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Article

Physiological Mechanism of Pulsatility of Portal Venous Flow in Healthy Adults

by
Airi Onoda
1,
Michito Murayama
2,*,
Moe Wadayama
1,
Sumika Kobayashi
1,3,
Maho Tsukamoto
1,4,
Takahito Iwai
4,5,
Satomi Omotehara
4,5,
Yusuke Kudo
4,5,
Mutsumi Nishida
5,6 and
Sanae Kaga
2,5,*
1
Graduate School of Health Sciences, Hokkaido University, N12, W5, Kita-ku, Sapporo 060-0812, Japan
2
Department of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, N12, W5, Kita-ku, Sapporo 060-0812, Japan
3
Department of Laboratory Medicine, Hokkaido Cardiovascular Hospital, S27, W13, 1-30, Chuo-Ku, Sapporo 064-8622, Japan
4
Division of Laboratory and Transfusion Medicine, Hokkaido University Hospital, N14, W5, Kita-ku, Sapporo 060-8648, Japan
5
Diagnostic Center for Sonography, Hokkaido University Hospital, N14, W5, Kita-ku, Sapporo 060-8648, Japan
6
Management Strategy Department, Hokkaido University Hospital, N14 W5, Kita-ku, Sapporo 060-8648, Japan
*
Authors to whom correspondence should be addressed.
Appl. Sci. 2025, 15(17), 9334; https://doi.org/10.3390/app15179334
Submission received: 15 July 2025 / Revised: 21 August 2025 / Accepted: 21 August 2025 / Published: 25 August 2025
(This article belongs to the Section Applied Biosciences and Bioengineering)
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Abstract

Portal venous (PV) flow Doppler velocimetry assesses venous congestion in heart failure, showing PV pulsatility due to backward transmission of right atrial pressure (RAP) through the sinusoids. However, PV pulsatility has also been observed under physiological conditions. We aimed to elucidate the mechanisms and contributing factors of PV pulsatility in healthy adults. Pulsed-wave Doppler recordings of the hepatic venous (HV) and PV flow were obtained with electrocardiography. A- and V-wave velocities and their timings relative to the P- and R-waves (P-HVA, R-HVV) were measured from the HV waveforms. From PV waveforms, atrial and ventricular systolic descent flow velocities and their timings (P-PVA, R-PVV) were measured. The PV pulsatility index (VPI) was calculated. There were no differences between P-PVA and P-HVA, and between R-PVV and R-HVV, indicating similar waveforms. Seventy-nine percent of participants showed a VPI ≥ 0.3, with a higher VPI in younger vs. older participants (0.7 vs. 0.3, p < 0.01). Only age was independently associated with VPI (β = −0.56, p < 0.01). PV pulsatility was common in healthy adults, suggesting RAP transmission via the sinusoids; this physiological phenomenon was attenuated with aging. These findings highlight the importance of considering age-related physiological changes when interpreting the PV flow.

1. Introduction

The pulsed-wave Doppler ultrasonographic evaluation of portal venous (PV) flow waveforms is used to assess the pathophysiological features associated with diffuse liver disease [1,2,3,4] or the severity of venous congestion in patients with heart failure [5]. Recently, several studies have highlighted the clinical relevance of the PV flow Doppler velocimetry in emergency medicine [6,7,8]. In patients with heart failure showing venous congestion, elevated right atrial pressure (RAP) is transmitted retrogradely through the sinusoids to the PV, reducing the systolic PV flow, and thereby increasing its pulsatility [9]. By contrast, under physiological conditions, such as those observed in healthy individuals, the PV flow is considered a minimally pulsatile continuous flow [9]. However, a few studies have demonstrated a pulsatile PV flow even in healthy adults [10,11]. Therefore, although PV flow pulsatility is recognized as a sign of venous congestion in heart failure, recent studies have reported pulsatility in healthy individuals, raising questions about its underlying physiological mechanisms. Accordingly, the features of PV flow in healthy individuals remain controversial. Furthermore, the mechanisms underlying pulsatile PV flow in healthy individuals and the factors influencing the PV flow remain unclear.
We hypothesized that pulsatile PV flow in healthy individuals may result from a mechanism similar to that observed in patients with heart failure, namely, the retrograde transmission of RAP via the sinusoids. We also hypothesized that inconsistencies in the features of the PV flow in healthy individuals [9] might be attributable to the impact of aging on PV flow pulsatility. To test these hypotheses, we performed pulsed-wave Doppler ultrasonography in younger and older healthy participants to compare the PV flow waveforms with hepatic arterial and venous flow velocity waveforms, including hepatic venous (HV) flow waveforms, which mirror the RAP waveforms. Therefore, this study aims to investigate the physiological mechanisms underlying the pulsatility of the PV flow in healthy individuals and to determine the factors influencing PV flow pulsatility.

