Systolic flow reversal pulmonary vein mitral regurgitation

Journal Article

Kiho Itakura,

Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences

,

1-2-3 Kasumi, Minami-ku

, Hiroshima 734-8551,

Japan

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Received:

28 November 2020

Editorial decision:

22 April 2021

Corrected and typeset:

13 August 2021

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  Kiho Itakura, Hiroto Utsunomiya, Hajime Takemoto, Kosuke Takahari, Yusuke Ueda, Kanako Izumi, Hiroki Ikenaga, Takayuki Hidaka, Yukihiro Fukuda, Yukiko Nakano, Prevalence, distribution, and determinants of pulmonary venous systolic flow reversal in severe mitral regurgitation, European Heart Journal - Cardiovascular Imaging, Volume 22, Issue 9, September 2021, Pages 964–973, https://doi.org/10.1093/ehjci/jeab098

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Abstract

Introduction

Pulmonary venous systolic flow reversal (PVSFR) is observed in severe mitral regurgitation (MR). Extended quantitation of MR is a prerequisite for surgical decision-making or a determinant of outcome. A normal pulmonary venous (PV) flow pattern as assessed by Doppler echocardiographic studies is biphasic with a combination of physiological events, which include right ventricular (RV) stroke volume, compliance of the pulmonary vasculature and left atrium (LA), and phasic changes in LA pressure.1–4 Previous studies have shown that this biphasic pattern actually reflects changes in LA pressure.2–4 Abnormal PV flow patterns have been described in patients with atrial fibrillation (AF), left ventricular (LV) systolic and diastolic dysfunction, constrictive pericarditis, PV obstruction, or significant mitral MR.5 Among them, some reports have examined the relationship between PVSFR and severe MR.6–9 However, most of these studies were based on transthoracic echo or only one of the four PVs was observed by transoesophageal echo. Therefore, this relationship has not been sufficiently examined. Which PVs are most likely to show PVSFR in patients with severe MR, to what extent all four PVSFRs are present in the same patient, and the relationship between presence of PVSFR and clinical symptoms or echocardiographic and haemodynamic parameters remain unclear. Transoesophageal echocardiography (TOE) is a useful modality for detailed and successful recording of all four PVs and providing each PV flow velocity, and it can also show a previously unavailable mechanism for estimating the haemodynamic effects of MR.

Therefore, this study aimed to evaluate the prevalence and distribution of transoesophageal Doppler-derived PVSFR in patients with severe MR. We also aimed to examine the effects of PVSFR in MR and to examine the relationship between the PVSFR profile and cardiac parameters.

Methods

Study population

We reviewed consecutive patients with severe MR who underwent TOE in Hiroshima University Hospital between January 2017 and March 2020. Severe MR was defined as MR with a >0.4 cm2 effective regurgitant orifice, >60 mL regurgitant volume, or >50% regurgitant fractions by transthoracic echocardiography (TTE).10 We divided these patients into three groups depending on the aetiology of MR as follows: (i) degenerative MR (DMR), (ii) ventricular functional MR (V-FMR), and (iii) atrial functional MR (A-FMR). The aetiologies were classified as DMR if MR was due to intrinsic valvular disease, V-FMR if MR was due to a primary abnormality of the LV, and A-FMR if the MR had a large LA for no reason except for long-standing AF. Clinical data were gathered from the patients’ clinical records. Heart rate and blood pressure were measured at the end of each echocardiographic examination. AF was recorded if the patient’s heart rhythm showed AF at TOE. Blood sample data that were obtained at the nearest TOE examination were collected. The protocol of this study was approved by the Institutional Review Board.

Transthoracic echocardiography

TTE was performed in all patients within 6 months from TOE by using commercially available equipment (iE33, Phillips; Artida and Artida2, Toshiba; Vivid7 and Vivid E9, GE). Assessment of the degree of MR was performed using the volumetric method, which was determined by quantitative Doppler and quantitative 2D echocardiography. The regurgitant volume, regurgitant fraction, and effective regurgitant orifice were then calculated. Other TTE measurements included LV volume using Simpson’s method and end-systolic LA volume using the biplane area-length method according to the American Society of Echocardiography (ASE) guideline.10 LA and LV volumes were indexed to the body surface area. The right atrial (RA) area at end-systole and RV area at end-systole or end-diastole were also measured, and the RV fractional area change (FAC) was calculated. The severity of tricuspid regurgitation (TR) was determined by integrative assessment using multiple parameters, such as the TR jet area, the ratio of the TR jet area to the RA area, continuous Doppler contour.

