Mitral regurgitation

Mitral regurgitation (MR) is a common valvular disorder that can arise from abnormalities of any part of the mitral valve apparatus.

These include the valve leaflets, annulus, chordae tendineae, and papillary muscles. 

MR is the most common valvular abnormality worldwide, affecting over 2% of the total population and has a prevalence that increases with age.

Pathophysiology

The definition of mitral regurgitation is a retrograde flow from the left ventricle into the left atrium. 

Mitral regurgitation leads to left ventricular volume overload due to increased stroke volume, caused by an increase in blood volume within the left atrium and hence an increased preload delivered to the left ventricle during diastole.

In chronic progressive MR, ventricular remodeling occurs, allowing maintenance of cardiac output, and an initial increase in ejection fraction (EF) is usually observed.

‍Symptoms

Many patients with severe MR are initially asymptomatic.

When associated with coronary artery disease (CAD) and acute myocardial infarction (MI), significant acute MR is accompanied by the following symptoms:

• Dyspnea
• Fatigue
• Orthopnea
• Pulmonary edema (often the initial manifestation)

The following may be noted with chronic MR:

• Some patients may remain asymptomatic for years
• Patients may have normal exercise tolerance until systolic LV dysfunction develops, at which point they may experience symptoms of a reduced forward cardiac output
• Patients may feel chest palpitations if AF develops as a result of chronic atrial dilatation
• Patients with LV enlargement and more severe disease eventually progress to symptomatic congestive heart failure (CHF) with pulmonary congestion and edema

Heart sounds

• Diminished S1 in acute MR and chronic severe MR with defective valve leaflets
• Wide splitting of S2 as a result of early closure of the aortic valve
• S3 as a result of LV dysfunction or increased blood flow across the MV
• Accentuated P2 if pulmonary hypertension is present
• Characteristic holosystolic murmur (or mid-systolic if etiology of MR is mitral valve prolapse)

‍Etiology (Image 1)

‍1) Primary MR — Also called degenerative or organic - any MR resulting from structural deformity of or damage to the leaflets, chordae, and/or papillary muscles causing leaflets to close insufficiently during systole.

• Degenerative mitral valve disease (including mitral valve prolapse) - most common cause of primary MR in developed countries. The underlying pathophysiologic basis for degenerative mitral regurgitation is most commonly related to myxomatous degeneration of the mitral valve, resulting in mitral valve prolapse (MVP). Also it can be caused by  fibroelastic deficiency disease, seen primarily in older populations.
• Congenital
• Infective endocarditis
• Rheumatic heart disease (Is uncommon in developed countries, but continues to constitute a significant burden in the rest of the world. Rheumatic valve disease often results in MR in the first two decades of life, while mitral stenosis and mixed mitral stenosis plus MR are more often seen in adults.) 

• Trauma, which can cause ruptured chordae and acute MR
• Use of certain drugs
• Mitral annular calcification

2) The secondary MR - Also called functional or ischemic, no structural problems with the valve itself. Leads to mitral annular dilatation or displacement of papillary muscles causing retrograde flow from improperly closed mitral valve leaflets.

• Ischemic MR (Coronary heart disease) - MR in patients with coronary disease most often is due to a regional wall motion abnormality distorting the mitral valve apparatus resulting in inadequate leaflet closure. In patients with previous myocardial infarction, chronic MR is seen due to adverse ventricular remodeling. .
• Atrial Fibrillation Associated
• Hypertrophic or Dilated cardiomyopathy

Carpentier’s classification

The Carpentier classification divides mitral valve regurgitation into three types based on leaflet motion (Image 2):

Type 1 – Normal leaflet motion

• predominantly caused by annular dilation, rarely by leaflet perforation secondary to infective endocarditis or an iatrogenic complication
• annular dilation commonly due to LV dilatation, but significant LA dilation is a possibility (Atrial Fibrillation associated)
• ECHO: regurgitation jet directed centrally due to coaptation defect

Type 2 – Excessive leaflet motion

• MV leaflets exhibiting disproportionate excursion into the left atrium = flail leaflet prolapse
• secondary to papillary muscle rupture, chordal rupture, chordal elongation
• ECHO: The MR jet in this type is always eccentric directed away from the involved leaflet

• anteriorly directed in posterior MV leaflet prolapse 
• posteriorly directed in anterior MV leaflet prolapse

