REVIEW ARTICLE

https://doi.org/10.5005/jp-journals-10089-0041
Journal of Acute Care
Volume 2 | Issue 3 | Year 2023

Echocardiographic Assessment of Mitral Valve

Satyen Parida1https://orcid.org/0000-0003-4752-3653, Muthapillai Senthilnathan2https://orcid.org/0000-0001-8418-5046, Chitra R Thangaswamy3

1–3Department of Anaesthesiology and Critical Care, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry, India

Corresponding Author: Satyen Parida, Department of Anaesthesiology and Critical Care, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry, India, Phone: +91 7708746042, e-mail: jipmersatyen@gmail.com

Received: 20 February 2023; Accepted: 15 March 2023; Published on: 19 February 2024

ABSTRACT

Echocardiography is the principal method for the estimation of the structure and function of the mitral valve (MV). Impedance to mitral inflow is caused essentially by mitral stenosis (MS) of rheumatic origin. Less common causes involve tumors, principally myxomas, calcification of the mitral annulus, carcinoid heart disease, and congenital MS. When associated with exclusive valvular and subvalvular affliction, severe MS is diagnosed with a pressure half-time (PHT) of >150 ms and valve area ≤1.5 cm2. In MS of rheumatic origin, echocardiography enables evaluation of the likelihood of success for percutaneous balloon valvotomy. Echocardiography allows appraisal of the degree of mitral regurgitation (MR) and helps discern various causes such as prolapse or flail of MV segments, endocarditis of mitral leaflets, rheumatic etiology, ischemic MR, or functional MR as seen in cardiomyopathy.

How to cite this article: Parida S, Senthilnathan M, Thangaswamy CR. Echocardiographic Assessment of Mitral Valve. J Acute Care 2023;2(3):144–152.

Source of support: Nil Conflict of interest: None

Keywords: Echocardiography, Mitral, Mitral regurgitation, Mitral stenosis, Mitral valve

INTRODUCTION

The MV synchronizes blood flow from the left atrium (LA) to the left ventricle (LV). It has a saddle shape (described as a hyperbolic paraboloid), with two leaflets, as opposed to the other atrioventricular valve, the tricuspid, which has three (Fig. 1). Echocardiography has evolved as the foremost technique to image and identify the structure and functionality of the MV.1,2 A discussion of the assessment of the structure and function of the normal MV by echocardiography and common mitral valvular abnormalities will be provided here.

Fig. 1: Location of the MV

STAGES OF MITRAL VALVE DISEASE

The 2020 American College of Cardiology/American Heart Association (ACC/AHA) guidelines for evaluation and decision-making in patients having cardiac valve diseases categorizes both mitral stenosis and regurgitation into four stages based on valve anatomy, hemodynamics, hemodynamic consequences on LA, LV and the pulmonary vasculature, as well as symptoms.3 Stage A defines patients at risk, stage B defines progressive valve disease, stage C defines the asymptomatic and severe disease, and stage D defines symptomatic and severe disease (Tables 1 to 3).

Table 1: Stages of primary MR
Grade Definition Valve anatomy Valve hemodynamics* Hemodynamic consequences Symptoms
I At the risk of MR Mild MV prolapse with normal coaptation Mild valve thickening and leaflet restriction No MR jet or small central jet area <20% LA on Doppler Small vena contracta <0.3 cm None None
II Progressive MR Severe MV prolapse with normal coaptation Rheumatic valve changes with leaflet restriction and loss of central coaptation Prior IE Central jet MR 20–40% LA or late systolic eccentric jet MR Vena contracta <0.7 cm Regurgitant volume <60 mL Regurgitant fraction <50% ERO <0.40 cm2 Angiographic grade I–II+ Mild LA enlargement No LV enlargement Normal pulmonary pressure None
III Asymptomatic severe MR Severe MV prolapse with normal coaptation or flail leaflet Rheumatic valve changes with leaflet restriction and loss of central coaptation Prior IE Thickening of leaflets with radiation heart disease Central jet MR >40% LA or holosystolic eccentric jet MR Vena contracta ≥0.7 cm Regurgitant volume ≥60 mL Regurgitant fraction ≥50% ERO ≥0.40 cm2 Angiographic grade III–IV+ Moderate or severe LA enlargement LV enlargement Pulmonary hypertension may be present at rest or with exercise C1: LVEF >60% and LVESD <40 mm C2: LVEF ≤60% and LVESD ≥40 mm None
IV Symptomatic severe MR Severe MV prolapse with loss of coaptation or flail leaflet Rheumatic valve changes with leaflet restriction and loss of central coaptation Prior IE Thickening of leaflets with radiation heart disease Central jet MR >40% LA or holosystolic eccentric jet MR Vena contracta ≥0.7 cm Regurgitant volume ≥60 mL Regurgitant fraction ≥50% ERO ≥0.40 cm2 Angiographic grade III–IV+ Moderate or severe LA enlargement LV enlargement Pulmonary hypertension present Decreased exercise tolerance Exertional dyspnea

