Effect of upper body position on arterial stiffness: Influence of hydrostatic pressure andautonomic function
PublisherJournal of Hypertension
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Objective: To evaluate changes in arterial stiffness with positional change and whether the stiffness changes are due to hydrostatic pressure alone or if physiological changes in vasoconstriction of the conduit arteries play a role in the modulation of arterial stiffness. Methods: Thirty participants’ (male=15, 24±4 years) upper bodies were positioned at 0°, 45°, and 72° angles. Pulse wave velocity (PWV), cardio-ankle vascular index (CAVI), carotid beta-stiffness index, carotid blood pressure (cBP), and carotid diameters were measured at each position. A gravitational height correction was determined using the vertical fluid column distance (mmHg) between the heart and carotid artery. Carotid beta-stiffness was calibrated using three methods: 1) non-height corrected cBP of each position, 2) height corrected cBP of each position, 3) height corrected cBP of the supine position (theoretical model). LFSAP was analyzed as a marker of sympathetic activity. Results: PWV and CAVI increased with position (p<0.05). Carotid beta-stiffness did not increase if not corrected for hydrostatic pressure. Arterial stiffness indices based on Method 2 were not different from Method 3 (p=0.65). LFSAP increased in more upright positions (p<0.05) but diastolic diameter relative to diastolic pressure did not (p>0.05). Conclusion: Arterial stiffness increases with a more upright body position. Carotid betastiffness needs to be calibrated accounting for hydrostatic effects of gravity if measured in a seated position. It is unclear why PWV increased as this increase was independent of blood pressure. No difference between Method 2 and 3 presumably indicates that the beta-stiffness increases are only pressure dependent, despite the increase in vascular sympathetic modulation.