2. Materials and Methods

2.1. Study Population

This prospective study recruited 74 participants, including students from a Japanese national university aged 18–28 years (young participants), and members of the Silver Human Resource Centers, aged > 60 years (older participants). The Silver Human Resource Centers promote community engagement and provide a sense of purpose for older adults through work. Individuals participating in these centers are generally healthy older adults. The participants were recruited between May 2023 and September 2024. The eligible participants underwent abdominal ultrasonography, transient elastography, and echocardiography. The exclusion criteria were as follows: (1) history of cardiovascular disease (n = 2), (2) abnormal echocardiographic findings (n = 3), (3) suspected hepatic steatosis based on B-mode ultrasonography (both hepatorenal contrast and liver brightness) and/or controlled attenuation parameter [CAP] ≥ 275 [12] (n = 10), and (4) poor PV flow images (n = 3). Ultimately, 56 healthy participants (30 younger and 26 older) were eligible for this study (Figure 1).
This study was approved by the Ethics Committee of Hokkaido University Faculty of Health Sciences (approval number: 23-5). Informed consent was obtained from all participants prior to their participation in this study. All the study procedures were performed in accordance with the principles of the Declaration of Helsinki.

2.2. Abdominal Ultrasonography

Abdominal ultrasonography was performed using an Aplio 500/i700 system equipped with a PVT-375BT/PVI-475BX probe (Canon Medical Systems, Otawara, Japan) with the participants in a supine position. The participants fasted for at least 4 h before ultrasonography was performed. The diameter of the left liver lobe was measured in front of the abdominal aorta, and the diameter of the right liver lobe was measured in front of the right kidney and on the anterior clavicular line [13]. The HV flow, which mirrors the RAP waveforms [9], the hepatic arterial (HA) flow, and the PV flow, was recorded using pulsed-wave Doppler images with a simultaneous electrocardiogram recording. Breath-holding at shallow expiration was used for all venous and arterial flow measurements. The Doppler beam was directed to the hepatic vein, hepatic artery, and PV with an incident angle of <60°, and an angle-correction technique was used for velocity measurements. For the HV flow waveform recordings, a sample volume gate was set at approximately 3–5 mm, and placed at approximately 2–3 cm distal to the inferior vena cava (IVC) [14,15]. The HA flow waveforms were measured by identifying the proper hepatic artery branching from the common hepatic artery [16], and the sample volume gate was set to more than two-thirds of the vessel diameter. The PV flow waveforms were measured by identifying the main PV near the hepatic hilum after the confluence of the splenic and superior mesenteric veins in the subcostal region [16]. The sample volume gate was set to more than two-thirds of the vessel diameter [16]. The maximum and minimum flow velocities (Vmax and Vmin, respectively) of the PV flow were measured, and the portal venous pulsatility index (VPI) was calculated as (maximum − minimum)/maximum frequency shift [17]. In accordance with the previous studies, pulsatility was defined using two cutoff values: a portal VPI ≥ 0.3 indicating mild abnormality and ≥ 0.5 indicating severe abnormality [6,18].

2.2.1. Analysis of the HV, HA, and PV Flow Waveforms

From the HV flow waveforms, we measured the velocity of the atrial systolic retrograde wave (HVA), which corresponds to the RAP a wave and appears corresponding to the P-wave on the electrocardiogram, as well as the velocity of the ventricular end-systolic wave (HVV), which corresponds to the RAP v wave and occurs corresponding to the end of the T wave. The time from the start of the P- and R-waves on the electrocardiogram to the HVA and HVV waves on the HV flow waveform was also measured, respectively (P-HVA and R-HVV) (Figure 2a). The time from the R-wave to the peak systolic velocity was measured from the HA flow waveforms (R-HAS) (Figure 2b). From the PV flow waveforms, we measured the velocities of the atrial-systolic descent (PVA), which follows the P-wave on the electrocardiogram; the ventricular-systolic descent (PVV), which appears after the end of the T-wave; and the systolic forward flow (PVS). In addition, we measured the time from the P- or R-wave to the PVA (P-PVA), PVV (R-PVV), and PVS (R-PVS) (Figure 2c). These temporal measurements were performed to investigate whether the HV flow waveforms, which reflect the RAP waveforms, and the HA flow waveforms influence the PV flow waveforms. For quantitative purposes, waveform components above the baseline were measured as positive values, and those below the baseline as negative values. All temporal analysis parameters represent the mean of three beats and were corrected for RR intervals.

2.2.2. Preload Stress Pulsed-Wave Doppler Sonography

To assess the changes in each waveform associated with positional change, passive leg raising maneuvers were performed, and the HVA, HVV, PVA, and PVV were remeasured from the HV and PV flow waveforms. Leg raising was performed with the hip joint flexed at 45°, while the trunk and bed remained in the horizontal position [19]. Each waveform was recorded immediately after leg raising and completed within 5 min [20].

2.2.3. Transient Elastography

CAP and liver stiffness measurements with vibration-controlled transient elastography were conducted using FibroScan® 502 (Echosens, Paris, France). The examination was considered successful when 10 valid measurements with a success rate of at least 60% were conducted and the interquartile range was <30% of the median liver stiffness measurement value [21].