Type 3 - Restricted Leaflet motion

• there is a decreased excursion of one or both leaflets
• regurgitant jet will be directed away from the involved leaflet if the other is spared, and centrally directed if both leaflets involved
• Type 3 is divided into 2 categories:

Type 3a – leaflet motion restricted both in systole and diastole

• aberrant systolic excursion and diastolic coaptation
• The leaflets are thickened and shortened, resulting in inadequate coaptation and regurgitation

• typically rheumatic disease, but also post-inflammatory thickening and post-radiotherapy fibrosis

Type 3b – leaflet restriction limited to diastole

• structurally normal leaflets, underlying LV disease causes leaflet tethering into LV 
• papillary muscle dysfunction, LV dilatation

An understanding of the mechanism of valve failure is critical in determining patient selection for suitability of valve intervention, including repair.

The presence, location, and extent of prolapse are of crucial importance in defining the likelihood of successful MV repair.

Video 1 Posterior leaflet prolapse leading to mitral regurgitation - PLAX view

Video 2 Posterior leaflet prolapse causing mitral regurgitation - A4C view

Video 3 Moderate mitral regurgitation, annular dilatation - PLAX view (Color flow Doppler)

Video 4 Moderate mitral regurgitation, annular dilatation, LV dysfunction - PSAX view

Video 5 Moderate mitral regurgitation, annular dilatation, LV dysfunction - A4C view

Video 6 Mitral valve prolapse (posterior cusp) causing moderate/severe MR - A4C view

Video 7 Mitral annular calcification leading to moderate mitral regurgitation - PLAX view

Video 8 Mitral valve infective endocarditis, moderate mitral regurgitation - TEE

Video 9  Papillary muscle rupture leading to acute massive mitral regurgitation - TEE

Video 10 Acute massive mitral regurgitation due to PM papillary muscle rupture - TEE

Echo assessment of mitral regurgitation

Quantification of the severity of mitral regurgitation should be an integrative process of qualitative, semi-quantitative and quantitative parameters measured on TTE. 

Mitral regurgitation is heavily influenced by blood pressure and heart rate. These parameters should always be documented in the protocol, alongside with weight, height and body surface, and taken into account when comparing serial echo findings.

Whenever performing TTE to establish the diagnosis of MR, a precise anatomical description of the lesions in accordance to the Carpentier classification, mitral annular dimensions and presence of calcification should be defined.

TOE is recommended for patients with suboptimal image quality and 3D echocardiography provides detailed information for selecting the appropriate repair strategy. 

Image 3 Severe mitral regurgitation criteria based on 2D echocardiography

Vahanian A, Beyersdorf F, Praz F, et al. ESC/EACTS Scientific Document Group. 2021 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J. 2021 Aug 28:ehab395. doi: 10.1093/eurheartj/ehab395. Epub ahead of print. PMID: 34453165.

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What parameters do we measure?

1. MV morphology

TTE is the primary diagnostic test that provides initial detection of MR and evaluation of the etiology and mechanism of MR.

Examination of all mitral valve structures usually enables differentiation between primary and secondary (functional) MR.

It is crucial and mandatory to identify the mechanisms causing the MR in order to determine whether the patient will go for a valve repair, replacement or be treated conservatively (medically).

To assess MV morphology we need to view the mitral valve in a number of scanning planes. 

a) PLAX (Parasternal long-axis view) – MV is routinely first seen in the PLAX window.

This view in standard position goes through the centre of the MV showing the A2 and P2 scallops. You can also see the postero-medial papillary muscle extending from the inferolateral (posterior) LV wall.

To view the additional scallops simply change the angulation of the transducer:

• inferior tilt towards the RV inflow and Tri valve shows A3/P3 scallops
• superior tilt towards RV outflow and pulmonary view shows A1/P1 scallops

Video 11 Mitral valve - PLAX view (A2/P2 scallops)

‍b) PSAX (Parasternal short-axis) – at the level of the MV we can visualize all 6 scallops of the anterior A1/A2/A3 & posterior P1/P2/P3 leaflets and both commissures entirely. To view the papillary muscles tilt the transducer inferiorly towards the apex. At this position, the postero-medial PM is seen on the left and the antero-lateral on the right.

