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Fabrice Moret, Wolf A. Lagrèze, Charlotte M. Poloschek, Michael Bach; Time of Collapse of Spontaneous Venous Pulsation. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6861.
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The spontaneous venous pulsation is a negative marker for elevated intraocular pressure and papilledema. Its relationship to the venous outflow resistance is also of interest in the context of glaucoma. At this time, pulsation's etiology remains unclear. A key element to elucidate the pulsation mechanism is the time at which collapse occurs with respect to the heart cycle, but previous reports are contradictory. We seek here to assess this question using quantitative measurements of both vein diameters and arteries's lateral displacements; the later being used as marker of ocular systole time.
We recorded 4-s fundus sequences with a near-infrared SLO in 12 subjects of age 22 to 31 years and with normal ocular status. Image sequences were co-registered, cleaned from microsaccades and filtered via a principal component analysis (PCA) to remove non-pulsatile dynamic features. Time courses of maximal arterial lateral displacements and of venous diameters at sites of spontaneous venous pulsation or proximal to the disk were derived. We analyzed time courses from both raw and PCA-filtered data.
Signals in seven subjects offered recognizable arterial pulsatile waveforms and were analyzed. Signal waveforms presented the strongest interest. Veins diameter is not just binary: either open or collapsed; No single collapse is observed over time, instead the venous signal appears as a damped and delayed replica of the arterial signal. The "collapse" is thus a normal trough as observed in arterial pressure waveforms. Waveforms and delays vary significantly between subjects but delays between waveform up-slope feet are always positive and never exceed arterial systole duration.
On this young cohort, the results support the traditional view: venous "collapse" occurs near ocular arterial systole. Diameter's waveforms show no "collapse" as such but rather a delayed arterial pressure waveform. Waveforms and limited positive delays suggest that the arterial pressure pulsation may be carried over the retinal microcirculation and that intraocular pressure pulse - if involved at all - may not be a primary actor in venous pulsation generation.
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