2.3. Echocardiography

Transthoracic echocardiography was performed using an Aplio 500/i700 system equipped with a PST-30BT/PSI-30BX probe (Canon Medical Systems, Otawara, Japan) with the participants in a supine or left lateral decubitus position. A comprehensive echocardiographic examination was performed in accordance with the American Society of Echocardiography guidelines to evaluate cardiac chamber morphology and function [22]. The end-diastolic right ventricular (RV) diameter was measured at the basal level of the RV inflow using RV-focused views. The RV systolic function was assessed using the tricuspid annular plane systolic excursion, which was measured by placing an M-mode cursor through the tricuspid annulus of the RV free wall in the modified apical four-chamber image [23]. The IVC dimensions and respiratory changes were measured using subcostal longitudinal images. We estimated the RAP as 3 mm Hg when the IVC diameter was ≤21 mm and collapsed ≥ 50% and as 15 mm Hg when the IVC diameter was >21 mm and collapsed < 50%. For participants who were unable to adequately sniff, the criterion of 20% respiratory change during rest breathing was used [14]. In cases where the IVC diameter and collapse did not meet these criteria, the RAP was classified as 8 mmHg, and an additional evaluation using secondary indices was performed. If no secondary indices were present, the RAP was downgraded to 3 mmHg; if a secondary index was present, the RAP was reclassified to 15 mmHg. If uncertainty remained, an intermediate value of 8 mmHg was used [14].

2.4. Statistical Analysis

Statistical analyses were performed using the standard statistical software (IBM SPSS ver. 26 for Windows, IBM Co., Armonk, NY, USA). All numerical data are presented as mean ± standard deviation, and categorical variables are expressed as numbers (percentage). For comparisons of continuous variables between the two groups, Student’s t-test was used for normally distributed data, and the Wilcoxon rank-sum test was used for non-normally distributed data. A paired t-test was used to investigate whether the HV and HA flow waveforms influence the PV flow waveforms, and to compare the changes in the HV and PV flow waveforms during a positional change. Multiple linear regression analysis was used to assess the associations with several confounding variables hypothesized to influence the portal VPI (age, sex, body mass index [BMI], body surface area, IVC diameter, IVC respiratory change, liver size, and CAP). Parameters with p values < 0.05 in the univariable analyses were incorporated into the multivariable model to identify independent determinants of the portal VPI. Two-sided significance levels of 0.05 were used for all analyses.

3. Results

3.1. Baseline Characteristics

Of the 74 participants in our study, 59 met the inclusion criteria. Ultimately, 56 healthy participants for whom the PV flow could be measured were included in the final analysis (Figure 1). A comparison of the baseline characteristics between the younger and older participants is summarized in Table 1. Among the 56 participants, 30 were young (22 ± 2 years old, 19–28 years old) and 26 were old (70 ± 5 years old, 60–79 years old). The older participants had higher blood pressure, smaller left ventricular end-diastolic dimension, and greater interventricular septum thickness and left ventricular posterior wall thickness than the younger participants. The IVC diameter was larger in the younger participants than in the older participants; however, none of the participants in either group had an elevated RAP of 15 mmHg. While the liver size was similar in both the groups, CAP was significantly higher in the older participants than in the younger participants.

3.2. Temporal Analysis of the PV, HV, and HA Flow Waveforms

Of the 56 healthy participants, PVA was observed in 23 (41%), and PVV was observed in 42 (75%). The timing of PVA and PVV appearance were near to those of HVA and HVV, respectively (P-PVA vs. P-HVA: 0.17 ± 0.08 vs. 0.14 ± 0.03, p = 0.109; R-PVV vs. R-HVV: 0.42 ± 0.09 vs. 0.43 ± 0.06, p = 0.246) (Figure 3 and Table 2), suggesting an association between the RAP and the PV flow. By contrast, the R-PVS was shorter than the R-HAS (0.20 ± 0.07 vs. 0.24 ± 0.06, p = 0.048), indicating no contribution of the HA flow to the PV flow (Figure 3 and Table 3).

3.3. Changes in the HV and PV Flow Waveforms During Passive Leg Raising

Among the 30 young participants, there were no significant changes in the HV and PV flow waveforms between the supine position and the leg-raising conditions (Figure 4). By contrast, among the 26 older participants, the HVA significantly increased during leg raising and the HVV showed an increasing trend. Corresponding to these changes in the HV flow waveforms, both the PVA and PVV in the PV flow waveforms significantly increased during leg raising (Figure 5 and Figure 6).

3.4. Frequency of PV Flow Pulsatility and Its Differences Between Younger and Older Participants

A portal VPI ≥ 0.3 was observed in 29 younger (97%) and 15 older (58%) participants (p = 0.029). A portal VPI ≥ 0.5 was observed in 27 younger (90%) and 4 older (15%) participants (p < 0.001). Figure 7 shows two examples of the portal VPI ≥ 0.3 in the younger and older participants. The portal VPI was significantly higher in the younger participants than in the older participants (0.65 ± 0.15 vs. 0.34 ± 0.16, p < 0.001).