ERO, effective regurgitant orifice; IE, infective endocarditis; LA, left atrium/atrial; LV, left ventricular; LVEF, left ventricular ejection fraction; LVESD, left ventricular end-systolic dimension; MR, mitral regurgitation, *, several valve hemodynamic criteria are provided for assessment of MR severity, but not all criteria for each category will be present in each patient. Categorization of MR severity as mild, moderate, or severe depends on data quality and integration of these parameters in conjunction with other clinical evidence

Table 2: Stages of secondary MR
Grade Definition Valve anatomy Valve hemodynamics* Associated cardiac findings Symptoms
I At the risk of MR Normal valve leaflets, chords, and annulus in a patient with coronary disease or cardiomyopathy No MR jet or small central jet area <20% LA on Doppler Small vena contracta <0.3 cm Normal or mildly dilated LV size with fixed (infarction) or inducible (ischemia) regional wall motion abnormalities Primary myocardial disease with LV dilation and systolic dysfunction Symptoms due to coronary ischemia or HF may be present that respond to revascularization and appropriate medical therapy
II Progressive MR Regional wall motion abnormalities with mild tethering of mitral leaflet Annular dilation with severe loss of central coaptation of the mitral leaflets Regurgitant volume <60 mL Regurgitant fraction <50% ERO <0.40 cm2 Regional wall motion abnormalities with reduced LV systolic function LV dilation and systolic dysfunction due to primary myocardial disease Symptoms due to coronary ischemia or HF may be present that respond to revascularization and appropriate medical therapy
III Asymptomatic severe MR Regional wall motion abnormalities and/or LV dilation with severe tethering of mitral leaflets Annular dilation with severe loss of central coaptation of the mitral leaflets Central jet MR >40% LA or holosystolic eccentric jet MR# Vena contracta ≥0.7 cm Regurgitant volume ≥60 mL Regurgitant fraction ≥50% ERO ≥0.40 cm2 Angiographic grade III–IV+ Regional wall motion abnormalities with reduced LV systolic function LV dilation and systolic dysfunction due to primary myocardial disease Symptoms due to coronary ischemia or HF may be present that respond to revascularization and appropriate medical therapy
IV Symptomatic severe MR Regional wall motion abnormalities and/or LV dilation with severe tethering of mitral leaflet Annular dilation with severe loss of central coaptation of the mitral leaflets Regurgitant volume <60 mL Regurgitant fraction <50% ERO <0.40 cm2 Regional wall motion abnormalities with reduced LV systolic function LV dilation and systolic dysfunction due to primary myocardial disease HF symptoms due to MR persist even after revascularization and optimization of medical therapy Decreased exercise tolerance Exertional dyspnea

2D, two-dimensional; ERO, effective regurgitant orifice; HF, heart failure; LA, left atrium; LV, left ventricle; MR, mitral regurgitation; TTE, transthoracic echocardiogram; *, several valve hemodynamic criteria are provided for assessment of MR severity, but not all criteria for each category will be present in each patient. Categorization of MR severity as mild, moderate, or severe depends on the data quality and integration of these parameters in conjunction with other clinical evidence

