Echocardiographic quantification of mitral apparatus morphology and dynamics in patients with dilated cardiomyopathy

Abstract

Mitral regurgitation is among the most common valvular heart diseases. Mitral regurgitation in patients with dilated cardiomyopathy is a complex pathology involving annular dilatation, papillary muscle displacement, systolic leaflet tethering, and left ventricular remodeling. Quantification of mitral apparatus damage in these patients is essential for successful interventional and surgical therapy. Mitral regurgitation in the presence of dilated cardiomyopathy is classified as Carpentier type IIIB, with restricted leaflet mobility as a standard feature. Echocardiography allows accurate evaluation of the complex anatomy and function of the mitral apparatus. Updated guidelines recommend two-dimensional followed by systematic three-dimensional echocardiographic evaluation in patients with mitral regurgitation. New three-dimensional echocardiographic software packages provide many parameters that help identify the precise morphology and function of the various components of the mitral apparatus, helping to determine the etiology of mitral regurgitation and evaluate disease severity. This review provides the first point-by-point approach to the assessment of all old and new echocardiographic methods, from the simplest to the most complex, used to examine the components of the mitral valve apparatus in patients with dilated cardiomyopathy. Although these parameters are still under research, this information will be helpful for establishing therapeutic procedures in a disease with a poor prognosis.

Keywords

Functional mitral regurgitation mitral valve apparatus component dilated cardiomyopathy echocardiography valvular heart disease narrative review

Introduction

Dilated cardiomyopathy (DCM) is a heart disease characterized by left ventricular (LV) or biventricular dilation and systolic dysfunction in the absence of pressure or volume overload (hypertension and valvular heart disease) or coronary artery disease sufficient to explain this dysfunction.^1,2 DCM accounts for approximately 70% of heart failure cases. According to the EuroHeart Failure Survey II, DCM occurs more often in men than in women.³ The risk of developing congestive heart failure in patients with DCM is approximately 30%.³

Echocardiography is an appropriate imaging tool for the diagnosis, management, and follow-up of patients with DCM.⁴ The two echocardiographic diagnostic criteria for DCM are an LV end-diastolic volume or diameter of >2 standard deviations from normal according to nomograms (Z-scores of >2 standard deviations) corrected for age and body surface area and an LV ejection fraction of <50%.⁴ Many patients with DCM have an unfavorable prognosis,⁵ especially those with New York Heart Association functional class III or IV, LV ejection fraction of <35%, and mitral regurgitation (MR). Survival has improved in the last few decades,⁵ but some patients with DCM still have unfavorable prognoses.⁶

MR secondary to LV remodeling is classified as Carpentier IIIb. This type of MR is characterized by decreased leaflets mobility.⁷ Patients with functional MR (FMR) exhibit restricted MV motion only in systole because of LV dilatation and remodeling.⁸ FMR can be due to nonischemic or ischemic cardiac remodeling⁹ and represents 65% of all MR cases. The 5-year survival rate in patients with MR secondary to DCM ranges from 46% to 50%.¹⁰ FMR is a powerful predictor of all-cause mortality, heart failure hospitalization, and heart transplantation.¹¹

Mitral valve (MV) pathology in patients with DCM is strongly associated with disease evolution and prognosis.¹⁰ Anatomical and functional damage of the MV in patients with DCM is secondary to LV injury.¹⁰ What remains incompletely understood is the nature and extent of mitral annulus (MA) damage leading to FVMR, creating a vicious circle in which MR maintains and aggravates itself. MV pathology in the setting of DCM and FVMR is associated with a poor prognosis despite the progress that has been made in the diagnosis and treatment of this disease.¹¹ Echocardiography is the primary imaging technique for both diagnosis and severity assessment.⁸ Finding methods to quantify MA damage in this group of patients is essential for successful interventional and surgical therapeutic approaches.¹¹

This narrative review of clinical studies and practice guidelines was designed to construct a practical approach to echocardiographic evaluation of the MV apparatus in patients with ventriculogenic FMR (VFMR) and DCM. Although these parameters are still under research, the information provided herein is useful for guiding therapeutic procedures in a disease with a poor prognosis. This review highlights the echocardiographic methods used to quantify the MV apparatus in patients with DCM.

