, these IOP-lowering effects are greater than in healthy subjects. In healthy subjects, OBF is unchanged during exercise due to vascular autoregulation. This autoregulation fails at ocular perfusion pressures greater than 70% above baseline. In conclusion exercise in glaucoma patients results in acutely lowered IOP and lower baseline IOP. The effects of exercise on the prevention of glaucoma and glaucomatous progression remain unknown. The role of exercise in glaucoma management should be investigated.

Chlorhexidine gluconate 0.02% as adjunct to primary treatment for corneal bacterial ulcers.

BACKGROUND: It is common practice to use topical antiseptic formulations prior to specific therapy in superficial infections and injuries, but not in corneal bacterial ulcers. There is accumulating evidence proving chlorhexidine gluconate 0.02%, an antiseptic agent, as an effective treatment for infectious keratitis. OBJECTIVES: To investigate the safety and efficacy of chlorhexidine gluconate 0.02% as an adjunct therapy for corneal bacterial ulcers. METHODS: Twenty-six patients with corneal bacterial ulcers were treated with standard empirical antibiotic treatment. The study group was treated with chlorhexidine gluconate 0.02% while controls received placebo for one week. The patients were followed for at least 1 month. RESULTS: No allergic or toxic reactions were noted. Although a higher baseline severity of ulcers existed in the study group, no differences were found in final vision, scarring extent, or recovery duration. CONCLUSIONS: Chlorhexidine gluconate 0.02% may improve the clinical course of corneal ulcers.

The effects of raloxifene hydrochloride on ocular hemodynamics and visual function.

OBJECTIVE: To assess the comprehensive effects of raloxifene hydrochloride on retinal, choroidal and retrobulbar hemodynamics and on visual function in post-menopausal women. DESIGN: Twenty-four post-menopausal women (age 55 +/- 3.8 years) were recruited for this cross-sectional study: 12 received placebo and 12 received raloxifene hydrochloride 60 mg once a day for 3 months. Baseline measurements of both groups included heart rate (HR), blood pressure (BP), visual acuity, contrast sensitivity and intraocular pressure (IOP) for both eyes. A comprehensive ocular blood flow (OBF) assessment was obtained for each patient in a randomly chosen study eye. Retinal blood flow data was obtained using confocal scanning laser Doppler flowmetry [Heidelberg Retinal Flowmeter (HRF)]. Color Doppler imaging (CDI) was used to assess retrobulbar hemodynamics in the ophthalmic, central retinal, short nasal and temporal posterior ciliary arteries. Baseline vision and hemodynamics in post-menopausal subjects were compared using paired Student's t tests, and the percentage change in baseline versus 3-month parameters was analyzed. RESULTS: There were no statistically significant differences between 3 months of raloxifene therapy and placebo in terms of age, HR, arterial or mean BP, visual acuity, contrast sensitivity, IOP or retinal or retrobulbar blood flow. CONCLUSION: Raloxifene therapy at 60 mg/day had no clinically significant impact on BP, IOP or OBF in post-menopausal women.

Age-related ocular vascular changes.

BACKGROUND: The global society is aging at an increasing rate, with a continually larger proportion of the population consisting of those over the age of 65. Age-related vascular changes have been demonstrated in ocular tissue, and the incidence and prevalence of diseases such as macular degeneration, glaucoma and vascular occlusive diseases increase significantly with age. METHODS: This article reviews the current body of literature examining age-associated ocular vascular changes, and summarizes the aggregate findings. We discuss the potential role of the aging vasculature in the etiology of age-associated ocular disease, focusing on glaucoma. RESULTS: Our working hypothesis is that although advancing age is a physiological phenomenon, there are stepwise hemodynamic and vascular changes that occur, predisposing the eye and other tissue beds to pathological conditions. Advancing age does not independently give rise to disease, but does generate increasingly vulnerable vascular beds that are susceptible to further insults. CONCLUSIONS: These results compel a need for further investigation of age-related changes in ocular physiology and pathophysiology.

Age-related macular degeneration and the aging eye.

Age-related macular degeneration (AMD) is an ocular disease that causes damage to the retinal macula, mostly in the elderly. Normal aging processes can lead to structural and blood flow changes that can predispose patients to AMD, although advanced age does not inevitably cause AMD. In this review, we describe changes that occur in the macular structure, such as the retinal pigment epithelium and Bruch's membrane, with advancing age and in AMD. The role of genetics in AMD and age-related changes in ocular blood flow that may play a role in the pathogenesis of AMD are also discussed. Understanding the pathophysiology of AMD development can help guide future research to further comprehend this disease and to develop better treatments to prevent its irreversible central vision loss in the elderly.

Dysfunctional regulation of ocular blood flow: A risk factor for glaucoma?

Primary open angle glaucoma (OAG) is a multifactorial optic neuropathy characterized by progressive retinal ganglion cell death and associated visual field loss. OAG is an emerging disease with increasing costs and negative outcomes, yet its fundamental pathophysiology remains largely undetermined. A major treatable risk factor for glaucoma is elevated intraocular pressure (IOP). Despite the medical lowering of IOP, however, some glaucoma patients continue to experience disease progression and subsequent irreversible vision loss. The scientific community continues to accrue evidence suggesting that alterations in ocular blood flow play a prominent role in OAG disease processes. This article develops the thesis that dysfunctional regulation of ocular blood flow may contribute to glaucomatous optic neuropathy. Evidence suggests that impaired vascular autoregulation renders the optic nerve head susceptible to decreases in ocular perfusion pressure, increases in IOP, and/or increased local metabolic demands. Ischemic damage, which likely contributes to further impairment in autoregulation, results in changes to the optic nerve head consistent with glaucoma. Included in this review are discussions of conditions thought to contribute to vascular regulatory dysfunction in OAG, including atherosclerosis, vasospasm, and endothelial dysfunction.