Table 3: Stages of MS
Grade Definition Valve anatomy Valve hemodynamics Hemodynamic consequences Symptoms
I At the risk of MS Mild valve doming during diastole Normal transmitral flow velocity None None
II Progressive MS Rheumatic valve changes with commissural fusion and diastolic doming of the MV leaflets Planimetered MVA >1.5 cm2 Increased transmitral flow velocities MVA >1.5 cm2 Diastolic PHT <150 ms Mild-to-moderate LA enlargement Normal pulmonary pressure at rest None
III Asymptomatic, severe MS Rheumatic valve changes with commissural fusion and diastolic doming of the MV leaflets Planimetered MVA ≤1.5 cm2 (MVA ≤1 cm2 with very severe MS) MVA ≤1.5 cm2 (MVA ≤1 cm2 with very severe MS) Diastolic PHT ≥150 ms (Diastolic PHT ≥220 ms with very severe MS) Severe LA enlargement Elevated PASP >30 mm Hg None
IV Symptomatic severe MS Rheumatic valve changes with commissural fusion and diastolic doming of the MV leaflets Planimetered MVA ≤1.5 cm2 MVA ≤1.5 cm2 (MVA ≤1 cm2 with very severe MS) Diastolic PHT ≥150 ms (Diastolic PHT ≥220 ms with very severe MS) Severe LA enlargement Elevated PASP >30 mm Hg Decreased exercise tolerance Exertional dyspnea

ACC, American College of Cardiology; AHA, American Heart Association; LA, left atrial; LV, left ventricular; MS, mitral stenosis; MVA, mitral valve area; PASP, pulmonary artery systolic pressure. The transmitral MPG should be obtained to further determine the hemodynamic effect of the MS and is usually >5–10 mm Hg in severe MS; however, due to the variability of the MPG with heart rate and forward flow, it has not been included in the criteria for severity. This table has been reprinted, nearly unchanged, in the 2020 ACC/AHA guideline for the management of patients with valvular heart disease; however, the 2020 guideline no longer includes criteria for “very severe MS” in the valve anatomy and valve hemodynamics columns

A transthoracic echocardiogram (TTE) is generally the initial and in most circumstances, an adequate imaging modality to assess the MV. If, however, there is a clinical finding not explained by TTE, or if better visualization or more accurate measurements are needed, a TEE could be indicated.

Normal MV

Anatomically, the orientation of the anterior mitral leaflet (AML) places this broad structure toward the anterior chest wall, making it an ideal target for the reflection of ultrasound waves while performing a TTE. Furthermore, because of its relatively large margin-to-base ratio (as opposed to the posterior ML (PML), which covers almost two-thirds of the mitral annular circumference, but has a much lower surface area), the AML is highly mobile. Several unique gradings and taxonomical descriptions for structural evaluation of the MV can be found in the literature, but Carpentier’s classification (2001) is widely integrated into clinical practice by most echocardiographers and cardiothoracic surgeons. Based on Carpentier’s classification, the leaflets of the MV are structurally sorted out into eight divisions (Fig. 2). PML demonstrates a total of three scallops—the medial scallop (P3), the middle scallop, which is the most overgrown of the three (P2), and the lateral scallop (P1). AML is partitioned into three morphologic segments—anteromedial (A3), middle (A2), and anterolateral (A1), based on the three scallops of the PML, which the corresponding segments of the AML coapt with. There is actually an absence of scalloping on the AML. The MV also has two divisions for the commissures, namely, the posteromedial commissure and the anterolateral commissure, each of which lie adjacent to trigones of the same name.

Fig. 2: MV leaflet anatomy

A layer of dense connective tissue, the annulus fibrosus, is situated between the LA and LV. The leaflets are framed out of an external envelope of the endocardium and a fibrous core of connective tissue, which blends seamlessly with the annulus fibrosus (Fig. 3).

Fig. 3: Histology of the MV apparatus

The MV can be assessed by echocardiography through a variety of anatomic windows, the parasternal, apical, and subxiphoid, all of which should be used in its transthoracic assessment. Similarly, several TEE midesophageal and transgastric views assist evaluation of MV anatomy.

