Mitral valve insufficiencyI34.0

Isolated mitral valve insufficiency was first described in 1938 by Semans and Taussing, after Abbott had already become aware of mitral valve insufficiency in the AV channel in 1932 (Apitz 2002).

Mitral valve insufficiency (MI) is characterized by changes in the area of the valve annulus. These changes lead to an inability to close the valve located between the left atrium and the left ventricle, which causes blood to flow back into the left atrium during systole.

Pathophysiology: In early systole, when the pressure in the left ventricle (LV) reaches the pressure in the left atrium (LA), the mitral valve sails close. Papillary muscles and chordae tendineae cause the sails to remain closed and under tension throughout systole, as the ventricle shrinks during systole.

If the mitral valve is unable to close, the ventricle can empty in two directions:

• part of the HZV flows into the system circulation
• another part flows as regurgitation volume into the left atrium.

The increased volume in the left atrium flows unhindered into the pulmonary veins, as these do not contain valves and the blood thus reaches the pulmonary vessels. This results in pulmonary congestion with reactive pulmonary hypertension, which leads to right heart strain and ultimately to right heart failure. In order to be able to maintain the CPV at all, the stroke volume must be increased. The volume increase in turn leads to dilatation and hypertrophy of the left ventricle. Severe pulmonary hypertension and the resulting dilatation of the right ventricle can lead to secondary tricuspid and pulmonary valve insufficiency (Kasper 2015).

{/en/internal-medicine/cardiomyopathy-hypertrophic-141918.amp" title="Cardiomyopathy hypertrophic Dependingon the course of MI a distinction is made between acute and chronic forms. An acute course is found with:

• bacterial endocarditis
• Currently myocardial infarction (due to papillary muscle rupture)
• Trauma
• Mitral valve prolapse
• torn tendon thread (so-called asymmetrical prolapse or flail leaflet) - (Kasper 2015)

A chronic course is found with:

• Mitral valve prolapse
• rheumatic fever
• Mitral valve calcification (occurs frequently in patients with advanced renal failure and in women over 65 years of age who suffer from diabetes and/or arterial hypertension [Kasper 2015])
• healed endocarditis
• congenital (e.g. in the case of the cleft of the anterior mitral valve leaflet and partial AV channel)
• ischemic due to remodelling processes of the left ventricle (LV remodeling)
• Hypertrophic cardiomyopathy (HOCM) with systolic anterior movement (SAM)
• dilated cardiomyopathy
• Radio (Kasper 2015)

MI is - after aortic stenosis - the second most common valve disease in adults. The incidence is 2 % / year (Herold 2018).

A distinction is made between primary and secondary MI, as both are triggered by different causes:

Primary mitral valve insufficiency: Primary insufficiency, also known as organic or degenerative (Herold 2018) MI, is caused by intrinsic changes in the valve itself (sails, chordae tendineae and papillary muscle [Pinger 2019]). These changes can lead to Rammos:

• Mitral valve prolapse
• Endocarditis
• Barlow's disease
• rheumatoid heart disease
• congenital condition (e.g. cleft, AV septal defect)
• iatrogenic (radio)
• inflammatory (e.g. in lupus erythematosus)

Secondary mitral valve insufficiency: The secondary form is also called functional MI. It occurs in the following diseases (Rammos 2015):

• coronary heart disease
• Cardiomyopathy

The symptomatology in mitral regurgitation is due to the small minute volume in the great circulation and the back up of blood into the pulmonary circulation (Herold 2018).

Acute MI: In acute MI, there is a lack of time for cardiac adaptation. Symptoms include rapidly developing left ventricular decompensation with pulmonary edema and even cardiogenic shock (Herold 2018).

Chronic MI: In slowly developing chronic MI, the body has time to compensate for the pathophysiological changes through adaptive mechanisms. Symptoms may therefore be absent or very mild for a long time, even in the presence of significant valve insufficiency. However, as soon as decompensation of the left ventricle has developed, symptoms such as:

• dyspnoea on exertion up to orthopnoea
• palpitations (usually heralding atrial fibrillation)
• nocturnal coughing fits
• Exercise intolerance
• Edema (Pinger 2019)

Differentially, the clinical symptoms are very similar to those of mitral stenosis .

Thoracic X-ray: Radiologically there is typically an enlargement of the left atrium as well as of the left ventricle. Other changes are:

• mitral-configured heart with elapsed heart waist
• Signs of pulmonary congestion with widened pulmonary veins in the hilus region
• Kerley B-lines in the subfields in interstitial pulmonary edema
• Milky glass drawing for alveolar oedema
• Sail calcification with long-standing rheumatic vitium (Kasper 2015)

MRI: MRI is not a routine examination in an MI, as it is costly and time-consuming. If it is performed, it can provide information on the anatomy and function of the heart and determine the degree of insufficiency by calculating the reflux (Herold 2018).