Transoesophageal echocardiography

Three-dimensional TOE with pulsed Doppler and colour flow imaging capabilities was performed using an iE33 ultrasound imaging system equipped with a fully sampled matrix-array transducer (X7-2t Live 3D transducer; Philips Medical Systems, Andover, MA, USA). This system provided successful recording of all four PV flows because of the posterior approach providing unimpeded interrogation of cardiac structures.

The left upper PV appeared at the lateral side of the LA appendage at a 60° angle. To obtain the left lower veins, the angle was set at 120° and the transducer was rotated counterclockwise. The left lower veins were visualized by advancing the probe from the position used for the left upper veins. When the transducer was widely rotated clockwise from the view of the left lower PV through the interatrial septal view at 120°, the right upper PV appeared. The right lower PV was observed at a 60° angle. In this view, the right upper and lower PVs appeared in the same window.1Figure1 shows representative PV colour Doppler of all four PVs. The sample volume in the PV was set to ∼1–2 cm above its entry into the LA and the pulsed-wave Doppler PV flow pattern was recorded. S wave was described several pattern and Figure 2 shows the types of PV flow that were observed. We divided PV flows into six types according to the shape of the S wave, as follows: (i) S dominant type; there is the S wave higher than D wave, (ii) D dominant type; there is the S wave lower than D wave, (iii) blunted S type; there is flat S wave, (iv) biphasic S type; there is negative S wave at end-systolic phase after positive S wave of the early systole, (v) mosaic S type; there is negative S wave at holosystolic phase and the S wave is mosaic pattern, and (vi) laminar S type; here is negative S wave at holosystolic phase and the S wave is laminar pattern. Of these, we defined the biphasic S, mosaic S, and laminar S types as PVSFR. The severity of MR was assessed by the 3D vena contracta area (3D-VCA), which was measured from 3D colour volume. Multiplanar reconstruction tools were used to orient orthogonal imaging planes (x and y) through the long axis of the MR jet and the z plane was adjusted perpendicularly through the narrowest area of the vena contracta. The VCA was then measured by manual planimetry of the colour Doppler signal according to the ASE guideline.10

Figure 1

Two-dimensional TOE of PV flow. Representative colour Doppler of each PV and how we detected these PVs. Evaluable PV Doppler flow was achieved in 96.8% of patients with MR. IAS, interatrial septum; LAA, left atrial appendage; Lt, left; PV, pulmonary venous; Rt, right; TOE, transoesophageal echocardiography.

Figure 2

PV Doppler flow patterns according to PVSFR. There are six types of PV flow pattern based on the shape of the S wave. Biphasic, mosaic, and laminar S types were defined as PVSFR. PV, pulmonary venous; PVSFR, pulmonary venous systolic flow reversal.

Invasive haemodynamic assessment

Seventy-nine (73.1%) patients had right heart catheter assessment performed. Catheter assessment was included in the analysis when it was assessed within 5 days of the TOE procedure. Patients underwent standard right heart catheterization from their right jugular vein, and pulmonary capillary wedge pressure (PCWP), pulmonary artery (PA) pressure, RA pressure, and cardiac output (CO) were measured using a balloon-tipped Swan-Ganz catheter. Mixed venous oxygen saturation (SvO2) was calculated by atrial oxygen saturation − (oxygen consumption/CO × haemoglobin × 13.4). CO was assessed by the Fick technique and indexed to the body surface area.

Statistical analysis

Standard statistical methods were used in this study. Significant differences were tested using the chi-square test or Fisher’s exact test for categorical variables. Categorical variables are reported as numbers with relative percentages. Continuous data are expressed as mean ± standard deviation or median (inter-quartile range), and were compared using ANOVA or the Wilcoxon test. Baseline clinical characteristics, TTE findings at baseline, and procedural and haemodynamic findings were included in univariate analysis. Multivariate analysis was performed with parameters that showed potentially significant in univariate analysis (P <0.1). A P value of <0.05 was considered to indicate statistical significance. Statistical analyses were performed using JMP 14 (SAS Institute, Cary, NC, USA).