3.5. Determinants of the Portal VPI

The relationships between the portal VPI and age, sex, heart rate, BMI, body surface area, and echocardiographic and abdominal ultrasonographic parameters are summarized in Table 4. Higher age, higher BMI, smaller IVC diameter, larger hepatic left lobe vertical diameter, and higher CAP were associated with a lower portal VPI. In a multivariable regression analysis, including age, BMI, IVC diameter, liver size, and CAP, only age (β = −0.56, p < 0.001) was selected as an independent determinant of the portal VPI.

4. Discussion

This study had five major findings. First, the timings of PVA and PVV were near to those of HVA and HVV, respectively, and the Doppler waveforms of the PV flow were similar to those of the HV flow. Second, the PVS appeared earlier than the HAS, and no temporal correspondence was observed between the HA and PV flows. Third, in older participants, changes in the HV flow waveforms induced by passive leg raising were mirrored by changes in the PV flow waveforms. Fourth, the PV flow was pulsatile in many healthy participants (VPI ≥ 0.3: 79%; VPI ≥ 0.5: 55%). Finally, the pulsatility of the PV flow decreased with aging.

4.1. Relationship Between the RAP and Pulsatility of the PV Flow

Abu-Yousef et al. reported that 11 healthy young volunteers without heart disease exhibited pulsatile flow in the PV, resembling the HV flow waveforms. However, respiratory changes in the PV flow were less pronounced compared with those observed in the HV waveforms, and the relationship between the PV and HV flows remained unclear. While their study suggested that even a low RAP may contribute to pulsatility in the PV flow, the mechanism remained unclear [24]. Nihei et al. conducted an experimental study using minipigs and demonstrated that the PV flow waveforms changed in response to the IVC flow. They concluded that the PV flow was influenced by the IVC flow via the sinusoids [25]. Although their study provided experimental evidence for the effect of RAP on the PV flow, this has not been confirmed in humans.
In the present study, a detailed temporal analysis revealed that the timings of PVA and PVV were near to those of HVA and HVV, respectively, which reflect the RAP waves, suggesting an association between the RAP and the PV flow. Furthermore, in older participants, the PV flow changed in conjunction with the HV flow by preload augmentation. These findings would support the hypothesis that the PV flow waveforms may be shaped by the HV flow waveforms and thus by the RAP waveforms. This suggests that pulsatility of the PV flow may occur not only in a pathologically elevated RAP [9,17,26,27] but under normal RAP conditions via sinusoidal transmission. Although indirect, this is the first study to demonstrate the potential influence of sinusoidal RAP transmission on the PV flow waveforms in humans.

4.2. Relationship Between Periportal Vasculature and Pulsatility of the PV Flow

Sugimoto et al. visually evaluated pulsed-wave Doppler tracings and reported that 22 of 33 participants without liver disorders showed systolic spike waves in the PV flow corresponding to the HAs, suggesting that the HA flow may directly influence the PV flow through the PV vasa vasorum [28]. By contrast, in a clamping experiment in minipigs, Nihei et al. showed that temporary interruption of the HA flow did not alter the PV flow waveforms, indicating that the HA flow does not contribute to PV flow pulsatility [25]. In our study, a temporal analysis showed that the PVS appeared significantly earlier than the HAS, supporting the absence of a causal influence of the HA flow on the PV flow. Other vascular factors potentially affecting the PV flow include mesenteric arterial pulsations transmitted via the capillary vessels of the intestine, as reported in an experimental study using minipigs [25]. However, owing to the anatomical differences between pigs and humans, and the strong dampening effect of capillary beds [29], whether such transmission occurs in humans remains uncertain.

4.3. Patient Characteristics Influencing Pulsatility of the PV Flow

Gallix et al. reported an inverse correlation between the portal VPI and the BMI in 23 healthy young-to-middle-aged volunteers, which was attributed to the correlation between the BMI and intraabdominal pressure [10]. Consistent with their findings, our study also demonstrated that a higher BMI was associated with a lower portal VPI; however, in the multivariable analysis, age, not the BMI, was selected as an independent determinant of the portal VPI (Table 4). Age-related histological changes in the hepatic lobule, including pseudocapillarization—characterized by endothelium thickening, the development of basal lamina, and collagen deposition in the Disse space—have been recognized and are associated with a narrowing of the sinusoidal lumens [30,31,32]. In addition, age-related lipid accumulation in the liver has been documented [33,34]. Balci et al. found that the portal VPI decreased in steatotic livers [2] and Akamatsu et al. attributed this to sinusoidal compression due to steatosis and hepatocyte expansion [35]. Mohammadi et al. reported that steatotic liver is accompanied by a decrease in hepatic sinusoidal vascular compliance, which leads to a decrease in the portal VPI [36]. Although our study excluded participants with steatotic liver disease, similar structural changes may occur in older participants in the present study. Therefore, age-related histological changes in the hepatic sinusoids may potentially impair the sinusoidal transmission of the RAP due to decreased hepatic vascular compliance, thereby reducing the portal VPI in older participants.