Left heart catheterization / Lävocardiography: The indication for invasive diagnostics is only indicated in case of insufficient evaluation by non-invasive measures (Pinger 2019)

In levocardiography, the graduation of an insufficiency is also possible and can be assigned to one of the 4 degrees of severity (Herold 2018). Graduation according to Sellers (Pinger 2019):

• Grade I: KM- reflux with minimal staining of the left atrium
• Grade II: Regurgitation jet with moderate coloration of the left atrium
• Grade III: complete staining of the left atrium with the same density as in the left ventricle
• Grade IV: The KM density is stronger in the left atrium than in the left ventricle, the atrium is distinctly enlarged, but the left ventricle is dilated; the reflux of the contrast medium reaches the pulmonary veins.

Inspection and palpation

• peripheral cyanosis is rarely found
• the pulse is regular or there is an absolute arrhythmia
• in case of additional insufficiency of the tricuspid valve a systolic venous pulse may be present
• due to eccentric hypertrophy of the left ventricle, there is a widened, amplified and leftward displaced cardiac apex (Pinger 2019)
• lifting pulsations over the right ventricle are possible
• Pulsus celer et altus may occur with low systolic pressure
• Signs of right heart failure may be present (Pinger 2019)

Auscultation: Auscultation should ideally be performed in the left lateral position, as the murmurs are then amplified. The following murmur phenomena may be auscultable:

• soft 1st heart sound (especially in severe MI)
• the 1st heart sound may also be absent or (in severe MI) may be lost in the systolic (Kasper 2015)
• immediately after the 1st heart sound, high-frequency, band-like (holo-) systolic with p. m. over the cardiac apex and continuation into the axilla
• systolic may be silent and brief or absent in acute, severe MI (Pinger 2019)
• the systolic usually ends well before the 2nd heart sound in mild MI (Pinger 2019)
• the systolic may resemble a croak (seagull sound) or have a melodic (flail leaflet) character in rupture of the chordae tendineae (Kasper 2015)
• short interval diastolic during rapid ventricular filling (in higher-grade stenosis)
• low-frequency 3rd heart sound possibly auscultable (occurs only in severe MI)
• 4th heart sound may also be auscultable (in acute severe MI [Pinger 2019])

ECG: It is not uncommon for the ECG to show no clear evidence of left ventricular strain (Kasper 2015).

Typical ECG findings in MI would be:

• P- sinistroatrial or also called P- mitral (P > 0.11 sec., double-peaked P- wave with emphasis of the 2nd peak).
• P- dextroatrial or also called P- pulmonary occurs only in a late stage (P- wave is ≥ 0,2 mV)
• possibly atrial fibrillation (occurs in severe MI in up to 75% [Pinger 2019])
• initially left type, then right type in pulmonary hypertension
• Signs of hypertrophy of the left ventricle due to volume loading (e.g., increase in R- amplitude; widening of the QRS complex; flattening of the T-wave up to T-negativization; incomplete or complete LSB; Sokolow- Lyon index: RV5 +SV1> 3.5 mV; left deviation of the cardiac axis)
• Signs of right heart strain due to pulmonary hypertension onset in the later stages (e.g., high right precordial R- amplitude; Sokolow- Lyon index: RV1 + SV 5 / 6 > 10.5 mm; right deviation of the cardiac axis)
• possibly both left and - in a later stage - right precordial excitation regression disorders

Echocardiography: Echocardiography is the most important examination in mitral regurgitation.

The following statements can be made by echocardiography:

• Determination of the atrial size
• Measurement of the contracta vein
• Determination of the effective regurgitation orifice area
• Calculation of regurgitation volume and fraction
• Estimation of the pressure conditions in the right ventricle and in the small circulation
• Indication of the cause of MI (mitral valve prolapse, calcifications, rupture of tendon filaments, vegetations in bacterial endocarditis)
• Assessment of both ventricles regarding size and function
• LVEF- determination (left ventricular ejection fraction): a dysfunction of the left ventricle is found with an EF < 60 % and an LVESD (left ventricular end-systolic diameter) > 40 mm (Pinger 2019)
• Evaluation of the remaining valves for involvement.
• Detection of thrombi in the left atrium (TEE).