Video 12 Mitral valve - PSAX (anterior A1/A2/A3 & posterior P1/P2/P3 leaflets)

‍c) A4C (Apical four chamber view): shows an oblique plane of the anterior leaflet with A3, A2 and P1 visible. This view gives us a perspective of the AV valves, with the MV annulus in a superior position to the tricuspid annulus (further from the apex) and inter-annular distance of 5-11 mm. Any abnormalities in this distance suggest a congenital anomaly.

Video 13 Mitral valve - A4C view (A3, A2 and P1)

‍d) A2C (Apical two chamber view): only shows the left side of the heart by rotating the probe anti-clockwise. MV is shown at the level of leaflet coaptation (bi-commisural view) with P3, A2 and P1 visible. A2 scallop disappears during diastole.  

Video 14 Mitral valve - A2C (P3, A2 and P1)

‍e) A3C (Apical three chamber view): rotate the probe further anti-clockwise to show A3C with the central portion of the MV, where A2 and P2 are visualised (similar to PLAX view).

Video 15  Mitral valve - A3C view (A2, P2)

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Important anatomical findings in severe MR

• flail leaflet segment – eversion of the leaflet tip into LA = major coaptation defect
• coaptation gap – loss of leaflet coaptation suggests a large regurgitant orifice

Video 16 Anterior flail leaflet leading to severe mitral regurgitation - PLAX view

Video 17 Central malcoaptation caused by prolapse of both leaflets - TEE

Video 18 Central malcoaptation caused by prolapse of posterior leaflet (left side of the screen) - TEE

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2) Colour flow Doppler (CFD) MR jet

Colour flow Doppler is the primary method for detecting the presence of regurgitation. CFD gives us information on the presence, size and location of the jet. 

We can identify the origin of the jet, its jet area spatial orientation (width & length) and flow convergence into regurgitant orifice. Every jet looks different and there may be more than one jet present. When looking for the regurgitant jet, always optimize the 2D image before using colour Doppler as the quality of CFD depends on it. All segments of the mitral valve must be visualised in all available views, even atypical ones, to fully assess the size, origin and PISA of the jet. 

There are 3 important regions of the regurgitant jet:

1. Colour Jet Area – expansion of the jet within the LA (left atrium)
2. Vena Contracta – narrowest part of the jet in the regurgitant orifice
3. Flow Convergence on the ventricular surface of the leaflets (PISA)

a) Colour jet area

Colour jet area is a qualitative method good for exclusion of the presence of MR. It is easy to measure, but it is not recommended for grading the severity of MR as it is dependent upon actual hemodynamics.

The basic principle is that greater MR severity results in a larger jet within the LA. 

It is usually measured in apical 4 chamber view (A4C) by tracing the CFD signal within the LA. At the next step the LA area is traced and a ratio is calculated.

Ratio= Color Jet Area/LA area

As a result, you get a percentage of the LA area that is filled with MR jet. A severe MR should be suspected at a value of >50%.

b) Vena contracta (VC)

Vena contracta is the narrowest part of the regurgitant jet as it passes through the regurgitant orifice area.

‍Width of the vena contracta corresponds to the diameter of the regurgitant orifice and is a good semi-quantitative parameter of the severity of MR as it is not dependent on the driving pressure of LV and flow rate.

Vena contracta is measured in a view where all 3 parts of the jet are seen. The principle assumes that the regurgitant orifice is circular and has a similar diameter in orthogonal planes. In reality, regurgitant orifices may have many geometric shapes and often more than one jet is present. Measurement should therefore be averaged from near-orthogonal planes, usually the A4C and A2C views, and should be averaged over two to three beats. 

Ultrasound beam should be perpendicular to flow and the narrowest part immediately superior to the regurgitant orifice is measured.

Severity of regurgitation estimated from VC diameter:

• <3 mm – mild regurgitation
• >7 mm – severe regurgitation

MR orifice is usually circular in shape and the VCW (vena contracta width) accurately represents the EROA. On the other hand, secondary MR usually has an elliptical-shape orifice (or a slit-shaped orifice), that runs along the coaptation line of MV. An elliptical shape can share the same diameter as a circle yet have a much greater area than the circle. The VCW measurement is therefore almost always underestimated in secondary MR.

Image 4 Moderate mitral regurgitation, vena contracta 6 mm - PLAX

c) Flow convergence

Flow convergence is a phenomenon seen when liquid flows from a large chamber through a smaller orifice at a fixed rate.

