Effect of Upper Body Position on Arterial Stiffness: Influence of Hydrostatic Pressure and Autonomic Function
Authors: Schroeder Elizabeth C , Hilgenkamp Thessa , Rosenberg Alexander J , White Daniel W , Baynard Tracy , Fernhall Bo 
Published: November 2023

Conventional markers of arterial stiffness, such as carotid beta‐stiffness index, are traditionally obtained in the supine position. In the seated position, it is not known if correcting for hydrostatic pressure is an adequate adjustment for estimation of beta‐stiffness index or if other factors need to be considered, such as autonomic modulation.

Objective

To determine if the change in arterial stiffness in a seated position is due to the effects of gravity alone or if there is an additional effect of autonomic modulation after correcting for changes in hydrostatic pressure.

Methods

Thirty young participants (male=15, 24 ± 4 years, 25.6 ± 3.9 kg/m2) were randomly positioned at 0°, 45°, and 72° angles (semi‐recumbent position). Beat‐to‐beat blood pressure, carotid blood pressure (cBP), beta‐stiffness index, and carotid diameters were measured at each position after 5 min rest. The gravitational height correction was determined by measuring the vertical fluid column distance (mmHg), between the heart and the carotid artery. Beta‐stiffness index was calibrated using three different 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). Method 3 was implemented under the assumption that pressures from the supine to the seated position only change due to the effects of gravity. LFSAP was analyzed as a marker of sympathetic activity.

Results

See table. Beta stiffness did not increase if not corrected for hydrostatic pressure changes. Arterial stiffness indices based on method 2 were not significantly different from the one based on method 3(p=0.65). LFSAP increased in more upright positions (p<0.05) but diastolic diameter relative to diastolic pressure did not change (p>0.05).

Conclusions

The change in arterial stiffness in Method 2 did not differ from Method 3, presumably indicating that the beta stiffness index increases with change in position are pressure dependent, despite the apparent increase in vascular sympathetic modulation. This is supported by the lack of change in diameter relative to diastolic pressure.

0°
45°
72°

Heart rate, bpm
58 (9)a
61 (11)
62 (11)

Height Correction, mmHg
0 (0)a
−11 (3)b
−16 (3)

Carotid SBP, mmHg (Method 1)
116 (13)a
122 (15)
122 (12)

Carotid DBP, mmHg (Method 1)
74 (8)a
78 (7)
78 (6)

Carotid SBP height corrected, mmHg (Method 2)
116 (13)a
110 (15)b
105 (12)

Carotid DBP height corrected, mmHg (Method 2)
74 (8)a
66 (7)b
61 (6)

Carotid SBP theoretical. mmHg (Method 3)
116 (13)a
105 (13)b
99 (13)

Carotid DBP theoretical, mmHg (Method 3)
74 (8)a
63 (8)b
58 (8)

Beta stiffness (Method 1)
4.1 (1.3)
4.0 (1.5)
4.0 (1.2)

Beta stiffness height corrected (Method 2)
4.1 (1.3)b
4.6 (1.7)
4.8 (1.5)

Beta stiffness theoretical (Method 3)
4.1 (1.3)a
4.7 (1.6)b
5.0 (1.7)

Diastolic diameter, mm
6.1 (0.8)a
5.7 (0.7)b
5.6 (0.7)

Diastolic diameter/Carotid DBP height corrected, mm/mmHg
0.08 (0.02)
0.09 (0.01)
0.09 (0.01)

Relative diameter, %
11.7 (3.3)
11.7 (3.1)
12.2 (3.7)

LFSAP
6.4 (4.7)a
11.6 (6.6)
13.1 (10.1)

significantly different from all other positions, p<0.05

significantly different from 72°, p<0.05

Data presented as mean (SD). SBP: systolic blood pressure; DBP: diastolic blood pressure