4.4. Clinical Implications

In daily clinical practice, pulsed a Doppler analysis of the PV flow is used to evaluate venous congestion in heart failure and severity of diffuse liver disease [6,9]. Bouabdallaoui et al. reported that a high portal VPI at discharge was associated with increased all-cause mortality in patients with heart failure [5]. Simultaneously, Beaubien-Souligny et al. demonstrated that the portal VPI could predict acute kidney injury after cardiac surgery [6]. Our study demonstrated that the PV flow can be pulsatile, even in individuals with a normal RAP, such pulsatility is present in many healthy participants, and it declines with age. These findings emphasize the importance of interpreting the portal VPI in the context of age. Physiological pulsatile PV flow in young healthy adults may resemble the pathological pulsatility observed in patients with congestive heart failure, potentially leading to misinterpretation. Therefore, when using the PV flow to assess venous congestion in patients with heart failure, clinicians should consider patient age in conjunction with other clinical findings. Taken together, our findings provide valuable physiological data on the PV flow in healthy adults and contribute to a more accurate interpretation of PV abnormalities in clinical settings.

4.5. Limitations

This study has several limitations. First, although we made efforts to maintain the Doppler incident angle below 60 degrees by tilting the probe and/or applying pressure, it is possible that the angle may have affected the PV velocities. Second, because the study population consisted of healthy individuals, right heart catheterization was not performed; therefore, a direct comparison between the RAP waveforms and the PV flow was not possible. Although we compared the PV flow with the HV flow, which reflects the RAP waveforms, and inferred the influence of the RAP on the PV flow, this interpretation remains speculative. Additionally, since invasive measurements were not performed, we cannot completely rule out the possibility of an elevated RAP (two young individuals were classified with an estimated RAP of 8 mmHg). However, all participants underwent comprehensive echocardiography, and no findings suggestive of an elevated RAP were observed. Third, blood tests were not performed. We excluded participants suspected of having steatotic liver disease based on B-mode abdominal ultrasonography and/or transient elastography and confirmed that no participants exceeded a liver stiffness of 7.0 kPa [37]. However, the possibility of including participants with diffuse liver disease cannot be ruled out. Fourth, a histopathological evaluation was not performed. Thus, we were unable to confirm age-related structural changes in the hepatic sinusoids, such as pseudocapillarization or lipid accumulation in the liver, particularly for older participants. Fifth, the sample size was small. Future studies should involve larger populations to further validate the current findings. Sixth, middle-aged participants were not included. Future studies involving a wider age range of healthy individuals may help clarify the age at which the pulsatility of the PV flow begins to decline. Finally, since most young participants showed a high portal VPI, the mean flow velocity of the PV flow may be a more appropriate parameter than VPI for the diagnosis or prognostication of patients with heart failure. However, further studies are needed to determine whether parameters, such as mean PV flow velocity, are indeed more informative than VPI for evaluating venous congestion in clinical practice.

5. Conclusions

In healthy adults, the PV flow waveforms frequently demonstrated pulsatility and resembled the HV flow waveforms. Our findings suggest that such pulsatility occurs via RAP transmission through the hepatic sinusoids, even in the absence of RAP elevation. Furthermore, this transmission appeared to be attenuated with age, resulting in a lower portal VPI in older participants. When interpreting the portal VPI as a parameter of venous congestion or in the assessment of diffuse liver disease, the physiological characteristics of the PV flow should be considered. Further studies involving larger cohorts are warranted to validate these findings and clarify their clinical implications.

Author Contributions

Conception/design of the study: A.O., M.M. and S.K. (Sanae Kaga); management of the participants: A.O., M.W. and S.K. (Sumika Kobayashi); collection and interpretation of the data: A.O., M.M., M.W., S.K. (Sumika Kobayashi), M.T. and S.K. (Sanae Kaga); analysis and interpretation of the data: A.O., M.M., M.W., S.K. (Sumika Kobayashi), M.T., T.I., S.O., Y.K., M.N. and S.K. (Sanae Kaga); drafting the article: A.O. and M.M.; critical discussion of the results: M.T., T.I., S.O., Y.K., M.N. and S.K. (Sanae Kaga); critical revision of the manuscript: M.M., T.I., S.O., Y.K., M.N. and S.K. (Sanae Kaga); funding: A.O. All authors have read and agreed to the published version of the manuscript.

Funding

This study was supported by the Support for Pioneering Research Initiated by the Next Generation (SPRING) program of the Japan Science and Technology Agency at Hokkaido University (Grant Number: JPMJSP2119) for Airi Onoda.

Institutional Review Board Statement

This study was approved by the Ethics Committee of Hokkaido University Faculty of Health Sciences (approval number: 23-5). Informed consent was obtained from all participants prior to their participation in this study. All the study procedures were performed in accordance with the principles of the Declaration of Helsinki.

Informed Consent Statement

Informed consent was obtained from all subjects involved in this study.