The severity of the insufficiency can also be determined and assigned to one of 3 severity levels. In the 2013 EAE guidelines, the need to describe the Carpentier- classification is pointed out (Pinger 2019):

• Type I: normal sail mobility
• TYPE II: excessive sail mobility
• Type III: impaired leaflet mobility
  • Type III a: sail motility is impaired in systole and diastole
  • Type III b: sail motility is impaired only in systole

However, accurate quantification of MI remains difficult. There is both examiner-dependent variability in severity and very large intraobserver variability (Pinger 2019). Quantification can be performed using the following methods:

• Measurement of the size of the regurgitation area:
  • Common, but very unreliable.
• Width of the contracta vein:
  • Vc < 3 mm in mild-grade MI.
  • Vc ≥ 7 mm for severe-grade MI.
• PISA- method / flow convergence zone:
  • ERO < 20 mm2 and R Vol < 30 ml for mild MI
  • ERO < 20 - 39 mm2 in moderate MI
  • ERO ≥ 40 mm2 and R Vol ≥ 60 ml in severe MI
• Mitral valve inflow profile:
  • E- wave > 1.2 m/s identifies severe MI in pure MI with a sensitivity and specificity of 86% each
• Time velocity integral:
  • the ratio TVI (mitral valve) / TVI (aortic valve) is measured
  • a value < 1 indicates a mild MI
  • a value > 1.4 indicates a severe MI
• Signal strength of CW Doppler signal:
  • a weak parabolic signal is found in mild MI
  • a high density of the reflux signal is indicative of severe MI
• Pulmonary vein flow profile:
  • pulmonary venous inflow into the left atrium is obstructed with increasing severity of MI. Systolic reversal of flow direction in at least 2 pulmonary veins is specific but not sensitive.
• Regurgitation fraction and volume:
  • In mild MI, there are:
    • Contracta vein ≤ 0.3 cm
    • normal valve
    • a- Wave dominated flow profile.
  • In severe MI, we find:
    • Vena contracta ≥ 0.7 cm
    • flail leaflet
    • e- wave > 1.5 m/s
• Stress echocardiography:
  • If discordance of symptoms and TTE (transthoracic echocardiography) at rest, there is a IIa- indication.
• 3-D echocardiography:
  • This examination seems to be superior to 2-D echocardiography in several studies and also offers new possibilities. However, further studies are needed here for validation (Pinger 2019).

• Pulmonary edema in cardiac decompensation
• Caution with atrial fibrillation, as this can trigger decompensation
• Thromboembolism (in atrial fibrillation)
• bacterial endocarditis

There are both conservative and different surgical options for the treatment of mitral valve insufficiency.

Conservative therapy:

Drug treatment of any existing heart failure is possible as long as it does not delay the surgical intervention. However, the prognostic benefit is not certain (Herold 2018). Pinger (2019) recommends conservative treatment:

• Diuretics as soon as edema occurs
• Vasodilatants: By lowering the peripheral resistance, the regurgitation fraction is reduced in the short term while the EF remains constant. These drugs are indicated in acute MI; possibly in combination with inotropics. This is different in chronic MI without heart failure. Vasodilatants are not recommended here.
• ACE inhibitors: These drugs are indicated in patients with HFReF (heart failure with reduced ejection fraction). Especially if the option of surgical intervention is not available.
• Spironolactone: Should be administered in heart failure with reduced ejection fraction (EF).
• Betablockers: There are no randomized prospective studies on the use of beta-blockers. However, a retrospective study has shown that patients with severe MI and normal left ventricular function have a survival advantage (Varadarajan 2008).

According to AHA/ACC 2014 (American heart association or American college of medicine), symptomatic patients with EF < 60% have a class IIa indication for treatment with beta blockers if surgery is not performed (Pinger 2019).

• Digitalis: Digitalis should be used in patients with absolute tachyarrhythmia (TAA). Another indication may be LV (left ventricular dysfunction).
• Cardioversion: Cardioversion may be indicated in patients with mild to moderate MI and short-term atrial fibrillation (Pinger 2019)

As soon as atrial fibrillation occurs, drug therapy with anticoagulants should be initiated immediately. Vitamin K antagonists should be used here, as new oral anticoagulants are not approved for this indication (Kasper 2015).

Dosage recommendation: Marcumar 3 mg 2 x 1 tbl/d in the first 3 days, afterwards dose adjustment according to the INR value. Alternatively, the preparation Falithrom 3 mg can be given in the same dosage. The INR target value should be between 2 - 3 (Kasper 2015).

Percutaneous interventional catheter therapy with mitral sail clipping:

Also known as mitral sail clipping; this treatment method should be performed in patients at increased risk for surgery (e.g., impaired left ventricular function, advanced age, comorbidities, etc.) and with an equally suitable anatomy (Kasper 2015).