M-mode Echocardiogram

The M-mode echocardiographic evaluation can be performed via TTE from the parasternal long-axis (PLAX) or short-axis (PSAX) window at the level of the MV. Generally, the AML presents a motion signature that reveals the phasic nature of ventricular filling and produces a familiar M-shaped pattern. The posterior leaflet moves in a near mirror image “W” signature with a much smaller excursion. The separation of the septum from the maximal excursion of the AML is called the E-point septal separation, and is generally smaller than 5 mm, but can be increased with impaired LV function (Fig. 4). In such patients, the M-shaped pattern of the AML may be immediately followed by a “B hump.”

Fig. 4: M-mode echocardiogram of the MV

Two-dimensional (2D) Echocardiogram

Mitral valve (MV) 2D imaging with TTE depends upon the imaging window and view used for evaluating the same. The PSAX view visualizes the MV as an ovoid, often described as a “fish mouth” orifice (Fig. 5), while the PLAX and apical views, demonstrate the thickness and motion of the leaflets of the MV, with the AML longer and more mobile than the PML (Figs 6 and 7). In general, the normal MV should appear as a mobile, two-leaflet structure that moves freely enough to respond to the normal flux of diastolic filling but forms a stable coaptation plane in systole without breaking the plane of the mitral annulus and entering the LA.

Fig. 5: 2D TTE in the short-axis plane of LV at the level of the MV

Fig. 6: 2D TTE PLAX view

Fig. 7: 2D TTE apical four-chamber position

Transesophageal Echocardiogram (TOE)

Because the esophagus is situated directly posterior and adjacent to the LA, TEE generally provides superior visualization of the entire apparatus of the MV, inclusive of the leaflets, annulus, chordae, and papillary muscles, as well as the adjoining LV wall, compared to TTE. By TEE in the 0–30 plane, at the midesophageal level, A1, and P1 segments are seen first as the probe is gradually advanced to the five-chamber view; with deeper insertion in the four-chamber view, A3–A2 (base-to-edge) and P2 or P1–P2 (base-to-edge) come into view, and subsequently, with still gradual deeper insertion, A3 and P3 are visualized. In the midesophageal commissural view (45–90°), all six segments of the valve leaflets can be visualized by rotating the probe clockwise and counterclockwise. Finally, in the long-axis view (120–150°), all segments can again be visualized by rotating the probe. By comprehensively examining all segments from different planes, MV lesions can be accurately localized and characterized (Fig. 8).4 From the transgastric window, the MV, along with the subvalvular structures could be evaluated in the basal short-axis, two-chamber, long-axis and deep transgastric views.

Fig. 8: 2D TOE showing the MV leaflets in different views. A1, A2, A3, P1, P2, and P3 are scallops of anterior and posterior MV leaflets, respectively. Ao, aorta; LC, lateral commissure; MC, medial commissure; ME, Midesophageal

Doppler Echocardiogram

Pulse wave Doppler examination of the normal MV reveals that the velocity pattern of blood entering the LV during diastole closely duplicates the M-shaped signature of the M-mode of that structure; the flow of blood is maximal in the early (E) filling phase, falls substantially during the mid-diastolic conduit phase, and accelerates again during atrial (A) contraction. Transmitral flow is sampled from the apical four-chamber (A4C) view; the sampling site used to obtain this signal is between the MV leaflets (Fig. 9). When transmitral flow is used to quantitate flow volume, the sample volume typically rests at the mitral annular plane. The normal peak velocity of flow across the MV is generally lower than 1 m/seconds and its normal area is 4–6 cm2. A color flow Doppler (CFD) is also used to evaluate flow abnormalities across the MV, as we shall see in subsequent sections.