Data Availability Statement

The original contributions presented in this study are included in the article. Further inquiries can be directed to the corresponding author.

Acknowledgments

The authors thank the members of the Cardiovascular Ultrasound Laboratory at Hokkaido University (https://hokudai-hs-echolab.com) (accessed on 15 July 2025) for their assistance in conducting this study. We also thank all participants from the Silver Human Resource Center for their contributions. We would like to thank Editage (www.editage.jp) (accessed on 15 July 2025) for the English language editing.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
PVPortal venous
RAPRight atrial pressure
HVHepatic venous
CAPControlled attenuation parameter
HAHepatic arterial
IVCInferior vena cava
VPIVenous pulsatility index
HVAA-wave in hepatic venous flow
HVVV-wave in hepatic venous flow
P-HVATime from the P-wave to the A-wave in hepatic venous flow
R-HVVTime from the R-wave to the V-wave in hepatic venous flow
R-HASTime from the R-wave to peak systolic velocity in hepatic arterial flow
PVAAtrial-systolic descent in portal venous flow
PVVVentricular-systolic descent in portal venous flow
PVSSystolic forward flow in portal venous flow
P-PVATime from the P-wave to atrial-systolic descent in portal venous flow
R-PVVTime from the R-wave to ventricular systolic descent in portal venous flow
R-PVSTime from the R-wave to peak systolic forward flow in portal venous flow
RVRight ventricular
BMIBody mass index