Results

Patient characteristics

A total of 125 patients with severe MR underwent TOE at our institution. Only four (3.2%) patients were excluded because of unclear detection in all four PVs. After additional exclusion of patients who had severe MR combined with mitral stenosis (n = 1), infectious endocarditis (n = 3), systolic anterior movement due to hypertrophic cardiomyopathy (n = 3), and post-mitral valve replacement (n = 5), 108 patients [median age: 68.0 ± 12.7 years, women: 46 (42.6%)] were included in this study. Table 1 shows the baseline clinical characteristics of the patients. A total of 72 patients had DMR, 20 had V-FMR, and 16 had A-FMR. Patients with V-FMR and A-FMR had a higher New York Heart Association functional class and N-terminal pro-brain natriuretic peptide levels, and higher frequency of medication by diuretics than those with DMR. Seven (35%) patients with V-FMR had a previous history of coronary intervention.

Table 1

Baseline characteristics

Data are presented as mean ± SD, median (interquartile range), or n (%).

CABG, coronary artery bypass grafting; DBP, diastolic blood pressure; eGFR, estimated glomerular filtration rate; Hb, haemoglobin; NT-pro BNP, N-terminal pro-brain natriuretic peptide; NYHA, New York Heart Association functional class; PCI, percutaneous coronary intervention; SBP, systolic blood pressure.

Table 1

Baseline characteristics

Data are presented as mean ± SD, median (interquartile range), or n (%).

CABG, coronary artery bypass grafting; DBP, diastolic blood pressure; eGFR, estimated glomerular filtration rate; Hb, haemoglobin; NT-pro BNP, N-terminal pro-brain natriuretic peptide; NYHA, New York Heart Association functional class; PCI, percutaneous coronary intervention; SBP, systolic blood pressure.

Prevalence and distribution of PVSFR

Figure 3A shows the prevalence and distribution of PVSFR. The left upper PV had the lowest and the right upper PV has the highest prevalence of PVSFR. The difference of frequency of PVSFR in these two PVs was >1.5 times. Eighteen (16.7%) patients had PVSFR in all four PVs and 15 (13.9%) patients had no PVSFR. Seventy-five (69.5%) patients had one, two, or three PVSFRs, which meant that the four PVs in individuals did not match the appearance of PVSFR.

Figure 3

Overview of the study population. (A) Prevalence, extent, and distribution of PVSFR. The left upper PV has the lowest and the right upper PV has the highest representation of PVSFR. The appearance of PVSFR in 69.5% patients did not match the four PV flows. (B) Correlations of the number of PVSFRs with PCWP, 3D-VCA, and the CI. Mean PCWP and 3D-VCA showed a positive correlation, and the CI showed a negative correlation with the number of PVSFRs. CI, cardiac index; PCWP, pulmonary capillary wedge pressure; PVSFR, pulmonary venous systolic flow reversal; 3D-VCA, 3D vena contracta area.

Echocardiographic and haemodynamic determinants of the number of PVSFRs

The relationship between the number of PVSFRs and cardiac parameters in all patients is shown in Table 2 and Figure 3B. In univariate analysis, the 3D-VCA in MR, RV end-systolic area, RV systolic pressure, PA pressure (systole, diastole, mean), PCWP (a wave, v wave, mean), SvO2, and the cardiac index (CI) showed significant correlations with the number of PVSFRs. When these univariable determinants were entered into multiple stepwise linear regression analysis, 3D-VCA in MR (P <0.001) and mean PCWP (P =0.004) were independently associated with the number of PVSFRs (Table 3).

Table 2

Clinical characteristics and cardiac parameters according to the number of PVSFRs

Data are presented as mean ± SD, median (interquartile range), or n (%).