Methods

We searched PubMed, Crossref, and Google Scholar for literature published from 2007 to 2023. We identified 68 clinical studies, practice guidelines, and reviews matching the criteria of FMR, MA components, DCM, and echocardiography. After analyzing all these materials, we identified 49 articles relevant to this review.

Complex anatomy of the MV

Detailed knowledge of the anatomy and function of the MV apparatus components is mandatory for successful implementation of therapeutic procedures such as MV repair and mitral ring implantation. The MV apparatus includes the MA, leaflets, chordae tendineae, and papillary muscles (PMs).¹²

The MA comprises a straight anterior segment and muscular posterior segment.¹² The anterior segment is equivalent to the hinge line of the anterior mitral leaflet.¹² The posterior segment anchors the posterior leaflet and is involved in sphincteric-like contraction¹² (Figure 1). The MA has a saddle-shaped configuration. The “highest points” are located at the mid-level of the anterior and posterior leaflets, and the “lowest points” are located at the commissural level¹² (Figure 1). This configuration optimizes leaflet coaptation and minimizes leaflet stress.¹³ The size and shape of the MA vary during the cardiac cycle. Contraction reduces the MA area by 20% to 30%.¹⁴ Its area is smallest during isovolumetric contraction and largest during isovolumetric relaxation.¹⁴ Dilatation predominantly affects the muscular posterior annulus.¹⁴

Figure 1.

Graphic representation of the mitral valve apparatus. A1, A2, A3: segments of the anterior mitral valve. P1, P2, P3: segments of the posterior mitral valve.

In normal conditions, the annulus moves toward the apex by approximately 1 cm.¹⁴ The area change and apex-to-basal motion are closely linked to LV function and significantly blunted in DCM.¹⁴ The angle between the MA and the aortic annulus also changes during the cardiac cycle.¹⁴

There are two mitral leaflets: the anterior (aortic) mitral leaflet and the posterior (mural) mitral leaflet.¹⁴ The posterior leaflet is divided by two incisures into three scallops: P1 (lateral), P2 (central), and P3 (medial).¹⁴ The anterior leaflet has no incisures but is correspondingly divided into three scallops: A1, A2, and A3¹⁴ (Figure 1). The anterior MV leaflet is triangular, and its insertion covers one-third of the annular circumference. The posterior MV leaflet is quadrangular and covers two-thirds of the annular circumference¹⁴ (Figure 1). Commissural (accessory or junctional) leaflets can be found at the anterolateral (A1–P1) and posteromedial (A3–P3) commissures.¹⁴ The normal ratio of the MA to mitral leaflet area is 1.5 to 2.0, and maintaining this ratio is vital to prevent significant MR in normal and dilated left ventricles.¹⁵

Two groups of PMs, the anterolateral and posteromedial PMs (named according to their relationship to the mitral commissures), contribute to closure of the mitral leaflets¹⁴ (Figure 2). In early systole, accentuation of the saddle shape along with coordinated and symmetric movement of the PMs to the MA favors apposition of the mitral leaflets.¹⁶

Figure 2.

Papillary muscles and chordae tendinae. (a) Papillary muscles visualized from the two-dimensional short-axis papillary muscle view. A-L PM: anterolateral papillary muscle, P-M PM: posteromedial papillary muscle and (b) Chordae tendinae visualized from the parasternal long-axis view.

