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DOI: 10.1055/a-1085-9250
Analysis of Retinal Vessel Pulsations with Electrocardiographic Gating
Analyse der Gefäßpulsationen in der Netzhaut mittels EKG-VerankerungPublication History
received 15 September 2019
accepted 26 November 2019
Publication Date:
04 March 2020 (online)
![](https://www.thieme-connect.de/media/klimo/202004/lookinside/thumbnails/10-1055-a-1085-9250_kl0113-1.jpg)
Abstract
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.
Zusammenfassung
Hintergrund Die Herkunft und die dahinterstehenden genauen Mechanismen der Pulsationen von retinalen Venen sind bis dato umstritten. Eine klassische Erklärung ihres Ursprungs war, dass der Herzzyklus systolische Spitzen im Augeninnendruck induziert, was zu einer Reduktion des Durchmessers führt. Ein vor Kurzem publiziertes theoretisches Modell geht jedoch davon aus, dass nicht der Augendruck die Hauptantriebskraft für die Venenpulsation ist und dass somit eine Reduktion der Venendurchmesser während der Augendruckdiastole vorkommen kann. Das Ziel dieser Studie war, diese Hypothese in einem klinischen Versuch zu überprüfen.
Methoden und Probanden Kontinuierliche IOP und Retinal-Vessel-Analyzer-Messungen (RVA-Messungen) wurden an 21 gesunden Probanden zwischen 20 und 30 Jahren ohne ophthalmologische Erkrankungen gemacht, während sie mit einem EKG verbunden waren. Mit dieser Methode konnten gemittelte und synchronisierte Pulsationskurven von dem Augendruck und den Netzhautgefäßen für jeden Probanden berechnet werden. Jeder Zyklus wurde auf 50 Zeitpunkte standardisiert, was einen direkten Vergleich der zeitlichen Verschiebungen ermöglicht hat.
Ergebnisse Alle Probanden zeigten vergleichbare Ergebnisse. In der Papillennähe (entfernt von 0 – 1,5 Papillendurchmesser vom Papillenrand) führen Netzhautarterien mit ihrer Spitze an Position 16/50, gefolgt vom Augeninnendruck mit seiner Druckspitze bei 23/50 und dann von den Netzhautvenen an der Position 26/50 im Zyklus.
Schlussfolgerung Die angewendete Methode zeigt, dass in der Tat der Venendurchmesser in der Retina nicht zum Zeitpunkt des höchsten Augendruckes am kleinsten ist, sondern eher umgekehrt – dass ihre Zyklen praktisch phasengleich sind. Dies Ergebnisse unterstützen die Hypothese, dass der Augeninnendruck nicht die hauptsächliche Antriebskraft für die Netzhautvenenpulsationen ist.
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