Evaluation of the relationship between mitral valve morphology and left atrial function in severe mitral regurgitation

Introduction

Mitral regurgitation (MR) is the most common heart valve disease worldwide (1). Approximately 7.5 million patients with MR require clinical intervention in China (2). A study conducted in the United States reported that the prevalence of mild, moderate, moderate-to-severe, and severe MR in the general population is 19.2%, 1.6%, 0.3%, and 0.2%, respectively (3). In individuals aged over 75 years, the incidence of MR approaches 10%, and its prevalence tends to increase as age advances (4,5). If left untreated, severe MR has a mortality rate of up to 6%, and severe MR is closely associated with high hospitalization rates and progressive heart failure (5).

The functional integrity of the mitral valve depends on the precise coordination of its apparatus, including the valve annulus, leaflets, chordae tendineae, papillary muscles, and underlying myocardium. Pathological changes in any of these components can lead to varying degrees of MR (6). Echocardiography (Echo) serves as the primary modality for evaluating MR. For example, the leaflet length, annular geometry (such as the annular diameter, leaflet coaptation area, and height), and coaptation angle of the anterior and posterior leaflets of the mitral valve can be measured by Echo, and mitral valve morphology, motion, origin of regurgitation, left atrial (LA) function, and dynamic changes in the mitral valve can be observed in real time (7,8).

LA reservoir function, measured by speckle-tracking echocardiography (STE), has incremental prognostic value for patients with moderate and severe degenerative mitral regurgitation (DMR) (9). Notably, three-dimensional (3D) Echo provides a stereoscopic imaging perspective, significantly enhancing the assessment of mitral valve morphology and dynamics, thereby aiding in the determination of MR etiology and its underlying pathological mechanisms (10), and the quantification of MR (11). Echo multi-parameter assessment of pathological changes in patients with different types of MR is essential for treatment planning (12). Thus, in patients with MR, regular Echo examinations can actively monitor disease progression and related changes (13,14).

This study sought to quantitatively analyze the mitral valve and LA function of patients with severe MR using real-time 3D-Echo combined with four-dimensional automated mitral valve quantification (4D Auto MVQ), and to identify the risk factors associated with MR progression. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1682/rc).

Methods

Subjects

A total of 72 patients with severe MR diagnosed by routine 3D transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) from January 2024 to January 2025 at the Department of Cardiology, the First Affiliated Hospital of Soochow University, were enrolled in the study. A control group of 47 patients, matched for body surface area, gender, and age (Figure 1), was also enrolled in the study. All the enrolled study patients signed the informed consent form, and the study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of the First Affiliated Hospital of Soochow University (No. 20250222082623391).

Figure 1 Flowchart of the study of mitral regurgitation. BSA, body surface area; MR, mitral regurgitation; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

Inclusion criteria

Patients were included in the study if they had been diagnosed with severe MR by TTE and TEE, and had complete and clear images.

Exclusion criteria

Patients were excluded from the study if they had mitral annulus calcification (n=2), a history of mitral valve surgery (n=1), moderate or greater aortic valve disease (n=6), poor quality images (n=3), rheumatic heart valve disease (n=9), or congenital heart disease (n=1).

Definition of severe MR

According to the 2020 American College of Cardiology/American Heart Association (ACC/AHA) guidelines for valve disease management (15) and the ACC expert consensus on MR management, severe MR was diagnosed if four or more of the following criteria were met (16): flail leaflets; a vena contracta width ≥0.7 cm; a proximal isovelocity surface area isokinetic sphere radius ≥1.0 cm; a central regurgitation area/LA area ≥50%; systolic pulmonary venous blood flow reversal; or left ventricular enlargement with preserved left ventricular systolic function. For cases meeting only two or three criteria, the diagnosis required additional quantitative evidence, specifically a regurgitant volume ≥60 mL, a regurgitant fraction ≥50%, or an effective regurgitant orifice area ≥0.4 cm².