CI, cardiac index; CO, cardiac output; DBP, diastolic blood pressure; EF, ejection fraction; FAC, functional area change; LAVI, left atrial volume index; LV EDVI, left ventricular end-diastolic volume index; LV ESVI, left ventricular end-systolic volume index; MR 3D VCA, mitral regurgitation 3D vena contracta area; NT-pro BNP, N-terminal pro-brain natriuretic peptide; NYHA, New York Heart Association functional class; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVSFR, pulmonary venous systolic flow reversal; RA, right atrium; RAP, right atrial pressure; RV Ad, right ventricular diastolic area; RV As, right ventricular systolic area; RVP, right ventricular pressure; SvO2, mixed venous oxygen saturation.

Table 2

Clinical characteristics and cardiac parameters according to the number of PVSFRs

Data are presented as mean ± SD, median (interquartile range), or n (%).

CI, cardiac index; CO, cardiac output; DBP, diastolic blood pressure; EF, ejection fraction; FAC, functional area change; LAVI, left atrial volume index; LV EDVI, left ventricular end-diastolic volume index; LV ESVI, left ventricular end-systolic volume index; MR 3D VCA, mitral regurgitation 3D vena contracta area; NT-pro BNP, N-terminal pro-brain natriuretic peptide; NYHA, New York Heart Association functional class; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVSFR, pulmonary venous systolic flow reversal; RA, right atrium; RAP, right atrial pressure; RV Ad, right ventricular diastolic area; RV As, right ventricular systolic area; RVP, right ventricular pressure; SvO2, mixed venous oxygen saturation.

Table 3

Linear regression analysis for the number of PVSFRs

CI, cardiac index; CO, cardiac output; DBP, diastolic blood pressure; EF, ejection fraction; FAC, functional area change; LAVI, left atrial volume index; LV EDVI, left ventricular end-diastolic volume index; LV ESVI, left ventricular end-systolic volume index; MR 3D VCA, mitral regurgitation 3D vena contracta area; NT-pro BNP, N-terminal pro-brain natriuretic peptide; NYHA, New York Heart Association functional class; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVSFR, pulmonary venous systolic flow reversal; RA, right atrium; RAP, right atrial pressure; RV Ad, right ventricular diastolic area; RV As, right ventricular systolic area; RVP, right ventricular pressure; SvO2, mixed venous oxygen saturation.

Table 3

Linear regression analysis for the number of PVSFRs

CI, cardiac index; CO, cardiac output; DBP, diastolic blood pressure; EF, ejection fraction; FAC, functional area change; LAVI, left atrial volume index; LV EDVI, left ventricular end-diastolic volume index; LV ESVI, left ventricular end-systolic volume index; MR 3D VCA, mitral regurgitation 3D vena contracta area; NT-pro BNP, N-terminal pro-brain natriuretic peptide; NYHA, New York Heart Association functional class; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVSFR, pulmonary venous systolic flow reversal; RA, right atrium; RAP, right atrial pressure; RV Ad, right ventricular diastolic area; RV As, right ventricular systolic area; RVP, right ventricular pressure; SvO2, mixed venous oxygen saturation.

Prevalence and distribution of PVSFR stratified by aetiology of MR

PVSFR appeared more frequently in right PVs compared with left PVs in all aetiologies. In DMR, 56 (77.8%) patients had one, two, or three PVSFRs, which meant that they did not have a matched distribution of PVSFR in each PV. However, 12 (60.0%) patients with V-FMR had a matched distribution of PVSFR (0 or 4) in individuals. Patients with A-FMR had the highest frequency of PVSFR (Table 4 and Figure 4A).

Figure 4

Substudy results stratified by the aetiology of MR. (A) Prevalence, extent, and distribution of PVSFR stratified by the aetiology of MR. PVSFR appeared more frequently in right PVs compared with left PVs in all aetiologies. Bar graphs show the prevalence of the number of PVSFRs in each aetiology of MR. The horizontal axis shows the number of PVSFRs. In DMR, 77.8% patients did not have a matched distribution of PVSFR (1, 2, or 3) in individuals. In V-FMR, 60.0% patients had a matched distribution of PVSFR (0 or 4) in individuals. (B) Correlations of the number of PVSFRs with PCWP and 3D-VCA stratified by the aetiology of MR. DMR, degenerative MR; MR, mitral regurgitation ; PCWP, pulmonary capillary wedge pressure; PVSFR, pulmonary venous systolic flow reversal; V-FMR, ventricular functional MR; 3D-VCA, 3D vena contracta area.