Flow velocity gradually increases and is greatest as it converges on the narrowest region of the flow. If the orifice is planar, round and narrow, the flow convergence has spherical geometry.

Same thing happens when the blood flow accelerates towards the regurgitant orifice and can be visualized as concentric isovelocity hemispheres with colour Doppler (the velocity on the surface of each of the hemispheres is equal).

The smallest hemisphere closest to the orifice has the highest velocity. This phenomenon is the basis of the PISA method (Proximal Isovelocity Surface Area) which uses the proximal flow convergence zone to measure the volume of regurgitation (Image 5).

Camm A, Luscher T, Serruys P, et al. (2009). The ESC textbook of cardiovascular medicine. Oxford, Oxford University Press, page 64.

PISA method

Proximal Isovelocity Surface Area (PISA) method is based on the flow convergence and conservation of mass. That means that all blood passing through the flow convergence in the LV must also pass through the effective regurgitant orifice area (EROA) to LA. This is used to estimate the total volume of blood flowing through the EROA. 

PISA measures are usually made in the A4C view, but the PLAX may provide better alignment with regurgitant flow in cases of posteriorly directed eccentric MR (ischaemic MR, anterior leaflet prolapse). To better identify these isovelocity hemispheres reduce the CFD velocity at which blood flow aliases (Nyquist limit) to between 20 and 40 cm/s in the direction of the flow. Eccentric jet PISA should be measured in the view that the greatest radius is seen.

There are 2 steps to performing the PISA method:

1. Measuring the radius and calculating the area of PISA using CFD
2. Continuous Wave (CW) Doppler MR jet velocity measurement

1. To measure the radius (r) from the EROA to the PISA, we use the hemisphere where aliasing occurs – the point where colour abruptly changes from blue or red to turbulent multicoloured flow. Obtain a mid-systolic frame by freezing and measuring from the point of colour aliasing to vena contracta.

PISA radius >1.0 cm favours severe mitral regurgitation

Once we have the radius, we can calculate the area of PISA (2πr2). When we multiply this surface area by the aliasing velocity (Val) (cm/s) we can get the instantaneous volume flow rate through the PISA = flow rate through the EROA.

Volume flow rate (ml/s)= 2πr2* Val

EROA (effective regurgitant orifice area – basically the size of the “hole” in the MV) is now estimated by dividing the volume flow by the regurgitant velocity, which can be measured by performing a CW Doppler through the MR jet. The size of EROA is a quantitative parameter for grading the MR severity.

EROA = MR volume flow-rate ÷ MR peak velocity (cm/s)‍

EROA (mm2) Mild MR = <20 mm2, Moderate MR = 20-39 mm2, Severe MR = >40‍

Image 6 Moderate to severe mitral regurgitation, PISA radius=0.8 cm - A4C view

Image 7 Moderate mitral regurgitation, PISA radius=0.6 cm- TEE

Continuous wave (CW) Doppler measurements

In continuous wave (CW) Doppler the Doppler line is placed in the valve orifice.

The two most used measurements are maximal velocity of the MR jet (MR Vmax) and VTI (Velocity Time Integral). 

Velocities (flows) directed away from the transducer are displayed below the baseline and velocities towards the transducer are above the baseline.

Image 8 Severe mitral regurgitation, Vmax measurement (5.05 m/s) - A3C view

Image 9  Severe mitral regurgitation, VTI (153.7 cm) and Vmax  (5.11 m/s) measurement - A4C view

MR Jet Velocity

The max velocity of the jet represents the instantaneous systolic pressure gradient between the LV and LA.

Maximal MR jet velocities by CW Doppler typically range between 4 - 6 m/s. This reflects the high systolic pressure gradient between the LV and LA. 

Wave density on CW Doppler

The density and velocity of the CW Doppler signal can also be used as a qualitative guide to MR severity. Number of blood cells (=volume of blood) within the sampling area is proportional to the CW signal density. The denser the signal, the more severe MR usually is.

Waveform shape on CW Doppler

Waveform shape also aids in identifying the severity of MR.

• Triangular with peaking in early systole – rapid pressure equalisation, suggestive of very severe or torrential, often acute MR
• Paraboral – moderate MR

Velocity Time Integral (VTI)

VTI is the area of the spectral curve that indicates how far blood travels during the flow period. 