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Figure 1. Participant selection flowchart. PV, portal venous.
Figure 1. Participant selection flowchart. PV, portal venous.
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Figure 2. Temporal analysis of the hepatic venous (a), hepatic arterial (b), and portal venous (c) flow waveforms. HVA, velocities of the A-wave in hepatic venous flow; P-HVA, time from the P-wave to the A-wave in hepatic venous flow; HVV, velocities of the V-wave in hepatic venous flow; P-HVV, time from the R-wave to the V-wave in hepatic venous flow; R-HAS, time from the R-wave to the peak systolic velocity in hepatic arterial flow; PVA, velocities of atrial-systolic descent in portal venous flow; P-PVA, time from the P-wave to atrial-systolic descent in portal venous flow; PVV, velocities of the ventricular-systolic descent in portal venous flow; R-PVV, time from the R-wave to ventricular systolic descent in portal venous flow; R-PVS, time from the R-wave to peak systolic forward flow in portal venous flow.
Figure 2. Temporal analysis of the hepatic venous (a), hepatic arterial (b), and portal venous (c) flow waveforms. HVA, velocities of the A-wave in hepatic venous flow; P-HVA, time from the P-wave to the A-wave in hepatic venous flow; HVV, velocities of the V-wave in hepatic venous flow; P-HVV, time from the R-wave to the V-wave in hepatic venous flow; R-HAS, time from the R-wave to the peak systolic velocity in hepatic arterial flow; PVA, velocities of atrial-systolic descent in portal venous flow; P-PVA, time from the P-wave to atrial-systolic descent in portal venous flow; PVV, velocities of the ventricular-systolic descent in portal venous flow; R-PVV, time from the R-wave to ventricular systolic descent in portal venous flow; R-PVS, time from the R-wave to peak systolic forward flow in portal venous flow.
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Figure 3. Results of temporal analysis of the portal venous, hepatic venous (a), and hepatic arterial (b) flow waveforms. P-PVA, time from the P-wave to atrial-systolic descent in portal venous flow; R-PVV, time from the R-wave to ventricular-systolic descent in portal venous flow; P-HVA, time from the P-wave to the A-wave in hepatic venous flow; R-HVV, time from the R-wave to the V-wave in hepatic venous flow; R-PVS, time from the R-wave to peak systolic forward flow in portal venous flow; R-HAS, time from the R-wave to peak systolic velocity in hepatic arterial flow.
Figure 3. Results of temporal analysis of the portal venous, hepatic venous (a), and hepatic arterial (b) flow waveforms. P-PVA, time from the P-wave to atrial-systolic descent in portal venous flow; R-PVV, time from the R-wave to ventricular-systolic descent in portal venous flow; P-HVA, time from the P-wave to the A-wave in hepatic venous flow; R-HVV, time from the R-wave to the V-wave in hepatic venous flow; R-PVS, time from the R-wave to peak systolic forward flow in portal venous flow; R-HAS, time from the R-wave to peak systolic velocity in hepatic arterial flow.
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Figure 4. Changes in the hepatic and portal venous flow waveforms during passive leg raise in young participants. HVA, A-wave in hepatic venous flow; HVV, V-wave in hepatic venous flow; PVA, atrial-systolic descent in portal venous flow; PVV, ventricular-systolic descent in portal venous flow.
Figure 4. Changes in the hepatic and portal venous flow waveforms during passive leg raise in young participants. HVA, A-wave in hepatic venous flow; HVV, V-wave in hepatic venous flow; PVA, atrial-systolic descent in portal venous flow; PVV, ventricular-systolic descent in portal venous flow.
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Figure 5. Changes in the hepatic and portal venous flow waveforms during passive leg raise in older participants. HVA, A-wave in hepatic venous flow; HVV, V-wave in hepatic venous flow; PVA, atrial-systolic descent in portal venous flow; PVV, ventricular-systolic descent in portal venous flow.
Figure 5. Changes in the hepatic and portal venous flow waveforms during passive leg raise in older participants. HVA, A-wave in hepatic venous flow; HVV, V-wave in hepatic venous flow; PVA, atrial-systolic descent in portal venous flow; PVV, ventricular-systolic descent in portal venous flow.
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Figure 6. A representative case showing changes in the hepatic and portal venous flow waveforms during passive leg raise in older participants. HVA and HVV are increased during leg raising (HVA: 6.2 cm/s to 15.4 cm/s, HVV: −9.7 cm/s to −9.5 cm/s). Corresponding to these changes in the HV flow waveforms, both PVA and PVV are increased during leg raising (PVA: −28.6 cm/s to −18.4 cm/s, PVV: −23.5 cm/s to −21.8 cm/s). HVA, A-wave in hepatic venous flow; HVV, V-wave in hepatic venous flow; PVA, atrial-systolic descent in portal venous flow; PVV, ventricular-systolic descent in portal venous flow.
Figure 6. A representative case showing changes in the hepatic and portal venous flow waveforms during passive leg raise in older participants. HVA and HVV are increased during leg raising (HVA: 6.2 cm/s to 15.4 cm/s, HVV: −9.7 cm/s to −9.5 cm/s). Corresponding to these changes in the HV flow waveforms, both PVA and PVV are increased during leg raising (PVA: −28.6 cm/s to −18.4 cm/s, PVV: −23.5 cm/s to −21.8 cm/s). HVA, A-wave in hepatic venous flow; HVV, V-wave in hepatic venous flow; PVA, atrial-systolic descent in portal venous flow; PVV, ventricular-systolic descent in portal venous flow.
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Figure 7. Two representative cases showing a portal VPI ≥ 0.3 in younger and older participants: (a) the case of a young participant showing a portal VPI of 0.70; portal VPI = (20.1 − 6.0)/20.1 = 0.70; (b) the case of an older participant showing a portal VPI of 0.45; portal VPI = (29.0 − 16.0)/29.0 = 0.45. VPI, venous pulsatility index; PVA, atrial-systolic descent in portal venous flow; PVV, ventricular-systolic descent in portal venous flow.
