posted on 2018-07-03, 00:00authored byEC SCHROEDER, AJ ROSENBERG, TIM HILGENKAMP, DW WHITE, T BAYNARD, B FERNHALL
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.