Analysis of Retinal Vessel Pulsations with Electrocardiographic Gating.

Abstract

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. 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. 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. 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.