Each of the two PM groups gives rise to chordae tendineae (Figure 2) that insert into both leaflets.¹⁷ First-order chordae insert close to the free margin of the leaflets and are called marginal chordae or commissures (commissural chordae).¹⁷ The second-order chordae (strut or stay chordae) insert between both leaflets’ rough and clear zones.¹⁷ Third-order chordae (basal chordae) originate directly from the ventricular wall and insert into the posterior leaflet, reducing mobility.¹⁶

In normal conditions, the coaptation of the MV leaflet is symmetrical, occurring within 2 mm of the annular plane, and the coaptation zone measures more than 5 mm.^18,19 Damage to the integrity of any MA components is followed by valvular incompetence.^18,19

MV apparatus in patients with DCM

MR appears late in advanced DCM and is caused by interactions between the following factors: alterations in contractility, PM dysfunction, MA dilation, and, in particular, geometric alteration of the LV cavity, which changes from an elliptical to a spherical shape.²⁰ Dilatation increases MV tethering forces exerted by the chordae on the leaflets, while LV dysfunction reduces MV closing forces; both factors simultaneously contribute to the development of FMR.²⁰

The degree of LV distortion determines the severity of apical and lateral PM displacement in patients with idiopathic DCM and ischemic DCM.²⁰ This damage impacts the spatial relationship between the LV, PM, MV leaflets, and MA, finally leading to apical displacement of the coaptation zone, poor coaptation, and valve incompetency.²⁰

The PM displacement is symmetrical in patients with idiopathic DCM and ischemic DCM due to multiple vessel disease. Some patients with ischemic DCM may develop more focal LV remodeling, such as that following myocardial infarction (MI), and the PMs can therefore be unequally damaged.²¹ MV tethering is usually symmetric in patients with global LV dysfunction and remodeling, with increased LV sphericity. The MR jet is central in patients with global wall motion abnormalities, with equal lateral displacement of the PMs, similar to nonischemic cardiomyopathy²¹ (Figure 3(a), (b)). Asymmetric tethering might occur in patients with multiple vessel disease and old inferior MI, mainly affecting the posterior PM.²¹ The jet is posterior in patients with dominant posterior leaflet tethering²² (Figure 3(c), (d)). MA enlargement and flattening with increased leaflet stress is another factor contributing to the development of FMR.⁸ Leaflet remodeling, with the area growing up to 35%, is an adaptive response to minimize MR.^23,24 If coaptation is lost because of mismatch between the dilated annulus and leaflet length,^23,24 insufficient mitral leaflet growth leads to the development of severe MR.^24,25

Figure 3.

Mitral regurgitation features in patients with dilated cardiomyopathy. (a) Central color mitral regurgitation jet visualized from parasternal long-axis view. (b) Central color mitral regurgitation jet visualized from apical four-chamber view. (c) Posteriorly directed color mitral regurgitation jet visualized from parasternal long-axis view and (d) Posteriorly directed color mitral regurgitation jet visualized from apical four-chamber view.

Studies have revealed anatomic differences in MA components among patients with DCM who have and do not have MR. These variations include differences in the annulus area, the leaflet area, and the distance from coaptation in the left ventricle to the annular plane. The left atrial volume tends to be higher in the presence of VFMR.¹⁶ In patients with heart failure, a reduced LV ejection fraction with left bundle branch block and dyssynchrony also contribute to decreased closing forces and worsening remodeling.²⁶

Echocardiography

Imaging plays a central role in the evaluation of patients with DCM and VFMR,²⁷ with transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) being complementary.²⁶ Two-dimensional (2D) and three-dimensional (3D) TTE and 2D and 3D TEE are essential imaging techniques for anatomic evaluation of the MV apparatus.²⁶

2D TTE

The first echocardiographic modality for identification and evaluation of DCM and FMR is 2D TTE. Different views can be used in both systole and in diastole for evaluation of the MA parameters.