Table 4

Prevalence of PVSFR and echocardiographic and haemodynamic data classified by the aetiology of MR

Data are presented as mean ± SD, median (interquartile range), or n (%).

A-FMR, atrial functional MR; CI, cardiac index; CO, cardiac output; DBP, diastolic blood pressure; DMR, degenerative MR; EF, ejection fraction; FAC, functional area change; LAVI, left atrial volume index; LV EDVI, left ventricular end-diastolic volume index; LV ESVI, left ventricular end-systolic volume index; MR 3D VCA, mitral regurgitation 3D vena contracta area; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PV, pulmonary venous; PVSFR, pulmonary venous systolic flow reversal; RA, right atrium; RAP, right atrial pressure; RV Ad, right ventricular diastolic area; RV As, right ventricular systolic area; RVP, right ventricular pressure; SvO2, mixed venous oxygen saturation; TR, tricuspid regurgitation; V-FMR, ventricular functional MR.

Table 4

Prevalence of PVSFR and echocardiographic and haemodynamic data classified by the aetiology of MR

Data are presented as mean ± SD, median (interquartile range), or n (%).

A-FMR, atrial functional MR; CI, cardiac index; CO, cardiac output; DBP, diastolic blood pressure; DMR, degenerative MR; EF, ejection fraction; FAC, functional area change; LAVI, left atrial volume index; LV EDVI, left ventricular end-diastolic volume index; LV ESVI, left ventricular end-systolic volume index; MR 3D VCA, mitral regurgitation 3D vena contracta area; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PV, pulmonary venous; PVSFR, pulmonary venous systolic flow reversal; RA, right atrium; RAP, right atrial pressure; RV Ad, right ventricular diastolic area; RV As, right ventricular systolic area; RVP, right ventricular pressure; SvO2, mixed venous oxygen saturation; TR, tricuspid regurgitation; V-FMR, ventricular functional MR.

Echocardiographic and haemodynamic determinants of the number of PVSFRs stratified by aetiology of MR

Echocardiographic and haemodynamic parameters based on the aetiology of MR are shown in Table 4. The frail or prolapse point of the mitral valve was in A2 or P2 in 45 (62.5%) patients, in A3 or P3 or the posterior commissure in 21 (29.2%) patients, and in A1 or P1 or the anterior commissure in six (8.3%) patients among those with DMR. Patients with V-FMR had the largest LV volume, lowest ejection fraction and 3D-VCA in MR, and highest PA pressure and PCWP. Patients with A-FMR had the largest biatrial volume and 3D-VCA in MR, lowest RV FAC, SvO2, and CI, and highest frequency of significant TR. Mean PCWP was still significantly correlated with the number of PVSFRs in patients with V-FMR but not in patients with DMR and A-FMR. Three-dimensional VCA was still significantly correlated with the number of PVSFRs in patients with DMR and A-FMR, but there was no correlation in patients with V-FMR (Figure 4B).

Type of PVSFR

Figure 2 shows the types of PV flow pattern according to the shape of the S wave. The S dominant type was present in 28/432 (6.5%), the D dominant type in 140/432 (32.4%), the blunted S type in 36/432 (8.3%), the biphasic S type in 62/432 (14.4%), the mosaic S type in 105/432 (24.3%), and the laminar S type in 61/432 (14.1%) patients with severe MR. The biphasic-type PVSFR was almost detected in patients with DMR. On the other hand, the laminar-type PVSFR appeared more frequently in functional MR aetiologies (Figure 5). Univariate and multivariate analyses for the presence of various types of PVSFR are shown in Table 5. If the patients had at least one biphasic-, mosaic-, or laminar-type PVSFR, the patients were divided into each (+) group. In univariate analysis, LAVI, mean PCWP, and CI were potentially associated with the presence of biphasic-type PVSFR (all P <0.1). Also, LAVI, MR 3D VCA, mean PCWP, and CI were potentially associated with the presence of mosaic-type PVSFR (all P <0.1). Furthermore, most parameters including LAVI, MR 3D VCA, RV FAC, mean PCWP, and CI, had a significant impact on the presence of laminar-type PVSFR (all P <0.01). When these univariable determinants were entered into multiple stepwise linear regression analysis, LAVI (P =0.003) for the presence of biphasic-type PVSFR, and RV FAC (P =0.02) and mean PCWP (P <0.001) for the presence of laminar-type PVSFR remained significant.