Instrument and equipment

All the echocardiographic examinations were performed using a GE VIVID E95 color Doppler ultrasound system (Horten, Norway), equipped with the following transducers: a two-dimensional (2D) probe (M5S-C, frequency: 1.7–3.3 MHz), a transthoracic 3D probe (4Vc, frequency: 1.5–4.0 MHz), and a transesophageal real-time 3D probe (6VT-D, frequency: 2–7 MHz).

Echocardiographic image acquisition and post-processing analysis

Patient baseline characteristics

Baseline characteristics, including age, sex, and weight, were recorded for all patients. Heart rate and blood pressure were also measured. The patients had a medical history of hypertension, diabetes, coronary heart disease, or atrial fibrillation.

2D and 3D TTE

The 2D images were collected using an M5S-C transthoracic probe, and the 3D images were collected using a 4Vc transthoracic 3D probe. Complete and clear 3D images of the mitral valve were obtained. “Multibeat” imaging was used to evaluate image stitching quality to reduce “stitching” artifacts, and “4D Zoom Prepare” was used to obtain local real-time 3D images of the mitral valve structure in a single cardiac cycle (volume frame rate ≥40% of the subject’s heart rate) for those with imaging difficulties. Mitral valve geometry was quantified using 3D mapping software.

TEE image acquisition

Following the connection of standard electrocardiogram monitoring, the subject was positioned in the left lateral decubitus position. Each subject was screened for the presence of removable dentures, which were removed if present. The subject was instructed to gently clench their teeth, relax their neck muscles, and maintain regular breathing. The probe was gently bent forward, slowly advanced into the esophagus, and positioned approximately 30 cm from the incisors at the mid-esophageal level. The image was then adjusted to a –120° left ventricular long-axis view. The probe was adjusted to obtain a clear 2D image, including the complete mitral valve and aortic valve. The gain was adjusted to ensure satisfactory image quality, and the images were saved.

LA function measurements

Following 2D image acquisition, the datasets were transferred to an EchoPAC 204 offline workstation. Apical four-chamber and apical two-chamber views were selected. The region of interest (ROI) was determined, with the width set to 3 mm. The intima boundary, from the atrial intima at the level of the mitral annulus on one side, crossing the pulmonary vein and LA appendage orifices, and extending to the mitral annulus on the opposite side, was traced. After the ROI was completed, the software tracked the motion of the atrial wall throughout one cardiac cycle and calculated the deformation parameters (Figure 2). LA physiological function was assessed by speckle STE, which measured the following phasic strain parameters: Left atrial reserve strain (LAS-R), which refers to the period of ventricular contraction and isovolumic relaxation; left atrial conduit strain (LAS-CD), which refers to the rapid filling period in the early ventricular period; and left atrial contractile strain (LAS-CT), which refers to the late diastolic period of the ventricle.

Figure 2 Left atrial speckle tracking analysis. (A) Non-mitral regurgitation group. (B) Severe mitral regurgitation group. LA, left atrial.

MVQ analysis

Following 3D image acquisition, the datasets were transferred to an EchoPAC 204 offline workstation. Quantitative analysis of the mitral valve was then performed using the dedicated 4D Auto MVQ software (Figure 3). The post-processing procedure was as follows: the EchoPAC post-processing workstation was launched, and the dynamic images were imported. A satisfactory 3D dynamic image of the mitral valve was selected. Subsequently, the “valve” option was chosen from the measurement menu to initiate the 4D Auto MVQ software interface. The long axis was adjusted so that the left atrium was located above the left ventricle, and the marked line passed simultaneously through the mitral valve closure point and the left ventricular apex. Next, the mitral valve root, aortic valve root, and mitral valve leaflet closure point were selected sequentially as reference points, and the system automatically analyzed the mitral valve annulus morphological parameters, mitral valve leaflet morphological parameters, and mitral valve anterior and posterior leaflet coaptation angle. The mitral valve annulus morphological parameters included the annulus area 3D (A3D), annulus perimeter (AP), anterior-to-posterior diameter (DAP), anterolateral to posteromedial diameter (DAL-PM), annulus height (AH), and non-planar angle (NPA).

