Analyzing biomechanical parameters of the cornea with glaucoma severity in open-angle glaucoma.

PURPOSE: The purpose was to investigate a possible association of corneal hysteresis (CH) and corneal resistance factor (CRF) with open-angle glaucoma and the severity of disease. METHODS: In this prospective cross-sectional study we recruited 86 open-angle glaucoma patients, 16 patients with ocular hypertension (OHT,) and 44 age-matched controls. Each participant had a complete glaucoma workup including measurements with the Ocular Response Analyzer and computerized perimetry with the Humphrey 30-2 SITA Standard program. Visual field damage was based on mean deviation (MD) and considered as early glaucomatous with a MD > - 6 dB, moderate glaucomatous between -6 and -12 dB and advanced glaucomatous < -12 dB. The association between ORA parameters, glaucoma, and disease severity was evaluated using univariate and multivariate linear regression analyses. RESULTS: There was a statistically significant correlation between the biomechanical parameters and intraocular pressure, central corneal thickness, axial length, and age. On average, glaucoma patients had the lowest adjusted CH (8.96 ± 1.43 mmHg) and CRF (9.07 ± 1.93 mmHg) values in comparison to OHT patients (CH: 10.2 ± 1.5 mmHg; CRF: 10.6 ± 2.1 mmHg) and controls (CH: 9.7 ± 1.4 mmHg; CRF: 10.2 ± 1.9 mmHg). This difference was statistically significant (CH: p = 0.003; CRF: p = 0.008). There was also a statistically significant difference in adjusted CH (p = 0.001) and CRF (p = 0.004) values between the controls and the visual field groups, with the lowest values being in the most advanced group. CONCLUSIONS: 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.

Nocturnal blood pressure in primary open-angle glaucoma.

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 = - 16.6 dB, IQR = -18.9 to -2.7 dB) than glaucoma patients with daytime systemic hypertension, who had less visual field defects in the over-dipper group (MD = -3.9 dB, IQR = -6.2 to -1.9 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.

Statin treatment in hypercholesterolemic men does not attenuate angiotensin II-induced venoconstriction.

UNLABELLED: 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 REGISTRATION: ClinicalTrials.gov NCT00154024.