Figure 5

Substudy results stratified by the type of PVSFR. The prevalence of PVSFR is shown based on the type of PVSFR. Biphasic PVSFR was detected mostly in DMR and laminar PVSFR appeared in functional MR aetiologies. A-FMR, atrial functional mitral regurgitation; DMR, degenerative mitral regurgitation; PVSFR, pulmonary venous systolic flow reversal; V-FMR, ventricular functional mitral regurgitation.

Table 5

Univariate and multivariate analyses for the presence of various types of PVSFR

CI, cardiac index; LAVI, left atrial volume index; MR 3D VCA, mitral regurgitation 3D vena contracta area; ; PCWP, pulmonary capillary wedge pressure; PVSFR, pulmonary venous systolic flow reversal.

Table 5

Univariate and multivariate analyses for the presence of various types of PVSFR

CI, cardiac index; LAVI, left atrial volume index; MR 3D VCA, mitral regurgitation 3D vena contracta area; ; PCWP, pulmonary capillary wedge pressure; PVSFR, pulmonary venous systolic flow reversal.

Discussion

This is the first study to investigate the characteristics of PVSFR in four PVs in patients with severe MR. The main findings of the present study were as follows. (i) Four PV flows were detected by TOE in almost every patient. (ii) Appearance of PVSFR did not match the four PVs within many individuals. (iii) The number of PVSFRs was significantly correlated with the severity of MR and LA pressure, and this differed depending on the aetiology of MR. (iv) The shape of PVSFR was able to be divided into three types, and these three PVSFR shapes had different characteristics.

Characterization of PVSFR in previous studies

Approximately 60 years previously, blood flow through the pulmonary capillary vessels was suggested to be pulsatile.11 Since this time, evaluation of PV flow by Doppler echocardiography has been established as a useful indicator for evaluating LV diastolic dysfunction.12 PV flow is easily affected by age, heart rate, and pre-load, even in healthy subjects.2,13–15 Some studies have reported the presence of PVSFR in patients with severe MR.6–9 However, the design of these pilot studies had a small population and inherent limitations, such as no details on the aetiology of MR or detection of only one PV flow.

Prevalence, distribution, and determinants of PVSFR in severe MR

The appearance of PVSFR did not match the four PVs in ∼60% of patients with severe MR. Remarkably, the left upper PV, which is frequently used in TTE, has the lowest rate of PVSFR.16 On the other hand, the right upper PV, which is also easily detected in TTE, has the highest rate of PVSFR. This may be related to the direction of the MR jet because V-FMR and A-FMR have a relatively concentric jet. Because DMR also has a large proportion of P2 prolapse, the MR jet has a lower chance to flow to the medial or lateral side. There is a high probability that the straight jet from the A2–P2 coaptation line travels to the right PVs. A previous study showed that PV flow on the same side tends to have the same shape in patients with MR.17 This may also be related to the occasional condition of unilateral cardiogenic pulmonary oedema found in patients with severe MR.18

In the present study, 77.8% of patients with DMR and 68.7% of patients with A-FMR differed regarding the presence or absence of PVSFR in the four PVs, while 60% of patients with V-FMR had the same appearance of PVSFR in the four PVs. Patients with V-FMR also had a high frequency of laminar-type PVSFR. These differences among the aetiologies of MR could be due to the fundamental cause of PVSFR. As a whole, the number of PVSFRs was independently associated with not only MR 3D VCA but also mean PCWP (Table 3). When stratified by MR aetiology, the number of PVSFRs was well correlated with MR 3D VCA, which indicates the severity of MR, in patients with DMR and A-FMR, whereas in V-FMR, a strong relationship between the number of PVSFRs and mean PCWP, which is LA pressure, was observed (Figure 4B). Previous studies have reported that PV flow is greatly affected by LA pressure.19 Particularly in V-FMR, the cause of PVSFR would be associated with an increase in LA pressure, rather than direct insufflation.