Figure 3 Comparison of three-dimensional ultrasound parameters of mitral annulus in mitral valve non-regurgitation group and mitral valve severe regurgitation group. (A-D) Non-mitral regurgitation group. (E-H) Severe mitral regurgitation group. 3D, three-dimensional; ED, end-diastole; ES, end-systole.

Leaflet parameters

The leaflet parameters included the anterior leaflet area (A-Ant), posterior leaflet area (A-Post), anterior leaflet length (L-Ant), posterior leaflet length (L-Post), tenting height (TH), and tenting volume (TV).

Statistical analysis

SPSS 27.0 was used for the statistical analysis. For comparisons between two groups, continuous variables with a normal distribution were expressed as the mean ± standard deviation, and compared using the independent sample t-test. Continuous variables that did not follow a normal distribution were expressed as quartiles, and compared using the Mann-Whitney U test. Categorical variables were presented as cases (percentages), and compared using the Chi-squared test. A Pearson correlation analysis was conducted to examine the relationships among the mitral valve parameters. Variables with P values <0.05 in the univariate analysis were further subjected to stepwise regression to identify independent risk factors. A P value <0.05 indicated a statistically significant difference.

Results

There were no significant differences in the basic clinical characteristics of the subjects, including gender, age, height, weight, body mass index, body surface area, inflammatory indicators in blood, between the groups (Table 1). Compared with the no mitral regurgitation (NMR) group, the severe MR group had a faster heart rate (77.12±14.40 vs. 70.13±10.70, P=0.008), and lower systolic blood pressure (120.42±16.76 vs. 130.11±21.25 mmHg, P=0.014), but no significant difference in diastolic blood pressure was observed (72.46±9.78 vs. 76.26±11.73, P=0.086). Further, there were no significant differences in the prevalence of hypertension, diabetes, and renal insufficiency between the groups (P>0.05).

The left ventricular end-diastolic diameter and left ventricular end-systolic diameter were increased in the patients with severe MR compared to those with NMR (58.26±7.50 vs. 48.34±4.52, P<0.001; 41.13±10.81 vs. 32.96±5.65, P<0.001). No significant difference in left ventricular ejection fraction (LVEF) was observed between the NMR group and the severe MR group (55.56±15.86 vs. 59.17±8.66, P=0.179) (Table 1). Compared with the NMR group, the severe MR group showed a statistically significant increase in the size of the right atrium and right ventricle (39.13±7.07 vs. 34.19±3.23; 35.28±5.24 vs. 32.19±3.14, P<0.001). Early diastolic mitral inflow velocity (E wave), late diastolic mitral inflow velocity (A wave), and Ratio of early diastolic mitral inflow velocity to early diastolic mitral annular velocity (E/e’ ratio) during early diastole of the mitral valve differed significantly between the two groups. Specifically, the E peak was increased (113.11±31.11 vs. 67.34±18.23, P<0.001), the A peak was decreased (74.21±24.58 vs. 85.11±14.81, P=0.018), and the E/e’ ratio was increased (16.75±5.79 vs. 10.18±3.67, P<0.001) in the severe MR group, compared with the NMR group.

Both the A3D (8.49±2.28 vs. 4.75±0.98, P<0.001) and the NPA (161.82±14.20 vs. 154.60±11.67, P=0.008) were significantly increased in the severe MR group compared with the NMR group (Table 1). Both the areas of the anterior and posterior mitral valve leaflets (4.34±1.01 vs. 2.76±0.42; 5.95±1.98 vs. 2.71±0.81, P<0.001) and their lengths (2.09±0.36 vs. 1.60±0.21; 1.62±0.36 vs. 1.1±0.27, P<0.001) were significantly increased in the severe MR group compared with the NMR group. Additionally, the height, volume, and area of the mitral valve were significantly increased in the severe MR group compared with the NMR group (0.67±0.24 vs. 0.48±0.14; 1.52±0.63 vs. 0.80±0.26; 2.19±1.27 vs. 0.80±0.33, P<0.001).