When multiplied by EROA measured via the PISA method you can calculate the regurgitant volume (Rvol):

Regurgitant volume = EROA × MR VTI

‍Limitations of the PISA method

• The regurgitant orifice is rarely round. Thus the PISA is not a perfect hemisphere.
• Jets which are eccentric in origin demonstrate a PISA that is not hemispherical.
• Motion of the annulus during systole influences the calculation.
• Measurement of the PISA radius is difficult.
• Alignment with the direction of flow is sometimes impossible.
• Multiple jets are usually present.
• Regurgitation is usually dynamic. Thus, the mid-systolic frame might not be representative of MR.
• The method cannot be used in calcified and prosthetic valves.

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‍Supportive parameters assessing hemodynamic changes

As the mitral regurgitation progresses to moderate/severe, it starts to have an impact on the chambers and function of the heart, primarily on LV and LA. 

More blood regurgitates into the left atrium during systole and causes volume and pressure overload. In consequence, preload for LV is increased and leads to dilation, hypertrophy and ultimately to impaired function. All that results in a number of hemodynamic consequences we can identify on TTE. These parameters can help us distinguish moderate and severe MR. 

Associated findings:

• LA dilatation
• Dilated LV
• Elevated mitral inflow velocity
• Hyperdynamic LVF
• IAS bulging (towards RA)
• Dilated pulmonary veins
• Pulmonary hypertension

a) Left atrial volume

As the pressure in LA rises with progression of MR severity, dilatation of LA secondary to volume overload is an usual finding in chronic MR.

If the volume of LA is normal, we can rule out chronic severe MR. Only exception is when severe MR is acute and there is no LA dilation or adverse remodelling just yet.

The excess regurgitant blood entering the LA may induce a progressive rise in pulmonary arterial pressure and a significant tricuspid annular dilatation.

The LA volume is best estimated using the Simpson’s biplane method – trace the whole LA endocardium in two orthogonal views, usually in apical 4 chamber and apical 2 chamber views at ventricular end systole (maximum LA size).

Image 10 Severe biatrial enlargement (especially left atrium), planimetry - A4C view

Image 11 Severe left atrial enlargement, planimetry - A2C; LAVI calculation 104.3 cm3/m2

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‍b) Left ventricular size and function

The size and function of the left ventricle are indicators of the severity of MR.

In the chronic compensated phase, the patient may be asymptomatic and the systemic stroke volume is maintained through an increase in LV EF (typically >65%). 

When the phase turns to decompensation (the patient may still have little to none symptoms), the systemic stroke volume decreases and LA pressure increases significantly. There is a significant drop in LV contractility. The LV remodels and dilates – this is specific for chronic severe MR, but it is also caused by many other conditions and should be considered as a nonspecific finding. Assessment of LV size and systolic function helps identify the optimum timing of intervention.

Secondary MR has a different physiology, as it is the consequence of an initial ventricular disease. The LV and LA dilatation are in excess to the degree of MR. The LA pressure is often elevated despite lower regurgitant volume than in primary MR. 

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c) Pulse wave Doppler MV inflow

Unlike CW Doppler, PW Doppler is capable of analyzing waves reflected from a specific location. You can specify this location by moving the Sample volume (SV) along the Doppler line. However, this process takes time and as a result maximal velocity that can be measured is reduced to around 1,7 m/s (higher velocities are measured incorrectly).

PW Doppler inflow pattern and velocity can help us identify supportive signs of severe MR.

This is best measured in apical 4 window (A4C) with the Doppler line parallel to the direction of the flow.

With progression of MR severity, higher forward flow velocities during early diastolic filling (increased E velocity) across the MV usually occur. 

Signs of severe MR:

1. E wave is dominant with peak velocity >1,5 m/s
2. Increased E/A ratio
3. Shortened Deceleration Time

However, it is important to note hyperdynamic circulation, mitral stenosis (even minor degrees) and LV diastolic dysfunction can also increase E wave amplitude.

Image 12 High peak velocity of E wave (1.62 m/s), shortened DTE (166 ms)

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d) Mitral to aortic VTI ratio (Regurgitant index)

This index is easily measured and may be used for quantification of isolated pure organic MR. 

These measurements are best performed in the apical four chamber view (AC4). 

Trace the mitral inflow PW Doppler waves obtained at the level of mitral leaflet tips. Next obtain aortic PW Doppler waves at the level of the annulus and trace the area. 

