Before interpreting corneal biomechanical parameters, it seems important to adjust the measured data for their underlying influencing factors. Glaucoma patients with lower adjusted CH and CRF probably have more advanced disease and should, therefore, be treated more aggressively and monitored more carefully and frequently.
ABSTRACT.Purpose: To evaluate the nocturnal blood pressure (BP) dipping-pattern in patients with manifest primary open-angle glaucoma (POAG) and to find possible associations with the severity of visual field damage. Methods: A number of 314 patients suffering from POAG were consecutively enrolled in this cross-sectional hospital-based study. Each patient had diurnal intraocular pressure (IOP) measurements, 24-hr BP monitoring and computerized perimetry with the Humphrey 30-2 SITA Standard program. Inclusion criteria were a mean IOP of less than 15 mmHg with fluctuations of less than 5 mmHg and a visual acuity of at least 20/40. One eye was randomly selected. Based on the night-day BP ratio, a mean arterial nocturnal BP drop of less than 10% was considered as non-dipping, between 10% and 20% as physiological dipping and of more than 20% as over-dipping. Results: Glaucoma patients with daytime systemic normotension on the average had more visual field loss in the over-dipper group (MD = À 16.6 dB, IQR = À18.9 to À2.7 dB) than glaucoma patients with daytime systemic hypertension, who had less visual field defects in the over-dipper group (MD = À3.9 dB, IQR = À6.2 to À1.9 dB) (p = 0.004). This result was also found taking age, glaucoma duration, visual acuity, gender, systemic and topical medication as covariates into account. Conclusions: To judge the nocturnal BP situation of an individual patient, it is important to do this in relation to the daytime BP level. Twenty-four-hour BP evaluation might be important for all patients with POAG, as nocturnal BP could be a modifiable risk factor for glaucoma severity and progression.Key words: 24-hr ambulatory blood pressure -nocturnal blood pressure dipping -nocturnal safety range -ocular perfusion pressure -open-angle glaucoma -systemic hypertension -visual field severity Acta Ophthalmol. 2015: 93: e621-e626
A significant amount of research effort is being carried out by the research community to increase the scope and usefulness of wireless sensor networks; to optimise life time by developing energy efficient power management, self-organising, medium access and routing protocols; and to reduce the cost of sensing nodes so that dense and robust deployment is possible. Though much has already been achieved, currently the cost of commercially available wireless sensor nodes is considerable and the wide applicability of proposed or existing protocols is still under investigation. One essential problem associated with cost or wide applicability of protocols is that sensor networks are application-specific. Protocols and in-network algorithms are optimised for particular sensing tasks. On the other hand, in research environments researchers would like to experiment not with a single application but with many applications. Considering the not-so-cheap sensing nodes available on the market and the management overhead of deploying wireless sensor networks, it is not economical or efficient to dedicate wireless sensor networks just to a single application, not at present at any rate. We therefore propose a middleware that enables researchers to experiment with multiple applications while providing them with essential in-network functionalities to satisfy individual application's requirements. The middleware cleanly separates sensing from network management so that application developers can obtain data from the wireless sensor networks without having to deal with management concerns.
Experimental studies suggested that statins attenuate vascular AT1 receptor responsiveness. Moreover, the augmented excessive pressor response to systemic angiotensin II infusions in hypercholesterolemic patients was normalized with statin treatment. In 12 hypercholesterolemic patients, we tested the hypothesis that statin treatment attenuates angiotensin II-mediated vasoconstriction in hand veins assessed by a linear variable differential transducer. Subjects ingested daily doses of either atorvastatin (40 mg) or positive control irbesartan (150 mg) for 30 days in a randomized and cross-over fashion. Ang II–induced venoconstriction at minute 4 averaged 59%±10% before and 28%±9% after irbesartan (mean ± SEM; P<0.05) compared to 65%±11% before and 73%±11% after 30 days of atorvastatin treatment. Plasma angiotensin levels increased significantly after irbesartan treatment (Ang II: 17±22 before vs 52±40 pg/mL after [p = 0.048]; Ang-(1–7): 18±10 before vs 37±14 pg/mL after [p = 0.002]) compared to atorvastatin treatment (Ang II: 9±4 vs 11±10 pg/mL [p = 0.40]; Ang-(1–7): 24±9 vs 32±8 pg/mL [p = 0.023]). Our study suggests that statin treatment does not elicit major changes in angiotensin II-mediated venoconstriction or in circulating angiotensin II levels whereas angiotensin-(1–7) levels increased modestly. The discrepancy between local vascular and systemic angiotensin II responses might suggest that statin treatment interferes with blood pressure buffering reflexes.Trial RegistrationClinicalTrials.gov NCT00154024
Optic nerve disease can occur from a variety of different causes, with vascular, inflammatory or toxic pathologies. In such cases, it is hardly possible to clarify the aetiology. These diseases of the optic nerve are usually accompanied by progressive loss of visual field and visual impairment. We report a case of a 74-year-old woman complaining of loss of visual acuity, visual and blurred vision in the left eye in 2010. We made the diagnosis of non-arteritic ischemic optic neuropathy (NAION). With steroid therapy, there was an improvement in both visual acuity and visual field defects. But if an attempt was made to reduce steroids, her condition progressed. Except for a very small optic disk and arterial hypotension, there were no typical risk factors for NAION. We started treatment with methotrexate (MTX), with a starting dose of 10 mg per week, and observed the patient over two years. Using MTX therapy, the swelling of the optic nerve head and visual field loss were reversible, so we increased the dose of MTX up to 15 mg/week. Steroid therapy could be stopped and the patient's visual acuity and visual field have now been stable for two years. There was no visible pallor in the optic nerve head, as normally occurs after AION, so we considered different underlying pathologies, including autoimmune disease. There were no adverse events with MTX therapy. If the course of the disease is atypical, the pathology may include an autoimmune component. Immunosuppressive MTX therapy may be started in order to avoid long-term steroid use. It may then be possible to maintain a stable visual field and prevent remitting episodes.
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