LAS-R (19.72±9.56 vs. 23.40±8.53, P=0.048) and LAS-CT (−7.6±5.5 vs. −13.21±5.9, P<0.001) were significantly decreased in the severe MR group compared with the NMR group (Table 1). However, no significant difference in LAS-CD was observed between the two groups (−12.00±6.0 vs. −10.49±4.3, P=0.162). Further, LA emptying fraction was decreased in the severe MR group compared with the NMR group (40.64±14.76 vs. 50.98±15.23, P<0.001).

The patients in the severe MR group were further allocated to the DMR group or functional mitral regurgitation (FMR) group based on the shape and function of the mitral valve. Among these patients, 16 had severe MR of functional etiology but not due to prolapse (the FMR group), and 34 had severe MR caused by mitral valve prolapse (the DMR group) (Table 2). This study showed that in the patients with severe functional MR and mitral valve prolapse, LA function was significantly decreased, including LAS-R, LAS-CD, and LAS-CT. The results showed that LAS-R (14.19±3.885 vs. 22.32±10.339, P=0.004), LAS-CD (−9±4.163 vs. −13.41±6.32, P=0.014), LAS-CT (−5.19±4.355 vs. −8.74±5.707, P=0.033), and left atrial ejection fraction (LAEF) (34.06±8.81 vs. 43.74±16.04, P=0.029) differed significantly between the two groups. There was no significant difference between the FMR and DMR groups in terms of age (70.56±6.33 vs. 68.53±7.48, P=0.353), but B-type natriuretic peptide (BNP) was increased in the FMR group [1,429 (820–4,444.2) vs. 41 (178.6–1,484.75), P=0.029]. There were no significant differences between the FMR and DMR groups in terms of troponin I [11.26 (8.83–11.26) vs. 20.29 (12.17–24.92), P=0.119], and mitral quantitative parameters such as A3D, AP, DAP, DPM-AL, NPA, TH, TA, and TV.

There was no significant difference between the DMR and NMR groups in terms of LAS-R. However, LAS-CD was significantly increased (−13.41±6.32 vs. −10±4.3, P=0.016) and LAS-CT was significantly decreased (−8.74±5.707 vs. −13.21±5.9, P<0.001) in the DMR group compared to the NMR group.

BNP was significantly increased [1,429 (820–4,444.2) vs. 148.5 (59.0–371.8), P<0.001] and LAS-R was significantly decreased in the FMR group compared with the NMR group (14.19±3.885 vs. 23.40±8.5, P<0.001). There was no significant difference between the FMR and NMR in the terms of LAS-CD (−9±4.163 vs. −10±4.3, P=0.234), but LAS-CT was significantly decreased in the FMR group (−5.19±4.355 vs. −13.21±5.9, P<0.001).

In terms of linear correlations (Figures 4,5), the A3D showed a significant correlation with both the A-Ant and A-Post in the NMR group (R both =0.714, P<0.001) and the severe MR group (R both =0.829, P<0.001). The A3D was positively correlated with the L-Ant and L-Post (R=0.714, R=0.588; P<0.001) in the NMR group, and the A3D was linearly correlated with the length of the anterior and posterior mitral leaflets. In the severe MR group, the A3D was positively correlated with the L-Ant and L-Post (R=0.829, R=0.503; P<0.001). The A3D was linearly correlated with the DAP and DPM-AL in the NMR group (R=0.836, R=0.786, P<0.001), and the A3D was correlated with the DAP and DPM-AL in the severe MR group (R=0.859, R=0.898, P<0.001). The A3D was correlated with the TA and TV in both the NMR group (R=0.421, R=0.443, P=0.003, P=0.002) and the severe MR group (R=0.280, R=0.127, P=0.049, P=0.380). The A3D showed significant positive correlations with the length and area of the anterior and posterior mitral leaflets, as well as with the anteroposterior, anterolateral, and posteromedial diameters in both the severe MR and NMR groups.