The 2D parasternal (PS) long-axis (LAX) view reveals that the anterior MV leaflet is in continuity with the non-coronary cusp. This view reveals the A2 and P2 scallops (Figure 4(a)) as in the apical three-chamber view (Figure 4(d)). The diagnostic criterion for MA dilatation is a diastolic annulus/anterior leaflet ratio of >1.3 or annulus diameter of >35 mm.²⁷ The PS LAX view also provides the maximal value of the tenting area (TA) (Figure 4(a)).²⁷ In a study of 90 patients with non-ischemic cardiomyopathy and FMR, the TA accurately reflected the degree of FMR at a cut-off value of 3.4 cm² and was strongly correlated with the functional status, plasma B-type natriuretic peptide level, mortality rate, and hospitalization rate. The TA was also an independent predictor of mortality and hospitalization in patients with non-ischemic cardiomyopathy and FMR.²⁸ The apical four-chamber view also allows measurements of the MA, TA, and tenting height (TH). From left to right, the scallops visualized from this view are A3, A2, and P1 (Figure 4(b)), and those visualized from the apical two-chamber view are P3, A2, and P1 (Figure 4(c)).

Figure 4.

Mitral valve scallops evaluation using two-dimensional echocardiography. (a) Parasternal long-axis view showing A2, P2 scallops, mitral annulus dimensions, tenting height, and tenting area measurement. (b) Apical four-chamber view showing A3, P2, A1 scallops, mitral annulus dimensions, tenting height, and tenting area measurements. (c) Apical two-chamber view showing P3, A2, and P1. (d) Apical three-chamber view showing A2 and P2 and (e) Parasternal short-axis view at the mitral valve level showing A3, A3, A1, P3, P2, and P1.

In the normal heart, the PS short-axis (PS SAX) view at the MV level reveals the anterior MV in the upper position and posterior MV in the lower position of the image. From left to right, this view reveals A3, A2, and A1 and P3, P2, and P1, respectively (Figures 4(e), 5(a)). The PS SAX view at the PM level reveals the anterolateral PM at the 3-o’clock position and the posterolateral PM at the 8-o’clock position of the image (Figure 5(b)). In patients with DCM, the MV and PM are posteriorly displaced from the SAX views, with restricted movement of the leaflets²⁹ (Figure 5(c), (d)).

Figure 5.

Mitral annulus components visualization using two-dimensional echocardiography short-axis views. (a) Parasternal short-axis mitral valve in normal conditions. (b) Parasternal short-axis papillary muscle in normal conditions. (c) Parasternal short-axis mitral valve in dilated cardiomyopathy with mitral valve apparatus posterior displacement and (d) Parasternal short-axis papillary muscle in dilated cardiomyopathy with papillary muscle posterior and lateral displacement. AML: anterior mitral leaflet, PML: posterior mitral leaflet, ALPM: anterolateral papillary muscle, PMPM: posteromedial papillary muscle.

A coaptation depth of ≥1 cm, TA of ≥1.6 cm², and posterior leaflet angle of >45 degrees measured from the apical four-chamber view predict significant recurrent MR after annuloplasty³⁰ (Figure 4(b)).

Doppler tissue echocardiography

Doppler echocardiography imaging allows for evaluation of regional MA velocities. However, this method has two significant limitations. First, velocity measurements represent small regions of the MA usually recorded from standard apical views. Second, measurements are dependent on the incidence angle of the acoustic beam (Figure 6).³¹

Figure 6.

Mitral annulus velocity measurement by tissue Doppler echocardiography. (a) Interventricular septum velocity measurement and (b) Left ventricle anterolateral wall velocity measurement.

2D TEE

In 2D TEE, the MV apparatus is evaluated by rotating the probe from 0 to 180 degrees. In the mid-esophageal (ME) four-chamber view, at 0 degrees, the anterior mitral leaflet is on the left and the posterior mitral leaflet is on the right side of the image.³² The visualized MV leaflet segments are A3A2 and P2P1³² (Figure 7(a)).

Figure 7.

Mitral valve scallops visualization by two-dimensional transesophageal echocardiography. (a) Mid-esophageal four-chamber view. (b) Mid-esophageal commissural view. (c) Mid-esophageal two-chamber view. (d) Mid-esophageal long-axis view. (e) Transgastric short-axis mitral valve. (f) Transgastric short-axis papillary muscle and (g) Transgastric long-axis view. A-L PM: anterolateral papillary muscle, P-M PM: posteromedial papillary muscle.

