The validity of carotid-femoral pulse wave velocity in the seated posture as an index of central arterial stiffness
This study demonstrated for the first time that the increase in carotid-femoral pulse wave velocity (cfPWV) observed in the seated posture is likely due to elevated transmural pressure (TMP) caused by increased hydrostatic pressure, rather than an actual rise in central arterial stiffness. Intraclas...
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Published in | American journal of physiology. Regulatory, integrative and comparative physiology Vol. 328; no. 2; pp. R145 - R153 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
American Physiological Society
01.02.2025
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Subjects | |
Online Access | Get full text |
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Summary: | This study demonstrated for the first time that the increase in carotid-femoral pulse wave velocity (cfPWV) observed in the seated posture is likely due to elevated transmural pressure (TMP) caused by increased hydrostatic pressure, rather than an actual rise in central arterial stiffness. Intraclass correlation analysis also showed a parallel upward shift in the regression line between supine and seated postures. This suggests that cfPWV values obtained in the seated position should be adjusted for hydrostatic pressure and TMP.
A previous study reported an increase in carotid-femoral pulse wave velocity (cfPWV) during an upright posture compared to the supine position, partly due to sympathetic activation. However, given that cfPWV is influenced by the transmural pressure (TMP) of the artery, which is elevated in the abdominal aorta in the seated posture due to the increased hydrostatic pressure. Thus, it remains unclear whether this increased cfPWV reflects a true rise in arterial stiffness or is simply a result of the elevated TMP. To assess the validity of cfPWV in the seated posture for arterial stiffness assessment, 20 young healthy subjects underwent arterial stiffness measurements in both the supine and seated positions. There were no significant differences in carotid artery compliance, β-stiffness index, and aortic characteristic impedance between the two positions ( P = 0.209–0.380). However, cfPWV was higher in the seated posture than the supine posture (5.4 ± 0.6 vs. 6.2 ± 0.8 m/s, P < 0.0001), showing a high intraclass correlation coefficient (ICC) between positions ( r = 0.841, P < 0.0001) and a parallel upward shift by 14% ( y = 1.01 x + 0.54). Moreover, cfPWV was correlated with TMP at the groin level ( r = 0.532, P = 0.0004), and after adjusting for TMP at the groin level using analysis of covariance (ANCOVA), the posture-related difference in cfPWV was no longer significant ( P = 0.867). These findings suggest that the increase in cfPWV observed in the seated posture is primarily due to elevated TMP caused by increased hydrostatic pressure, rather than a genuine rise in arterial stiffness. Consequently, cfPWV measurements taken in the seated posture may overestimate arterial stiffness unless they are appropriately adjusted for TMP.
NEW & NOTEWORTHY This study demonstrated for the first time that the increase in carotid-femoral pulse wave velocity (cfPWV) observed in the seated posture is likely due to elevated transmural pressure (TMP) caused by increased hydrostatic pressure, rather than an actual rise in central arterial stiffness. Intraclass correlation analysis also showed a parallel upward shift in the regression line between supine and seated postures. This suggests that cfPWV values obtained in the seated position should be adjusted for hydrostatic pressure and TMP. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 0363-6119 1522-1490 1522-1490 |
DOI: | 10.1152/ajpregu.00073.2024 |