Figure 4 Scatter plots demonstrating the linear correlation between change in annulus area 3D. (A) Anterior leaflet area. (B) Posterior leaflet area. (C) Anterior leaflet length. (D) Posterior leaflet length. a, non-mitral regurgitation group. b, severe mitral regurgitation group. 3D, three-dimensional.

Figure 5 Scatter plots demonstrating the linear correlation between change in annulus area 3D. (A) A-P diameter. (B) PM-AL diameter. (C) Tenting area. (D) Tenting volume. a, non-mitral regurgitation group. b, severe mitral regurgitation group. 3D, three-dimensional; A-P, annulus of anterior to posterior; PM-AL, posteromedial-anterolateral.

The intra- and inter-observer reproducibility of the LA strain parameters based on TTE was examined (Table 3). Notably, LA strain demonstrated excellent intra-observer reproducibility and good inter-observer reproducibility for the assessment of LA function. The intra-observer reproducibility of LAS-R, LAS-CD, and LAS-CT was also carefully evaluated in the present study with intraclass correlation coefficients of 0.946, 0.935, and 0.910, respectively.

In the multivariate analysis (Table 4 and Figure 6), the A3D was identified as a risk factor for severe MR [hazard ratio (HR): 14.575 (2.886–73.615), P=0.001]. Decreased LAS-R and LAS-CT were also identified as major risk factors for severe MR [HR: 1.465 (1.061–2.024), P=0.02; HR: 2.183 (1.250–3.812), P=0.006].

Figure 6 Multivariable logistic regression analysis for risk factors of severe mitral regurgitation. 3D, three-dimensional; CI, confidence interval; HR, hazard ratio; LAS-CT, left atrial contractile strain; LAS-R, left atrial reserve strain.

Discussion

Innovation

The major findings of this study are as follows: (I) LA remodeling may be a key driver of the morphological and functional alterations observed in the mitral annulus and leaflets; (II) severe MR is influenced by multiple aggravating factors, including mitral annulus dilation, the flattening of the saddle shape, and impaired LA function; (III) mitral annular dilation appears to be the earliest and most significant factor affecting severe MR; and (IV) 4D Auto MVQ technology provides a comprehensive set of quantitative parameters, which may provide valuable guidance for risk stratification and lay the foundation for future longitudinal studies of MR progression.

The normal mitral annulus is saddle-shaped, and its shape changes dynamically throughout the cardiac cycle; the flattening of the annulus increases tension on the annulus, leaflets, and chordae tendineae (17). This study showed that the expansion of the mitral valve annulus and the reduction of its dynamic mobility can lead to an increase in LA pressure. The morphological parameters of the mitral valve annulus, including the A3D, DAP, DAL-PM, TH, and NPA, were larger in the MR group than in the control group. In terms of the pathological changes, the mitral valve annulus tended to become rounder and flatter. Hemodynamic alterations may lead to extracellular matrix remodeling in the leaflets. The abnormal accumulation of collagen and mucopolysaccharides leads to the biomechanical weakening of leaflets. Mechanical tension caused by a flattened valve annulus gradually leads to the elongation of the leaflets, which increases the likelihood of leaflet prolapse and chordae tendineae rupture. Increased leaflet-chordal stress in turn exacerbates annular dilation and flattening (18). As the severity of MR increased, the LA diameter and volume index increased, and the height of the mitral annulus decreased, while the enlargement of the mitral annulus was influenced by both the LA and left ventricle diameters across all types of MR. In this study, DAL-PM, AP, and NPA increased, while TH decreased, and the mitral annulus tended to flatten as a whole. A flattened annulus exposes the mitral valve to more mechanical stress, which disrupts the stable coaptation of the leaflets, leading to MR. Thus, the flattening of the mitral valve annulus may be one of the causes of MR.