In the ME commissural view (50–70 degrees), the MV scallops from left to right are P3-A2-P1 and adjacent A3 and A1 (P3-A3A2A1-P1). The ME commissural view can display the anterolateral and posteromedial PMs and corresponding chordae³² (Figure 7(b)). In the ME two-chamber view (80–100 degrees), the posterior mitral leaflet is on the left side and the anterior leaflet is on the right side of the image.³² The visualized leaflet segments of the MV are P3-A3A2A1³² (Figure 7(c)). The ME LAX view (120–150 degrees) displays the P2-A2 scallops³² (Figure 7(d)).

In the transgastric (TG) MV SAX view (0–20 degrees at the MV level), the anterior leaflet is on the left of the image and the posterior leaflet is on the right. The medial commissure is in the near field, and the lateral commissure in the far field³² (Figure 7(e)). In the TG midpapillary SAX view (0–20 degrees), the anterolateral PM is seen at the 5-o’clock position and the posteromedial PM is seen approximately between the 11- and 2-o’clock positions.³² The TG SAX view reveals MV and PM displacement in patients with DCM (Figure 7(f)). In the TG two-chamber view (90–110 degrees), the pathology of the subvalvular mitral apparatus is well displayed³² (Figure 7(g)).

In patients with FMR, TEE findings predict the feasibility of transcatheter edge-to-edge repair (TEER). These findings include the leaflet coaptation depth, coaptation length, grasping zone distance between leaflets, and presence, extent, and distribution of leaflet calcification. The cut-off values are a coaptation length of ≥2 mm and coaptation depth of <11 mm measured from the ME four-chamber view³² (Figure 8(b), (a)).

Figure 8.

Coaptation depth and length measured by two-dimensional transesophageal echocardiography. (a) Depth and (b) Length.

4D echocardiography

The recently updated valvular regurgitation guidelines recommend 3D echocardiography (3DE) for MR evaluation.^{19,27,29,32,33} 3DE and four-dimensional echocardiography (4DE), also known as real-time 3DE (RT3DE), are superior to 2DE for detailed assessment of the MV, identification of anatomical features, and evaluation of the MR mechanism.²⁹ 3D TEE has superior spatial resolution and provides better anatomic details of the MV apparatus components.²⁹ Studies have shown greater value of 3D TTE over 2D TTE in MR quantification.³⁰

Guidelines recommend a systematic 3DE evaluation after 2DE examination of the entire MV complex.^{19,27,29,32,33} This technique provides MV imaging from the ventricular perspective and atrial perspective (surgical view)²⁹ (Figure 9). The surgical view enables visualization of the leaflets and assessment of the relationship of the MV apparatus with other structures such as the left atrial appendage (left side), tricuspid valve (right side), and aortic valve (1-o’clock position)¹⁵ (Figure 10).

Figure 9.

Three-dimensional echocardiography mitral valve perspectives. (a) Atrial perspective, surgical view and (b) Ventricular perspective.

Figure 10.

Three-dimensional echocardiography mitral valve showing other structures. (a) Atrial perspective and (b) Ventricular perspective.

When using 3D TTE, the anterior MV leaflet is best visualized from the apical and PS views, while the PS view most effectively displays the posterior MV leaflet.¹⁵ 3D TEE using the atrial perspective can best depict the MA morphology and size quantification.^15,19

The sub-mitral apparatus and chordae tendineae lengths can be evaluated from the transesophageal and TG views.^15,25,27 However, the spatial resolution of 3D TTE/TEE is poorer than that of 2D TTE/TEE for chordae tendineae visualization.³⁴

MV competence depends on the morphological and functional integrity of the MV components (leaflets, chordae, and PMs) and surrounding cardiac chambers.^19,29,33 3DE has an essential role in demonstrating the spatial interactions between MV components.¹⁹ New software packages offer measurements useful for surgical repair techniques. Software for MV quantification (MVQ) creates a model of the valve.³⁵ The color-encoded, surface-rendered images serve as topographic maps of the leaflets and MV apparatus, and they provide information for the surgeon before intervention. Numerous standardized parameters can be measured³⁵ (Figures 11 and 12), which may improve repair techniques.³⁶

Figure 11.