We also focused on the shape of PVSFR because it seems to have different characteristics. We divided PVSFR into three types according to the shape of reversal S wave: biphasic-type, mosaic-type, and laminar-type PVSFR. Biphasic-type PVSFR appeared more frequently in patients with DMR and had a relationship with smaller LAVI, which may be explained by the fact that it is formed by jet insufflation simply. On the other hand, laminar-type PVSFR appeared more frequently in patients with FMR and had a relationship with a higher PCWP and a lower RV FAC, which may be explained by the fact that it is directly reflected by haemodynamic abnormalities. This finding is consistent with a previous report, which showed that the S wave was formed by a change in RV stroke volume and pressure of the LA.4 As for mosaic-type PVSFR, both MR 3D VCA and LAVI had significant determinants in univariate analysis, yet it lost in multivariate analysis probably because the mosaic types were frequently seen in both DMR and FMR (even in patients with FMR with laminar-type PVSFR, mosaic-type PVSFR was often seen in at least one of four PV). Hence, the significance of MR 3D VCA and LAVI observed in univariate analyses may be diminished.

Clinical implications

Four PVs can be visualized relatively easily on TOE, and the appearance of PV flow is an objective indicator of severity of MR. Additionally, the severity of MR and the presence or absence of elevated LA pressure can be estimated based on the shape of PVSFR. Patients with MR might be able to be further stratified when they are classified as severe by only effective regurgitant orifice evaluation. Additionally, with familiarization of the MitraClip procedure, there is an increasing need for simple and reproducible indicator of the severity of MR that can be reflected immediately. An increased Doppler velocity–time integral of the S wave post-Clip may lead to a favourable prognosis.20 In most cases who underwent MitraClip at our institution, PVSFR disappeared after a decrease in MR volume. This was particularly characteristic of the biphasic- and mosaic-type PVSFR. On the other hand, there were some cases with persistent laminar-type PVSFR even after MR reduction. In such cases, invasively measured LA pressure post-Clip was still high, and it may emphasize the necessity of intensive medical treatment to optimize LA pressure. Therefore, accurate assessment and understanding of PV flow profiles in patients with severe MR are of great interest.

Study limitations

The present study had several limitations. First, this was a single-centre, retrospective study with a relatively small sample size. Especially, the numbers of patients with V-FMR and A-FMR were small. The current data are for generating hypothesis and thus need to be validated with a larger volume. Secondly, PV flow or right heart pressure can be affected by various factors (e.g. PV flow may change with treatment for congested heart failure). However, we attempted that we only included a right heart catheter examination within 5 days from TOE in this study. Thirdly, the angles of Doppler may have affected the flow shape. However, we focused only on the shape of the S wave without the measurement of S wave amplitude or Doppler velocity–time integral, which helps to reduce this problem. Furthermore, nine patients enrolled in this study underwent TOE twice, and we have confirmed that the number of PVSFRs was the same value for each test in the same case. Finally, although the feasibility for the detection of PVSFR was acceptable in this study, our results may not guarantee excellent feasibility in general.

Conclusions

All four PV flows can be detected in most patients, and 16.8% patients with severe MR have PVSFR in all four PVs. The methods of determining the prevalence and distribution of PVSFR are different based on DMR or FMR in patients with severe MR. A larger volume of MR can be a reason for PVSFR in DMR, and higher LA pressure can strongly affect the appearance of PVSFR in patients with V-FMR. The shape of PVSFR also has an effect on evaluation of MR aetiologies.

Acknowledgements

We would like to thank Hiroyuki Nagata, Hiroshi Ofuji, Hiromi Naito, and Takayuki Hataoka, from Philips Electronics, Japan, for their technical assistance.

Funding

This work was partially supported by MSD Life Science Foundation, Public Interest Incorporated Foundation. This work was also supported by Takeda Science Foundation.

Conflict of interest: none declared.

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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: .

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: .

Topic:

• mitral valve insufficiency
• transesophageal echocardiography
• lung
• ventricular tachycardia, induced
• heart valve bioprosthesis stenosis
• heart ventricle
• pulmonary wedge pressure
• systole
• toes
• heart
• functional mitral regurgitation
• vena contracta
• causality
• fluid flow

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