The ratio mitral / aortic VTI:

• > 1,4 – strongly suggests severe MR
• < 1 – mild MR

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e) Pulmonary venous flow reversal

Depending on the severity of MR, pulmonary venous flow pattern is altered thanks to volume and pressure overload of the left atrium. This can be used as a good tool for evaluation of MR severity. 

In a normal heart without diastolic dysfunction and valve abnormalities, when using a PW Doppler on pulmonary veins, we can see a positive systolic wave (S) followed by a smaller diastolic wave (D) and A wave (peak reversal flow).

As the LA pressure increases with MR progression, the forward blood flow from the pulmonary veins during systole meets resistance and we can see a decrease of the S-wave velocity (blunting). In severe MR, the pressure in LA is so high it forces the blood back into the veins during systole and causes reversed systolic pulmonary flow = S wave is inverted. 

If the sampling is directed into a vein that has an eccentric MR jet flowing into it, a unilateral pulmonary flow reversal may be seen. It is therefore better to perform sampling on all pulmonary veins possible, especially when using TOE.

How to perform the pulmonary vein flow measurement?

• Apical 4 window
• Sample volume of Doppler 1 cm into pulmonary vein
• Do not Doppler a vein that regurgitation is dumping into; attempt more than one vein in this case

Image 13 Reversed systolic pulmonary flow = S wave is inverted in a patient with sever MR

 Image 14  Pulmonary vein flow in with and without MR

Lancellotti P, Moura L, Pierard LA, et al. European Association of Echocardiography. European Association of Echocardiography recommendations for the assessment of valvular regurgitation. Part 2: mitral and tricuspid regurgitation (native valve disease). Eur J Echocardiogr. 2010 May;11(4):307-32.

While flow reversal is specific for severe MR, blunting of the S wave is not sufficient for diagnosis of moderate MR, as fibrillation and elevated LA pressure from any cause can blunt forward systolic pulmonary vein flow. It is also less valuable in secondary MR, because we can’t exclude the influence of diastolic dysfunction.

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Quick algorithm for severe MR rule-out

For MR to meet the criteria of severity, without the need for additional advanced quantification, four or more specific criteria must be met.

• Flail leaflet
• VC > 0.7cm
• PISA radius > 1.0 cm
• Central large jet > 50% of LA area
• E wave is dominant with peak velocity >1,5 m/s
• Pulmonary vein systolic flow reversal
• Enlarged LV with normal function

If >4 criteria is not met, it is necessary to calculate other specific criteria in a table mentioned below:

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Management of mitral regurgitation

1) Primary mitral regurgitation

In primary MR, as mentioned above, a part of the mitral valve apparatus is directly affected. 

Urgent surgery is indicated in patients with acute severe mitral regurgitation. In the case of papillary muscle rupture as the underlying disease, valve replacement is in general required.

2) Chronic secondary MR‍

An algorithm in picture (Image 15) below sums up the approach to treatment according to LV function and response to medical therapy:

Vahanian A, Beyersdorf F, Praz F, et al. ESC/EACTS Scientific Document Group. 2021 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J. 2021 Aug 28:ehab395. doi: 10.1093/eurheartj/ehab395. Epub ahead of print. PMID: 34453165.

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Surgery

Indications for surgery in severe chronic primary mitral regurgitation are shown in the table below.

Surgery is indicated primarily for symptomatic patients with severe MR.

An LVEF ≤60% or LVESD ≥45mm, atrial fibrillation and a systolic pulmonary pressure ≥50mmHg predict a worse postoperative outcome independent of the symptoms and have therefore become triggers for surgery in asymptomatic patients (Image 16).

It is widely accepted that, when feasible, a durable valve repair is preferred to valve replacement. 

Vahanian A, Beyersdorf F, Praz F, et al. ESC/EACTS Scientific Document Group. 2021 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J. 2021 Aug 28:ehab395. doi: 10.1093/eurheartj/ehab395. Epub ahead of print. PMID: 34453165.

Watchful waiting is a safe strategy in asymptomatic patients with severe primary mitral regurgitation and none of the above indications for surgery.

‍Secondary mitral regurgitation

In secondary MR, the valve leaflets and chordae are structurally normal and mitral regurgitation results from alterations in LV geometry. 

It is most commonly seen in dilated or ischaemic cardiomyopathies.

Annular dilatation in patients with chronic atrial fibrillation and LA enlargement can also be an underlying mechanism (Image 17).