Mitral annulus parameters evaluation by three-dimensional echocardiography (mitral valve quantification). (a) Three-dimensional annulus area. (b) Annulus perimeter. (c) Anteroposterior diameter. (d) Posteromedial-anterolateral diameter. (e) Commissural diameter. (f) Inter-trigonal distance. (g) Annulus height. (h) Non-planar angle and (i) Mitro-aortic angle.

Figure 12.

Mitral valve leaflet parameters evaluation by three-dimensional echocardiography (mitral valve quantification). (a) Anterior mitral leaflet area. (b) Posterior mitral leaflet area. (c) Anterior mitral leaflet length. (d) Posterior mitral leaflet length. (e) Anterior leaflet angle. (f) Posterior leaflet angle. (g) Closure line length. (h) Tenting height. (i) Tenting area and (j) Tenting volume.

Because of the complex saddle shape of the MA, multiple parameters describing the MV apparatus measured with 2DE cannot adequately describe the geometry and function of the MV.³⁵ 3DE allows a comprehensive evaluation of the MV apparatus. Furthermore, 3D TEE MVQ reveals the MA size, shape, and function.³⁵

The MA plays an important role in the structural and functional integrity of the MV complex and can be characterized by several morphological and functional parameters using RT3DE: the 2D and 3D annulus area, annulus perimeter, anteroposterior diameter, posteromedial to anterolateral diameter, commissural diameter, inter-trigonal distance, annulus height, non-planar angle, mitral annular excursion, MA area (2D) fraction, mitral annular velocity, and mitral-aortic angle³⁵ (Figure 11). The saddle shape of the MA minimizes peak mitral leaflet stress.^36,37

RT3DE is useful for identifying differences in annular shape and function among various cardiac diseases.³⁸ Annular morphology and dynamics are abnormal in patients with MR.³⁹ The MA dimensions and dynamics change according to the underlying mechanisms of MR.³⁹ FMR is associated with annular dilation, flattening, and reduced contractility.⁴⁰ In FMR, the MA is dilated but less dynamic during the cardiac cycle than in primary (organic) MR.⁴⁰ This reduction in annular contractility is associated with loss of the physiologic morphology.³⁹ 3D MVQ in patients with VFMR reveals anteroposterior annular dilatation, loss of the typical saddle shape of the MA, a longer distance between the MA and inter-trigonal zone, a more significant annular nonplanarity scalar angle, and increased anteroposterior and anterolateral–posteromedial diameters.⁴⁰

Identification of annular changes may be important for surgical repair.³⁹ Some studies have been performed to identify MA characteristics in patients with DCM and FMR. Flachskampf et al.³⁰ compared the shape and dynamics of the MA in patients with DCM versus those in healthy patients by TEE and 3D reconstruction. They also calculated the MA area, the apicobasal motion of the MA, and nonplanarity over time. The authors found significant differences in the annular area between patients with DCM and the healthy group (15.2 ± 4.2 vs. 11.8 ± 2.5 cm²); this finding was consistent after correction for body size (5.9 ± 1.2 vs. 7.7 ± 1.0 cm²/m²; P < 0.02). They also found a difference in the area variation during the cardiac cycle (13.2% ± 2.3% vs. 23.8% ± 5.1%, P < 0.001).³⁰

Mihalatos et al.⁴¹ analyzed MA remodeling according to the MR mechanism. They used 3DE in 83 patients with different degrees and etiologies of MR. The measurements included the MA dimensions (anteroposterior, inter-commissural, surface area, and circumference) in end-systole and diastole; annular sphericity indices were determined by dividing the inter-commissural by anteroposterior dimensions. They found that the annular dimensions in the anteroposterior dimension, circumference, area, and MA sphericity increased in proportion to MR severity.⁴¹