Mitral valve compensatory hyperplasia is another cause of MR. As the mitral valve annulus enlarges, the leaflet area increases in a compensatory manner, but this is limited and gradual, such that the coaptation area and index decrease, resulting in coaptation gaps between the leaflets. The mitral valve adapts to mechanical stress changes caused by MR through endothelial-mesenchymal transformation and matrix remodeling, which promote the compensatory expansion of the leaflets. Endothelial-mesenchymal transition is the result of the MR-induced leaflet effect and is the cause of further stimulation of MR aggravation (19).

In this study, the A-Ant, A-Post, L-Ant, and L-Post of the moderate MR and severe MR groups were significantly increased. Additionally, the morphological parameters of the mitral valve annulus, including the A3D, DAP, DAL-PM, TH, and NPA, were larger in the MR group than in the control group. Mitral annular dilation is a common geometric change in severe MR. However, due to the flattening of the valve annulus and the increase in the 3D projection area of the valve annulus, the reserve capacity of anterior and posterior mitral leaflets may be unbalanced, which may also lead to an increased degree of MR. Thus, insufficient reserve of mitral valve leaflets is a cause of MR.

The mitral valve is a complex structure, mainly composed of the mitral annulus, leaflets, chordae tendineae, and papillary muscles. Its physiological function depends on the biomechanical properties and structural integrity of its components. Changes in the geometry of the mitral valve of the heart increase mechanical stress on the mitral valve apparatus, exacerbating the severity of regurgitation (20). The results of this study showed that mitral annular dilation is a common geometric change in severe MR. DMR is caused by leaflet insufficiency due to leaflet prolapse with or without chordal tendinous rupture. Functional MR can be subdivided into ventricular functional regurgitation and atrial functional regurgitation. Ventricular functional MR is characterized by mitral annular dilation and leaflet insufficiency caused by left ventricular remodeling and leaflet tethering. Atrial functional regurgitation is often caused by LA enlargement. The mitral valve is a part of the left atrium, and its configuration can be affected by changes in LA volume. The posterior wall of the left atrium is contiguous with the posterior leaflet of the mitral valve, so LA enlargement can displace the posterior inferior displacement of the posterior leaflet of the mitral valve, resulting in valve insufficiency.

A number of factors affect mechanical stress. In DMR, the abnormal accumulation of collagen and mucopolysaccharides in the mitral leaflet tissue leads to decreased mechanical stress, decreased tension, extracellular matrix remodeling, and an increased risk of leaflet prolapse (21). The flattening of the mitral valve annulus increases the stress of valve leaflets and chordae tendineae, makes valve leaflets gradually redundant, increases the possibility of chordae tendineae rupture, and promotes the occurrence of valve leaflet prolapse (9). Chordal rupture also increases the stress on adjacent unruptured chordal and leaflet tissue, which in turn leads to annular dilation and flattening, which interacts with leaflet prolapse to create a vicious cycle that increases the severity of regurgitation (9). The coordination of mitral valve devices and the imbalance of mechanical stress can also aggravate MR.

The mitral TV and mitral tenting area (TA) are key 3D structures of the mitral valve, and serve as the key quantitative parameters of pathophysiological changes. An increase in this key geometric parameter indicates mitral insufficiency. An increase in this parameter indicates worsening regurgitation, particularly in functional MR. In this study, we found that the mitral annulus area measured by 3D Echo had good collinearity with the length and area of the anterior mitral leaflet and posterior mitral leaflet. The TA of the mitral annulus measured by 3D Echo also had good collinearity with the anteroposterior diameter and the anterolateral posteromedial diameter of the mitral annulus, but the collinearity between the TV and TA was slightly lower. This may be partly related to mitral valve prolapse in the severe MR group, offsetting the increase in fornix height due to secondary leaflet tethering (22). TA and TV may also aggravate MR.