Vahanian A, Beyersdorf F, Praz F, et al. ESC/EACTS Scientific Document Group. 2021 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J. 2021 Aug 28:ehab395. doi: 10.1093/eurheartj/ehab395. Epub ahead of print. PMID: 34453165.

The treatment is therefore much more complicated and there is currently no evidence that an intervention of secondary mitral regurgitation improves survival.

The indications for surgical intervention are shown in a table below (Image 18):

Vahanian A, Beyersdorf F, Praz F, et al. ESC/EACTS Scientific Document Group. 2021 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J. 2021 Aug 28:ehab395. doi: 10.1093/eurheartj/ehab395. Epub ahead of print. PMID: 34453165.

Transcatheter mitral valve interventions are being developed to correct MR through transseptal or a transapical approach and lift the burden of open-chest surgery. 

MitraClip

MitraClip is a device for percutaneous edge-to-edge reconstruction of the mitral valve in patients with severe mitral regurgitation who are deemed at high risk for surgery. Using the femoral access, the atrial septum is punctured and a steerable guide catheter is advanced into the LA. Once the MitraClip is in a satisfactory position, grasping of the leaflets as they are captured in between the clip arms and the gripper is usually monitored using a 2D LVOT view.

Suitable patient group for MitraClip (Image 19)

• Severe mitral regurgitation (3-4/4) with restriction or prolapse of the valve leaflets (Carpentier II-IIIb)
• NYHA ≥ II, assumed survival > 12 months
• Surgery is contraindicated

Exclusion criteria

• Heavily calcified MV or rheumatic heart disease
• Previous surgical or percutaneous MV procedure
• Dual antiaggregation therapy intolerance
• Severe dilatation of LV with EF <25%

Video 19 Mitraclip implantation, TEE

‍Video 20 Mitraclip implantation, 3D TEE

Video 21 Mitraclip implantation, TEE, color (residual mitral regurgitation)

Video 22 Mitraclip in situ, TEE

Video 23 Mitraclip in situ - PLAX

Video 24 Mitraclip in situ - PSAX

Video 25 Mitraclip in situ - A5C

Video 26 Mitraclip in situ - A3C modification

Tendyne

Tendyne or Transcatheter Mitral Valve Implantation is a new emerging method designed to be implanted into a beating heart through a left minithoracotomy using a transapical approach. 

Suitable patients

• severe MR (3-4/4) of any etiology
• NYHA ≥ II, assumed survival > 12 months
• Surgery is contraindicated
•  EF LK >30% a EDD < 70mm 

Patients excluded for this method

• Heavily calcified MV or rheumatic heart disease
• Previous surgical or percutaneous MV or AV procedure
• Significant tricuspid regurgitation, PASP > 70mmHg
• Dual antiaggregation therapy intolerance
• Aneurysma or fibrotic changes of the LV apex

Image 20 Tendyne valve

https://www.cardiovascular.abbott/int/en/hcp/products/structural-heart/tendyne-mitral-valve.html

Video 27 Tendyne in situ - PLAX‍

Video 28 Tendyne in situ - PSAX

Video 29 Tendyne in situ - A4C

Video 30 Tendyne in situ- subxyphoideal view

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References

1. Patrizio Lancellotti, Christophe Tribouilloy, Andreas Hagendorff, Bogdan A. Popescu, Thor Edvardsen, Luc A. Pierard, Luigi Badano, Jose L. Zamorano, On behalf of the Scientific Document Committee of the European Association of Cardiovascular Imaging: Thor Edvardsen, Oliver Bruder, Bernard Cosyns, Erwan Donal, Raluca Dulgheru, Maurizio Galderisi, Patrizio Lancellotti, Denisa Muraru, Koen Nieman, Rosa Sicari, Document reviewers: Erwan Donal, Kristina Haugaa, Giovanni La Canna, Julien Magne, Edyta Plonska, Recommendations for the echocardiographic assessment of native valvular regurgitation: an executive summary from the European Association of Cardiovascular Imaging, European Heart Journal - Cardiovascular Imaging, Volume 14, Issue 7, July 2013, Pages 611–644, https://doi.org/10.1093/ehjci/jet105
2. CAMM, A. J., LÜSCHER, T. F., & SERRUYS, P. W. (2009). The ESC textbook of cardiovascular medicine. Oxford, Oxford University Press
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