Fig. 9: Normal pulse-wave Doppler echocardiographic transmitral diastolic inflow pattern

Three-dimensional (3D) Echocardiogram

Three-dimensional (3D) echocardiography has improved the appreciation of the unique structure and function of the hyperbolic paraboloid, in which the MV is 3D TTE image acquisition is performed from the parasternal and apical windows, using the zoomed or full-volume feature. Changing the display enables visualization of the MV, either from the LV or LA (“surgical”) perspective and allows for precise lesion localization. Additionally, 3D echocardiography facilitates accurate LV measurements as it avoids LV foreshortening.5 Subvalvular apparatus can be seen from the LV perspective, while the leaflets are better evaluated from the LA side (Video 1).6 3D TEE has superior resolution compared with 3D TTE and are a critical aid in percutaneous MV repair.7

MITRAL STENOSIS

Etiology

The most common cause of MS would be rheumatic origin in India. Other rare causes of MS include congenital, deposition of calcium, MV prolapse, and lupus.

Criteria for diagnosing MS:

The severity of MS based on MV area (MVA)

  • Normal MVA: 2.5–4.5 cm2
  • Progressive MS: <2.5 cm2
  • Severe MS: ≤1.5 cm2
  • Very severe MS ≤1 cm2

The severity of MS based on mean pressure gradients (MPG) across the MV:

  • Mild MS: < 5 mm Hg
  • Moderate MS: 5–10 mm Hg
  • Severe MS: >10 mm Hg

M-mode Echocardiography of MS

In the PLAX view or PSAX, the M-mode cursor can be kept at MV leaflets to obtain the movement of MV (Fig. 10). MS alters the appearance of the M-mode tracing of the MV so that its normal early diastolic closure is delayed or abolished. The early diastolic closure slope, the E–F slope, can be used to differentiate among the degrees of obstruction. Although this method is the least reliable means of quantitating the severity of obstruction, a slope of <10 mm/seconds (normal is >60 mm/seconds) from a valve recording made during suspended respiration is evidence for severe MS.8 In MS, the posterior leaflet moves forward in diastole, paralleling the anterior. Reversal of diastolic motion from the normal pattern makes the M-mode of the posterior leaflet one of the most valuable means of identifying MS.

Fig. 10: Mitral stenosis on M-mode echocardiography

Two-dimensional TTE of MS

Doming of AML, paucity of movement of PML, thickening of chordae and associated MR can be appreciated in patients with MS in either the A4C) (Video 2) or PLAX views (Video 3). One of the methods to assess the severity of MS is via planimetry (Fig. 11) in the PSAX view at the MV level. Unlike transvalvular pressure gradients, MV area measurement by planimetry is not affected by the flow.

Fig. 11: Planimetry of the MV

Doppler Echocardiogram

Doppler echocardiography may demonstrate an absent A wave in atrial fibrillation. The time required for the peak pressure to become half is the PHT, which needs to be measured from the E wave (Video 4). A PHT >150 ms indicates severe MS. MVA = 220/PHT (220 is derived from the product of compliance of LA and LV with root value of peak pressure gradient across the MV). The transvalvular MPG should be expressed along with heart rate as tachycardia overestimates the MPG. The pressure gradient across the MV will be calculated by Gorlin’s formula: ΔP = 4 × V2 The continuity equation can also be used to estimate MVA. As per the law of conservation of mass, the flow on either side of the MV must be equal. LV outflow tract (LVOT) diameter can be measured from an apical five-chamber (A5C) or PLAX view from which LVOT area can be calculated by the machine. The LVOT velocity time integral (VTI) can be traced from the A5C view; MV VTI can be estimated by continuous wave (CW) Doppler by placing the Doppler cursor at the MV inlet. In another method of calculating MVA = (LVOT VTI × LVOT area)/MV VTI. This method needs many measurements which are dependent on flow and hence, it may not reflect the true hemodynamic effect of MS. Noting the degree of transtricuspid valvular gradient and pulmonary hypertension, as determined by Doppler of the tricuspid regurgitant jet is an indirect way of identifying the severity of MS, as indeed, are other indicators including the degree of shortening of the chordae tendineae, estimating the extent of leaflet calcification, noting the degree of LA enlargement, noting the degree of LV underloading (i.e, volume decrease), noting the presence of right ventricular and atrial dilatation, etc.

