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      Diurnal Variation of the Incidence of Symptomatic Branch Retinal Vein Occlusion

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          Aim: To investigate the diurnal variation that is related to the incidence of branch retinal vein occlusion (BRVO). Methods: This is a cross-sectional study. 72 consecutive patients who were newly diagnosed with BRVO were precisely questioned about the time of their symptom onset. The clinical history, systemic illnesses, ocular findings, and body mass index were obtained for each patient. Results: Analysis of the diurnal variation of symptom onset showed a distribution with the peak in the period from 6 a.m. to noon compared with all the other time periods (p < 0.001). Multivariate analysis showed that involvement of the superior retina was the only factor that influenced the onset time of BRVO. Conclusion: Patients with symptomatic BRVO frequently noted their visual deterioration in the morning, which is the same as the other types of ocular and systemic vascular disease. Our results may be helpful for understanding the pathophysiology of BRVO. Our findings require conformation and further studies on this subject are certainly warranted.

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          Most cited references 6

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          Pathophysiology and hemodynamics of branch retinal vein occlusion.

          To describe the pathophysiologic and the hemodynamic changes associated with branch retinal vein occlusion (BRVO) on the basis of selected angiographic observations from a cohort of patients with BRVO and related anomalies of retinal blood flow. Retrospective, observational case series. A total of 250 patients with incipient or manifest BRVO and 5 patients with related anomalies. Color and red-free gray-scale fundus photography and intravenous fluorescein angiography. Morphologic signs of disturbed retinal blood flow. All occlusions occurred at arteriovenous crossing sites where the artery is positioned anterior to the vein. Presumptive precursor abnormalities of blood flow at arteriovenous crossings include turbulence and upstream venous dilation. After the onset of BRVO, the clinical course is determined by the location of the BRVO in relation to the fovea, the extent of the involved venous drainage area, and the collateral drainage capacity from the area with compromised venous drainage to the adjacent areas of intact venous drainage. Collateral maturation occurs over a period of 6 to 24 months after the onset of BRVO, when a transient retinal edema may be seen that has a preponderance for foveal involvement because the perifoveal area has the highest density of preformed collaterals between adjacent venous drainage areas. The treatment of BRVO may possibly benefit from a refined angiographic analysis of the process of collateral formation and new treatment methods aimed at accelerating the process of collateral maturation.
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            Circadian variation in the onset of unstable angina and non-Q-wave acute myocardial infarction (the TIMI III Registry and TIMI IIIB).

            Circadian variation has been demonstrated in several types of acute cardiovascular disease, including acute myocardial infarction (AMI), sudden cardiac death, silent ambulatory ischemia, and thrombotic stroke. In contrast, no diurnal variation was observed in 1 study of non-Q-wave AMI, and limited data are available for unstable angina. To assess whether circadian variation is present in unstable angina and non-Q-wave AMI, we examined the time of onset of ischemic pain in 7,731 patients who were prospectively identified in the Thrombolysis in Myocardial Ischemia (TIMI) III Registry, 3,318 of whom were enrolled in the prospective study, and in 1,473 patients enrolled in the TIMI IIIB trial. A circadian variation in the onset of pain was observed, with an increase in the number of patients experiencing the onset of pain in the morning hours between 6 A.M. and 12 noon (p <0.001). This circadian variation was observed both in patients with unstable angina and in those with evolving non-Q-wave AMI. A similar circadian pattern was observed in all subgroups tested. These findings were confirmed in the TIMI IIIB trial and complement previous studies suggesting that circadian variation exists in the onset of the full spectrum of myocardial ischemic syndromes.
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              Role of Nocturnal Arterial Hypotension in Optic Nerve Head Ischemic Disorders

              Objective: To investigate the role of nocturnal arterial hypotension, intraocular pressure (IOP) and heart rate in optic nerve head (ONH) ischemic disorders, and the effects of systemic factors and topical β-blocker eye-drops on nocturnal arterial hypotension and heart rate. Methods: We investigated prospectively, by 24-hour ambulatory blood pressure (BP) monitoring and diurnal curve of the IOP, 275 white patients with anterior ischemic optic neuropathy (AION – 114), normal tension glaucoma (NTG – 131) and primary open angle glaucoma (POAG – 30). Results: Hourly average BP data analyses showed a significantly greater drop in mean diastolic BP (p < 0.009) at night in NTG than AION. Cases with visual field deterioration had significantly (p = 0.05) lower minimum nighttime diastolic BP. Arterial hypertensives on oral hypotensive therapy showed a significantly lower mean nighttime systolic BP (p = 0.006) and larger mean percentage drop in systolic (p < 0.0001), diastolic (p = 0.0009) and mean (p < 0.0001) BPs. Normotensives and hypertensives without therapy had no such difference. IOP showed no significant correlation with visual field deterioration in any of these conditions. Patients using β-blocker eyedrops, compared with those not using them, had greater percentage drop in diastolic BP (p = 0.028), lower minimum nighttime diastolic BP (p = 0.072) and lower minimum nighttime heart rate (p = 0.002). Conclusions: Findings of our study suggest that nocturnal hypotension, by reducing the ONH blood flow below a crucial level during sleep in a vulnerable ONH, may play a role in the pathogenesis of AION and glaucomatous optic neuropathy (GON) and progression of visual loss in them. Thus, nocturnal hypotension may be the final insult in a multifactorial situation.

                Author and article information

                S. Karger AG
                June 2007
                20 June 2007
                : 221
                : 4
                : 251-254
                Department of Ophthalmology, Korea University College of Medicine, Seoul, Korea
                101927 Ophthalmologica 2007;221:251–254
                © 2007 S. Karger AG, Basel

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                Figures: 1, Tables: 1, References: 14, Pages: 4
                Original Paper


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