In most cases, as left ventricular contraction begins, the papillary muscles contract first and pull the leaflets downward. At this time, the valve annulus contracts, decreasing its area, and the valve remains closed all the time. The unique saddle shape of the mitral valve annulus deepens, which helps to disperse the pressure. In patients with valvular disease, the contractile force decreases before and after the valve annulus, and the joint part of the valve annulus is abnormally dilated, resulting in an increase in the mitral valve orifice area and the shallow saddle structure (23). Mitral valve coaptation decreases and regurgitation increases. MR-related remodeling affects the left atrium (24), and the increased afterload of the left atrium is due to the presence of left ventricular diastolic dysfunction (i.e., increased left ventricular end-diastolic pressure). Chronic MR affects the systolic and diastolic function of early LA myocardium. LA dysfunction is related to LA compliance. MR increases the volume load, reduces LA compliance, and accelerates the remodeling of the thin-walled left atrium (25). The reconstructed atrium presents as LA dilation, and increases the severity of MR.

In this study, LA function showed a significant decreased trend in the severe MR group compared with the NMR group. In the multivariate analysis, the LAS-R, LAS-CT, and the mitral valve area measured by 3D Echo were risk factors for severe MR. In the DMR group, the LAS-CD was increased, but the LAS-CD was not significantly different from that in the FMR group; the LAS-R was not statistically significant compared to that in the DMR group, but was significantly decreased in the FMR group, and the LAS-CT was significantly decreased in both the DMR and FMR groups. Thus, MR and LA remodeling may influence each other.

In the univariate analysis, a history of coronary heart disease and atrial fibrillation was associated with LA function and mitral valve morphology. However, this study mainly examined the risk factors of severe MR, which may be influenced by confounding factors. Due to the single-center study design, the sample size of this study was limited, and all potential confounding variables were not included in the multivariate analysis for full adjustment.

The interpretation of the E and E/e’ ratio as markers of diastolic dysfunction has limitations, especially in patients with secondary severe MR. It has been reported (26) that left ventricular filling pressure cannot be predicted by the E/e’ ratio in patients with secondary severe MR and preserved left ventricular function, since E/e’ is usually caused by increased regurgitation in these patients. In addition, patients with chronic MR maintain enhanced left ventricular relaxation and decreased left ventricular stiffness to compensate for excess volume. The findings of this study are consistent with previous literature. Recent studies (27) suggest that a decrease in LA function is a marker of left ventricular diastolic dysfunction. In this study, we found that the main manifestation of LA compliance (LA function) in patients with severe MR was significantly decreased, suggesting that patients with severe MR may, to some extent, have left ventricular diastolic dysfunction. Thus, LA function may be a marker of left ventricular diastolic function in severe MR.

It is difficult to accurately evaluate the dynamic characteristics of the mitral valve using 2D Echo only. However, using 3D Echo, the dynamic and quantitative parameters of mitral annulus and leaflet can be accurately calculated to explore structural changes in the mitral valve, providing a valuable reference for surgery. 3D Echo clearly shows the mitral valve structure, and effectively reduces inaccuracies in identifying the causes of MR. Further, 3D Echo can precisely localize mitral valve prolapse. It is instrumental in pre-procedural planning for interventions such as Mitra Clip, as it enables the analysis of leaflet motion, length, and coaptation area to assess procedural feasibility. It can also be used to evaluate immediate procedural results and monitor long-term outcomes during follow-up. Thus, 3D Echo quantitative evaluation has a number of advantages and prospects.

Limitations

This study had a number of limitations. It was a single-center retrospective study with a relatively small sample size, which may have introduced bias into the study results. Given that mitral valve geometry changes dynamically throughout the cardiac cycle, future studies with larger sample sizes need to be conducted to compare dynamic changes of the mitral valve annulus across different MR subtypes, and to further analyze the predictive value of annular dynamic changes for distinguishing between different MR subtypes.

Conclusions

3D Echo can quantitatively evaluate dynamic structural parameters of the mitral valve. Mitral annular enlargement contributes to the structural basis of both primary and secondary MR, while in functional MR, changes in the mitral apparatus combined with decreased LA function exacerbate MR.

Acknowledgments

We would like to thank all patients and researchers involved in this study.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1682/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1682/dss

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1682/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All enrolled study patients signed the informed consent form, and the study conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of The First Affiliated Hospital of Soochow University (No. 20250222082623391).

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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