Stress Echocardiography in MS

When the patient’s clinical presentation is disproportionate to the TTE finding, then stress echocardiography with exercise or dobutamine, can be considered to study the exercise capacity and to study the changes in the transvalvular gradients with exertion. Dobutamine infusion can be started to study the effect of stress on the MPG across the MV in the intensive care unit.

Three-dimensional Echocardiography in MS

The 3D echocardiography is one of the tools that can help to assess the hemodynamic severity of MS. Calcification, commissural fusion, chordal thickening, and prolapse of leaflets are better appreciated with 3D echocardiography (Video 5).

Echocardiography in Balloon Mitral Valvuloplasty (BMV)

Balloon mitral valvuloplasty(BMV) is performed by advancing the balloon catheter across the MV. While inflating the balloon, there will be a splitting of the commissures. Relatively mobile, thin leaflets, without calcification and without subvalvular fusion are a few anatomical variables that provide favorable outcomes after BMV. However MR remains a significant concern following BMV, as can be seen in this video of a 40 years male who underwent BMV and showed significant improvement in MVA, but with resultant MR (Video 6).

Mitral Annular Calcification (MAC)

It occurs due to degenerative processes. It results in the deposition of calcium, phosphate, and lipid over the annular fibrosis. MAC can be confirmed with the detection of accumulation of calcium predominantly along its posterior aspect with extension into the posterior leaflet. It progresses anteriorly as severity increases.

Congenital MS

The anomaly may be in the leaflets, chordae or in papillary muscles. Double orifice MV, Ebstein’s malformation of the MV, a mitral ring, and Hammock valve are the different morphological lesions of MV described.

Cor Triatriatum

Rare cardiac anomaly where there is a membrane separating the pulmonary veins from the LA. There will be two portions with LA—the confluence of pulmonary veins and actual LA and its appendage. Physiologically, it mimics total anomalous pulmonary venous connection. Few patients with cor triatriatum also have congenital MS.

Left Atrial Myxoma

Myxomas are the most common primary cardiac tumors. The most common site (up to 75%) originates from LA (either from the mitral annulus or interatrial septum). Myxomas are pedunculated. Clinical presentations include dyspnoea, paroxysmal nocturnal dyspnea, and pulmonary edema.

Supramitral Ring

The supravalvular mitral ring is a rare congenital anomaly of the MV apparatus. It restricts LV filling and results in pulmonary hypertension. There are at least two variants of this anomaly—the supramitral ring and the intramitral ring. In the supramitral ring, there is a fibrous ring between the LA appendage and the MV annulus. This variant does not affect valvular movement. It differs from the cor triatriatum as the supramitral ring lies between the MV apparatus and LA appendage. In CFD echocardiography, there will be flow turbulence above the MV due to the obstruction caused by the supramitral ring. Intramitral ring is located in the mitral tunnel itself and it restricts the mobility of the MV. This variant is associated with abnormal subvalvular apparatus. Supravalvular mitral ring is associated with many other congenital anomalies of the heart like Shone complex (consisting of at least four obstructive lesions—parachute MV, intramitral ring, coarctation of the aorta, and subvalvular aortic stenosis), ventricular septal defect (VSD), bicuspid aortic valve, cor triatriatum, double outlet right ventricle and tetralogy of Fallot. Echocardiographic evaluation will reveal the circumferential ring attached to the MV leaflets in patients with intramitral ring and restriction of MV movement. The above-mentioned congenital anomalies may also coexist with intramitral ring.

MITRAL REGURGITATION

Acute MR

Acute MR occurs as a result of posteromedial papillary muscle rupture resulting from an inferior wall infarct or owing to altered geometry of the LV causing restricted closing of mitral leaflets.9 The PML is more commonly affected than the AML and the regurgitant jet is central or directed posteriorly.

Chronic MR

Primary MR occurs due to damage to valve leaflets, chordae tendineae or papillary muscles.10 Conditions include MV prolapse, leaflet perforation, and papillary muscle rupture. Secondary MR occurs due to left ventricular remodeling or annular dilatation. Conditions include ischemic or dilated cardiomyopathy.