Figure 7. Two representative cases showing a portal VPI ≥ 0.3 in younger and older participants: (a) the case of a young participant showing a portal VPI of 0.70; portal VPI = (20.1 − 6.0)/20.1 = 0.70; (b) the case of an older participant showing a portal VPI of 0.45; portal VPI = (29.0 − 16.0)/29.0 = 0.45. VPI, venous pulsatility index; PVA, atrial-systolic descent in portal venous flow; PVV, ventricular-systolic descent in portal venous flow.
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Table 1. Clinical characteristics of the study participants.
Table 1. Clinical characteristics of the study participants.
VariableYounger Participants
(n = 30)		Older Participants
(n = 26)		p Value
Baseline characteristics
Age (years)22 ± 2 70 ± 5<0.001
Sex, male, n (%)15 (50)15 (42)>0.999
Height (cm)166 ± 10163 ± 80.121
Weight (kg)58 ± 1058 ± 100.987
Body mass index (kg/m2)21 ± 222 ± 20.112
Body surface area (m2)1.64 ± 0.181.61 ± 0.170.552
Heart rate (beats/min)59 ± 862 ± 90.147
Systolic blood pressure (mmHg)107 ± 9121 ± 17<0.001
Diastolic blood pressure (mmHg)65 ± 778 ± 11<0.001
Echocardiography
Left ventricular end-diastolic dimension (mm)47 ± 444 ± 50.031
Left ventricular end-systolic dimension (mm)29 ± 428 ± 30.165
Left ventricular ejection fraction (%)68 ± 768 ± 30.809
Interventricular septum thickness (mm)7.3 ± 0.78.0 ± 1.00.004
Left ventricular posterior wall thickness (mm)7.1 ± 0.87.6 ± 1.00.027
Right ventricular basal dimension (mm)36 ± 437 ± 60.533
Tricuspid annular plane systolic excursion (mm)25 ± 424 ± 40.390
IVC diameter during expiration (mm)18 ± 513 ± 3<0.001
IVC respiratory change (%)60 ± 965 ± 110.050
Estimated RA pressure, n (%)
15 mm Hg0 (0)0 (0)1.000
8 mm Hg2 (7)0 (0)0.184
3 mm Hg28 (93)26 (100)0.184
Abdominal ultrasonography
Hepatic left lobe vertical diameter (mm)47 ± 949 ± 130.546
Hepatic right lobe vertical diameter (mm)102 ± 9102 ± 110.773
Portal maximum flow velocity * (cm/s)46 ± 25 41 ± 280.430
Portal minimum flow velocity * (cm/s)15 ± 11 24 ± 140.007
Portal VPI 0.65 ± 0.150.34 ± 0.16<0.001
Portal VPI ≥ 0.3, n (%)29 (97)15 (58)0.029
Portal VPI ≥ 0.5, n (%)27 (90)4 (15)<0.001
PVA velocity (cm/s)−24 ± 17 −29 ± 180.514
PVV velocity (cm/s)−16 ± 11 −26 ± 160.017
PVS velocity (cm/s)−47 ± 27 −49 ± 380.859
Transient Elastography
Controlled attenuation parameter (dB/m)190 ± 34210 ± 300.022
Liver stiffness (kPa)4.3 ± 0.94.0 ± 1.00.327
Data are expressed as mean ± standard deviation or n (%). The p-values are from Student’s t-test or chi-squared test. * absolute value; IVC, inferior vena cava; RA, right atrial; VPI, venous pulsatility index; PVA, atrial-systolic descent in portal venous flow; PVV, ventricular-systolic descent in portal venous flow; PVS, systolic forward flow in portal venous flow.
Table 2. Temporal analysis of the portal and hepatic venous flow waveforms.
Table 2. Temporal analysis of the portal and hepatic venous flow waveforms.
NumberPortal Venous FlowHepatic Venous Flowp Value
P-PVA vs. P-HVA230.17 ± 0.080.14 ± 0.030.109
R-PVV vs. R-HVV410.42 ± 0.090.43 ± 0.060.246
Data are expressed as mean ± standard deviation. The p-values are from the paired t-test. P-PVA, time from the P-wave to atrial-systolic descent flow in portal venous flow; P-HVA, time from the P-wave to the A-wave in hepatic venous flow; R-PVV, time from the R-wave to ventricular-systolic descent flow in portal venous flow; P-HVV, time from the R-wave to the V-wave in hepatic venous flow.
Table 3. Temporal analysis of portal venous and hepatic arterial flow waveforms.
Table 3. Temporal analysis of portal venous and hepatic arterial flow waveforms.
NumberPortal Venous FlowHepatic Arterial Flowp Value
R-PVS vs. R-HAS340.20 ± 0.070.24 ± 0.060.048
Data are expressed as mean ± standard deviation. The p-values are from the paired t-test. R-PVS, time from the R-wave to peak systolic forward flow in portal venous flow; R-HAS, time from the R-wave to peak systolic velocity in hepatic arterial flow.
Table 4. Results of linear regression analysis to determine the portal VPI.
Table 4. Results of linear regression analysis to determine the portal VPI.
Dependent VariableUnivariableMultivariable
βp Valueβp Value
Age (years)−0.70<0.01−0.56<0.01
Sex, male, n (%)0.100.48
Heart rate (beats/min)−0.070.62
Body mass index (kg/m2)−0.40<0.01−0.220.10
Body surface area (m2)−0.080.54
IVC diameter during expiration (mm)0.330.010.150.22
IVC respiratory change (%)−0.230.09
Hepatic left lobe vertical diameter (mm)−0.320.02−0.160.15
Hepatic right lobe vertical diameter (mm)−0.140.30
Controlled attenuation parameter (dB/m)−0.320.02−0.010.94
Liver stiffness (kPa)0.200.13
IVC, inferior vena cava. No evidence of collinearity is found in this model (variance inflation factor < 5).
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Onoda, A.; Murayama, M.; Wadayama, M.; Kobayashi, S.; Tsukamoto, M.; Iwai, T.; Omotehara, S.; Kudo, Y.; Nishida, M.; Kaga, S. Physiological Mechanism of Pulsatility of Portal Venous Flow in Healthy Adults. Appl. Sci. 2025, 15, 9334. https://doi.org/10.3390/app15179334

AMA Style

Onoda A, Murayama M, Wadayama M, Kobayashi S, Tsukamoto M, Iwai T, Omotehara S, Kudo Y, Nishida M, Kaga S. Physiological Mechanism of Pulsatility of Portal Venous Flow in Healthy Adults. Applied Sciences. 2025; 15(17):9334. https://doi.org/10.3390/app15179334

Chicago/Turabian Style

Onoda, Airi, Michito Murayama, Moe Wadayama, Sumika Kobayashi, Maho Tsukamoto, Takahito Iwai, Satomi Omotehara, Yusuke Kudo, Mutsumi Nishida, and Sanae Kaga. 2025. "Physiological Mechanism of Pulsatility of Portal Venous Flow in Healthy Adults" Applied Sciences 15, no. 17: 9334. https://doi.org/10.3390/app15179334

APA Style

Onoda, A., Murayama, M., Wadayama, M., Kobayashi, S., Tsukamoto, M., Iwai, T., Omotehara, S., Kudo, Y., Nishida, M., & Kaga, S. (2025). Physiological Mechanism of Pulsatility of Portal Venous Flow in Healthy Adults. Applied Sciences, 15(17), 9334. https://doi.org/10.3390/app15179334

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