Purpose The origin of retinal venous pulsations has been a matter of debate for some time. One classical explanation to the origin of these pulsations has been that the cardiac cycle induces systolic peaks in the intraocular pressure (IOP) which leads to decreases in retinal vein diameters. Recently, theoretical concepts have been published which postulate that IOP changes during the pulse cycle is not the primary driving force for venous pulsation, and hence, predict that the retinal vein diameter is indeed reduced during IOP diastole. The aim of the study was to test this hypothesis in a clinical trial. Subjects and Methods Continuous IOP and retinal vessel analyser (RVA) measurements were taken from 21 subjects, ages 20 to 30 years, with no known ophthalmologic diseases, while connected to a standard electrocardiograph (ECG). With this methodology, average and synchronised curves for the pulse cycle of IOP and retinal vessel pulsations were calculated for each subject. Each pulse cycle was standardised to 50 timepoints, which enabled direct phase shift comparisons. Results All subjects showed comparable results. Close to the optic disc (within 0 to 1.5 optic disc diameters away from the disc), retinal arteries led with the first peak at the 16/50 pulse cycle position, followed by IOP peak at the 23/50 cycle position, and then by veins at the 26/50 cycle position. Conclusion The present method indeed shows that retinal veins do not collapse when the IOP is highest, on the contrary, IOP and retinal vein diameters seem to be in phase, which lends support to the hypothesis that IOP is not the major driving force of the retinal vein pulsations.

Background Lowering intraocular pressure (IOP) is a mainstay of glaucoma therapy. It is, however, still an open question whether a comparable level of long-term IOP lowering achieved by different medications results in comparable protection for the retinal ganglion cells. The purpose of this study was to retrospectively analyze glaucoma damage progression in two cohorts of primary open-angle glaucoma patients with different and unchanged therapy over a period of 3 years, and the main objective of this study was to determine possible differences in terms of structural [retinal nerve fiber layer thickness (RNFL)] and functional [visual field (VF)] outcome. Patients and Methods The retrospective observational cohort analysis compared two differently treated groups of glaucoma patients with their original, at study entry, topical therapy unchanged over 3 years. The main endpoint was the time course of RNFL thickness and VF mean defect (MD). Results Twenty-one eyes were included in each group. The first group (21 eyes) was on a fixed combination of timolol and dorzolamide twice a day and the second group on one drop of prostaglandin analog, either latanoprost alone (15 eyes) or travoprost alone (6 eyes), in an unchanged regimen over a period of 3 years. IOP in mmHg at baseline and at 36 months was 11.9 ± 2.4 and 13.0 ± 2.1 in the first, and 12.9 ± 3.0 and 14.1 ± 3.2 in the second group, respectively. RNFL thickness values in micrometers were at baseline and at 36 months 77.8 ± 12.3 and 76.6 ± 15.2 in the first, and 77.5 ± 15.2 and 72.8 ± 14.5 in the second group, respectively. VF MD in dB were 1.7 ± 2.5 and 1.2 ± 2.9 in the first, and 0.9 ± 2.3 and 0.7 ± 2.6 in the second group, respectively. Conclusion Both groups had comparable baseline, as well as mean overall IOP. However, the course of IOP levels over time was different in the two groups, showing earlier and more pronounced long-term drift in the prostaglandin analog-treated group. RNFL thickness was comparable at baseline, however, RNFL thinning over time was more pronounced in the prostaglandin analog-treated group. There were no statistical differences between the groups in terms of VF MD at baseline and over time.

Purpose To analyse the amplitude of vessel pulsation in the retina and to determine whether constriction of the vessels by oxygen would decrease their pulsation amplitude and could thus be used to quantify the rigidity of the retinal vessels. Patients and Methods The study included 20 healthy young subjects. With the RVA (retinal vessel analyser), we aimed to quantify vessel pulsations under normal and hyperoxic conditions. Electrocardiographic (ECG)-gated RVA was used for this purpose, with change in vessel pulsation as the primary endpoint and shift in vessel pulsation during the heart cycle as the secondary endpoint. Furthermore, we assessed the correlation between the amplitude of retinal vessel wall pulsation and blood pressure. Descriptive statistics, paired t-tests, and correlation analysis were applied. Results Retinal veins in proximity to the optic disc demonstrated the highest pulsation amplitude under all conditions. All retinal vessels significantly constricted under hyperoxic conditions. There was no significant change in the amplitude of vessel pulsation nor a significant shift in the pulsation cycle under hyperoxic conditions in the examined cohort. No correlation was found between systemic blood pressure parameters and amplitude of retinal vessel wall pulsation or any change in this. Conclusion ECG-gated RVA recording is not able to detect any relevant change in vessel pulsation behaviour under oxygen, despite clearly observed vasoconstriction in retinal vessels. New approaches are necessary to reliably quantify the rigidity of the retinal vessels.