Determination of the Severity of MR

Transthoracic echocardiogram (TTE) is the main modality for 2D valve assessment. TEE is reserved to assess suitability for transcatheter or surgical procedures and inconclusive studies. 3D is useful in the accurate localisation of the valvular lesion. Anatomical indicators of severity—a flail leaflet segment or major coaptation defect indicates severe MR. The coaptation surface of a competent MV is 8–10 mm which may be accurately measured by 3D TEE. The LV size and systolic function as measured by Simpson’s biplane method also depict the severity of MR. The LA volume in A4C and A2C images at end-systole could also indicate the degree of severity. 3D assessment is superior for the assessment of LA and LV volume and ejection fraction (EF). Color Doppler—this is the primary method to assess the severity both qualitatively and quantitatively. The MR jet must be evaluated in all possible views to note its origin and size, spatial orientation in the LA, and proximal flow convergence on the ventricular surface of the leaflets [proximal isovelocity surface area or (PISA)].11

  • Jet area and jet characteristics: As there are several limitations of using the jet area to assess severity, the American Society of Echocardiography does not recommend this technique.12
  • Vena contracta—the vena contracta width is the most useful semiquantitative method for determining severity. It should be estimated in the PLAX, A4C or A2C views (TTE) or midesophageal long-axis view (TEE). A zoom view of the MV should be used and the focus adjusted to optimise the view. The color box size and position should be adjusted to focus on the leaflet coaptation. Doppler gain should be just below the level at which spontaneous flecks of color are seen. Doppler scale set to 40–60 cm/second is satisfactory. Although independent of hemodynamics, underestimation can occur due to low color gain or multiple jets. Overestimation can occur due to high color gain, irregular jet shape or atrial fibrillation (AF).
  • Proximal isovelocity surface area (PISA) method: In MR, the blood converges upon the regurgitant orifice resulting in the formation of hemispheric shells of different velocities that progressively increase, as the surface area of the shells decreases. One could then use a zoomed view, use CFD, bring down the Nyquist limit to between 20 and 40 cm/second, and manipulate the probe to identify the greatest radius. The PISA radius is computed as the distance from the point where the color Doppler aliases up to the vena contracta. After unfreezing the image, the cursor can be placed through the centre and enter color flow M-mode to identify the dynamic PISA.

mitral regurgitation (MR flow rate (mL/second) = surface area of the proximal hemispheric shell × CFD Nyquist velocity. Effective regurgitant orifice area (EROA) (cm2) = MR flow rate/peak velocity of MR jet (cm/second) Regurgitant volume (mL) = EROA × MR VTI (cm)

  • Qualitative techniques—the CW Doppler could easily be aligned through the MR jet. The peak velocity and signal intensity are assessed. Mild MR is detected as an incomplete envelope of low systolic signal intensity, while dense complete systolic envelopes of approximately the same density as the diastolic signal indicate severe MR. In acute severe MR, a sudden rise in LA pressure causes a decrease in the transmitral gradient and regurgitant jet velocity during late systole which gives a Doppler signal with a shape that is asymmetrical, and is described as the cutoff of the V wave.
  • Transmitral early diastolic wave velocity—the sample volume is placed 1–3 mm between the tips of the MV leaflets during diastole. An Emax >1.4 m/second suggests severe MR.
  • Pulmonary venous flow reversal—the sample volume is placed 1–2 cm into the vein. A blunted S wave or systolic flow reversal might indicate significant MR. One needs to rule out diastolic dysfunction before reporting the severity of MR based on pulmonary venous flow. Any condition which can elevate the pressure in the LA can also blunt pulmonary venous flow.
  • Calculation of MR severity by continuity equation—this is calculated as MV stroke volume—LVOT stroke volume. This represents the regurgitant volume. The regurgitant volume may be underestimated in AR and LVOT obstruction. Overestimation occurs in MS or VSD. The regurgitant volume may be variably estimated in AF, which may not indicate the true severity of the MR. A regurgitant fraction greater than 50% suggests severe MR and is computed by dividing the regurgitant volume by the sum of the regurgitant volume and the LV stroke volume at LVOT.
  • Other important calculations that could potentially affect decision-making in MR include LV size, systolic function as assessed by the Simpsons biplane method, and LA volume assessed in the A4C and A2C images at end-systole. 3D assessment for LA and LV volume as well as EF is superior to 2D.