Topilsky et al.¹⁶ found a similar inter-commissural diameter in patients with a low EF with or without MR and a larger anteroposterior diameter than patients with systolic dysfunction but no MR. They also reported the loss of annular folding across the inter-commissural axis and the loss of saddle shape accentuation in early systole in patients with type IIIb MR.¹⁶ Moreover, the authors evaluated the MA in patients with LV dysfunction, patients with LV dysfunction + FMR, and healthy volunteers using 3D TTE. The saddle shape did not change from diastole to early systole in patients with FMR. In patients with anterior MI and global dysfunction, annular dysfunction and dilatation were the dominant parameters of FMR.¹⁶ The authors measured the MA size, shape, motion, and PM motion throughout the cardiac cycle in patients with FMR versus control subjects and patients with low EF but no FMR. In patients with LV dysfunction with or without FMR, the MA was enlarged in systole and diastole, and the inter-commissural diameter presented minimal changes. Asymmetric PM tip movement toward the mid-anterior MA was the primary determinant of mid- and late-systolic FMR in this group of patients.¹⁶

Veronesi et al.⁴² evaluated the MA area and motion throughout the cardiac cycle and PM position by RT3DE. Patients with DCM and MR had the most significant end-diastolic MA systolic area values.⁴² During systole, the leaflet tenting volumes (TVs) were significantly lower in the control group than in patients with DCM and MR and those with ischemic MR. The end-diastolic inter-commissural diameter was higher in patients with DCM and MR (control: 3.0 ± 0.4 cm, DCM-MR: 3.8 ± 0.4 cm, ischemic MR: 3.5 ± 0.6 cm), as was the anteroposterior annular diameter (control: 2.4 ± 0.4 cm, DCM-MR: 3.4 ± 0.5 cm, ischemic MR: 2.8 ± 0.4 cm). The maximum MA systolic area change was 13.9% in the DCM-MR group, 30.7% in the ischemic DCM-MR group, and 54.6% in the control group.⁴² The most significant MA systolic area value occurred during rapid LV filling but later in the cardiac cycle in patients with DCM-MR and ischemic DCM-MR. Regarding the MA motion, the systolic and diastolic MA velocities were significantly lower in both DCM groups than in the healthy group. The DCM-MR group had lower systolic MA velocities and displacement than the ischemic MR group. In patients with DCM-MR, PM symmetry was preserved, but in patients with ischemic MR, papillary tethering lengths were unequal because of wall motion abnormalities.⁴²

RT3D TEE in patients with ischemic DCM FMR reveals quantitative differences in MV geometry depending on the tethering patterns and the degree of tethering affecting MR severity. An asymmetric tethering pattern is associated with MR severity independent of MA dilatation and LV function.⁴³

Patients with ischemic DCM and MR exhibit asymmetrical MA distortion due to local remodeling of the LV.⁴³

Obtaining 3D information on the anatomy of the MV leaflets is very important for repair techniques. The leaflet parameters provided by MVQ are the anterior leaflet area, posterior leaflet area, anterior mitral leaflet length, posterior leaflet length, anterior leaflet angle, posterior leaflet angle, anterior leaflet closure line length, posterior leaflet closure line length, TH (distance from the leaflet’s coaptation point to the annular plane), TA (area between the leaflets and annular plane), TV, TV fraction, orifice area, and billowing height⁴⁴ (Figure 12).

Leaflet remodeling is a compensatory mechanism in patients with FMR.⁴³ When the remodeling is inappropriate, the MV becomes insufficient.⁴³ The ability of the leaflets to increase their surface area in response to chronic tethering is also revealed by 3DE.⁴⁰ Chaput et al.⁴³ reported that the MV leaflet area increased by 35% in patients with LV dysfunction and FMR compared with normal subjects. A leaflet to mitral annular closure area ratio of <1.7 was the threshold for secondary MR development.⁴³

In patients with a low EF, regardless of MR severity, Topilsky⁴⁵ reported a decrease in interpapillary muscle approximation, which was correlated with reduced circumferential and radial basal contraction.