Mechanism of MR

The varied mechanisms of MR are best categorized by the scheme presented by Carpentier in Table 4.

Table 4: Mechanism of MR Carpentier classification
Types Pathology
Type I Normal leaflet motion
Type II Excessive leaflet motion
Type III Restricted leaflet motion

MV billowing—a portion of the MV leaflet goes above the annular plane during systole, but the point of leaflet coaptation stays below the plane. Mitral valve prolapse (Videos 7 and 8)—elevation of one or both leaflet tips above the mitral annular plane in systole.13 Flail—refers to a situation where the edges of one of the mitral leaflets display free and unrestricted excursion into the LA (Video 9) because of one or more ruptured chordae tendineae. Ischemic MR—tethering of posterior mitral leaflet toward the posterior wall can lead to a posteriorly directed and eccentric jet (Videos 101112). If both leaflets tether toward the apex, the jet can be central. The tenting height is the maximum distance between the mitral leaflet tips and the plane of the mitral annulus, measured during mid-systole.14 Tenting area depicts the area calculated between the plane of the mitral annulus and the coaptation point of the AML and PML during midsystole. Tenting height <0.5 cm, tenting area 0 cm2 and PML angle <35° are normal. Tenting height > 1 cm, tenting area 2.5–3 cm2, and posterolateral angle >35° predict unsatisfactory outcomes following MV repair.

Fig. 12: Endocarditis of the MV leaflet

Rheumatic MR—rheumatic heart disease confers characteristic features to the MV on echocardiography.15 Leaflets appear thick and there may be chordal elongation with possible prolapse, often of the AML. The chordae tendineae may also rupture resulting in flail AML in severe acute rheumatic carditis, and sometimes following infective endocarditis (Fig. 12). Both pure MR as well as those with accompanying MS, the movement of leaflets may be severely restricted, typically at the tips, with consequent doming (Fig. 13), appearing like an elbow or dogleg deformity, especially the AML. Calcification of mitral leaflets is typically unusual in rheumatic disease in children as well as young adults but may occur in the elderly, having long-standing MR.

Fig. 13: Doming of mitral leaflets due to rheumatic affliction

SUPPLEMENTARY MATERIAL

The supplementary videos 1 to 12 are available online on the website of https://www.jacutecare.com/journalDetails/JAC
Video 1: 3D TEE of normal mitral valve from left atrial aspect.
Video 2: Apical 4-chamber view of stenotic mitral valve with color doppler.
Video 3: Parasternal long axis view of stenotic mitral valve with color doppler.
Video 4: Pulse wave doppler through the stenotic mitral valve.
Video 5: 3D TEE of stenotic mitral valve from left atrial aspect.
Video 6: S/P balloon mitral valvotomy showing significant improvement in mitral valve area, but with resultant MR in 2D TTE apical 4-chamber.
Video 7: 2D TTE showing prolapse of the anterior mitral leaflet in parasternal long axis view.
Video 8: 2D TTE with color doppler showing prolapse of the anterior mitral leaflet with severe eccentric mitral regurgitation in parasternal long axis view.
Video 9: 2D TTE apical 4-chamber view with a flail anterior mitral leaflet.
Video 10: 2D TEE mid-esophageal long axis view showing tethering of the posterior mitral leaflet in patient with ischemic mitral regurgitation.
Video 11: 2D TEE mid-esophageal long axis zoomed view showing tethering of the posterior mitral leaflet in patient with ischemic mitral regurgitation.
Video 12: 3D TEE showing ischemic mitral regurgitation due to posterior mitral leaflet tethering.

ORCID

Satyen Parida https://orcid.org/0000-0003-4752-3653

Muthapillai Senthilnathan https://orcid.org/0000-0001-8418-5046

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