Timing of FMR

The early systolic component of MR depends on loss of the normal deepening of the saddle shape in patients with anterior MI and/or global dysfunction. The mid-systolic component of MR depends only on the annular area in patients with anterior MI, whereas it depends on symmetry and coordination of PM motion in patients with inferior MI and global dysfunction.¹⁶

The two proposed mechanisms of the FMR components in patients with DCM are flattening of the annulus with decreased dynamics in early systole and loss of coordination between PM contraction and anterior annulus motion, resulting in leaflet deformation in mid and late systole.¹⁶

In patients with DCM, the MA shows not only enlargement and decreased contractility but also a delay in the MA systolic area. These changes are explained by asynchronous annular motion due to regional wall motion abnormalities in patients with ischemic MR and by decreased LV contractility in patients with DCM and MR.⁴⁶

RT3DE is the first imaging modality used to measure the coaptation length and surface⁴⁶ (Figure 12(g)). This technique can also quantify MV tethering by measuring the height, area, or volume from the leaflet tips to the annular plane.⁴⁶ The TH (Figure 12(h)), TA (Figure 12(i)), and TV (Figure 12(j)) are associated with MR severity.⁴⁶ TV evaluated by RT3DE has been proven to be the single major determinant of the regurgitant orifice area.⁴⁶ Saito et al.⁴⁷ performed TEE in 44 patients with FMR and 56 controls, revealing decreased coaptation in patients with FMR. The coaptation length was related to PM displacement, and the indexes of coaptation were associated with FMR severity.⁴⁷

Hübscher et al.⁴⁸ used 3D TEE to evaluate the TV in patients with FMR. The threshold value of 1.25 cm³/m differentiated moderate to severe FMR from no to mild FMR with a sensitivity of 85% and a specificity of 71%.⁴⁸

Hirasawa et al.²⁴ evaluated 119 patients undergoing TEER by 4D TEE. A larger MA area and smaller total leaflet area to MA area ratio predicted residual VFMR after TEER. This result was consistent with the findings reported by Levine et al.,⁴⁹ who examined leaflet augmentation as an adaptation to LV dilation and showed that it can ameliorate FMR severity as the LV dilates. They also reported other data showing that the MV actively adapts to MR and that the lack of this adaptation can mediate MR.⁴⁹

Echocardiographic indices describing MV leaflet tethering determine the likelihood of a successful MV intervention. It is critical to differentiate between ischemic and nonischemic secondary MR in patients with DCM because of the different therapeutic approaches.²⁶ The MA is more dilated and flattened than in patients with a symmetric than asymmetric pattern. Additionally, the tethering area and volume are larger than those in the asymmetric pattern.⁴⁹

Conclusion

Despite the progress in diagnosis, management, and treatment, patients with DCM and FMR still have a poor prognosis and high mortality. The current guidelines recommend a staged evaluation using 2DE and 3DE as complementary methods. This review reveals the importance of a step-by-step approach in disease evaluation. Because the MA morphometry is a cornerstone of the therapeutic approach, a detailed echocardiographic examination using 2D and 3D techniques is essential in this group of patients. 3D MVQ provides the values and features of the MA components, although most are still undergoing research. Future studies with larger patient populations will demonstrate the utility of these parameters for detailed diagnosis, management, follow-up, and prognosis.

Supplemental Material

sj-pdf-1-imr-10.1177_03000605231209830 - Supplemental material for Echocardiographic quantification of mitral apparatus morphology and dynamics in patients with dilated cardiomyopathy

Supplemental material, sj-pdf-1-imr-10.1177_03000605231209830 for Echocardiographic quantification of mitral apparatus morphology and dynamics in patients with dilated cardiomyopathy by Despina-Manuela Toader in Journal of International Medical Research

Footnotes

Author contributions

Despina-Manuela Toader was the sole contributing author.

Declaration of conflicting interest

The author declares that there is no conflict of interest.

Ethics

The requirements for ethics approval and consent were waived because of the nature of this study (narrative review).

Funding

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

ORCID iD

Despina-Manuela Toader

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