The EVERST II study showed brelatively good results in mitral sail clipping therapy.

Surgical Therapy

Surgical measures available are valve replacement therapy and valve reconstruction, the so-called interventional edge-to-edge procedure (also known as Mitraclip).

The operative mortality rate of valve reconstruction, at approx. 1 % - 2 %, is lower than that of valve replacement therapy, which is approx. 4 % - 6 %. Furthermore, postoperatively there is a better left ventricular function after valve reconstruction (Pinger 2019).

The individual mortality risk for valve replacement therapy can be calculated with the help of a score and has a very wide range of 0.2 % and 53 % (Amber 2005).

A. Acute mitral valve insufficiency:

Acute mitral valve insufficiency requires immediate surgery.

(Herold 2019)

B. Chronic mitral valve insufficiency:

In chronic mitral valve insufficiency a different approach is recommended depending on the genesis of the valve insufficiency:

1. primary MI:

For symptomatic patients the following applies for:

• Level of recommendation IB: left ventricular ejection fraction (LVEF) of ≥ 30 %.
• Level of recommendation IIC: LVEF of < 30 %, if capable of reconstruction
• Level of recommendation IIbC: LVEF of < 30% and non-reconstructable valve

(Herald 2019)

The following applies to asymptomatic patients

• Level of recommendation IB:
  • LVEF from ≤ 60 % and / or
  • a left ventricular end-diastolic diameter (EVESD) ≥ 45
• Level of recommendation IIaB:
  • in paroxysmal or newly occurring atrial fibrillation and
  • if the systolic pulmonary arterial pressure at rest is > 50 mmHg
• Level of recommendation IIbC:
  • if the volume of the left atrium is > 60 ml/m2
  • if the systolic pulmo-arterial pressure rises when the load is > 60 mmHg
  • in case of sail tearing with good reconstructibility of the flap

(Herald 2019)

2. Secondary MI:

In this group of patients the indication for surgery is controversial. It is recommended as an accompanying measure in patients with planned aortocoronary bypass or as a symptomatic measure, provided that left ventricular function is not yet severely restricted. It has been shown in recent studies that in secondary MI, valve reconstruction is likely to be considered equivalent to valve replacement.

• Level of recommendation IC: this level of recommendation applies - regardless of symptoms - to patients with severe MI and an ejection fraction (EF) > 30% with simultaneous ACVB surgery

In symptomatic patients:

• Level of recommendation IIaC: this level of recommendation applies to patients with moderate MI, an ejection fraction (EF) > 30% and simultaneous ACVB surgery

• Level of recommendation IIb: Patients with severe MI, an EF > 30 %, with a low risk of surgery, but without bypass indication

(Herald 2019)

Contraindications for operative measures:

Relative contraindications for operative valve replacement therapy or valve reconstruction exist in

• LVEF < 20 %, as the surgical risk is higher than the expected benefit

(Herald 2019)

Hospital mortality after mitral valve reconstruction is about 2 % and after valve replacement about 6 % (Herold 2019)

Postoperatively, patients require oral anticoagulation. This is required for life after implantation of a mechanical heart valve and at least 3 months postoperatively if a biological valve is used (Herold 2018).

Recommended dosage:

If initial Quick- or INR- values are within the normal range, the following dosage can be started in adults:

• Marcumar 3 mg 2 x 1 tbl/d in the first 3 days, then dose adjustment according to the result of the INR value.

Alternatively, the preparation Falithrom 3 mg can be given in the same dosage.

Foods rich in vitamin K (e.g. broccoli, cabbage, spinach etc.) do not have to be avoided during the therapy, but they should not be taken in excess and distributed over the week. For more details see thrombosis prophylaxis

(Herald 2918)

Patients with valve reconstruction or prosthetic heart valve have a significantly increased risk of endocarditis. The post-procedural bacteremia frequency after tooth extractions in gingivitis, for example, is up to 90%. For this reason, postoperative endocarditis prophylaxis is necessary for certain procedures.

The standard therapy is administered as a single dose approx. 30-60 minutes before the procedure, e.g. amoxicillin or ampicillin 2 g orally or i.v., or in the case of penicillin allergy clindamycin 600 mg also orally or i.v. (Pinger 2019).

For further details see Endocarditis prophylaxis

Patients should in any case spare themselves physically. Even asymptomatic patients with severe mitral regurgitation and (to date) normal-sized left ventricle, which contracts normally and whose frequency is in sinus rhythm, are recommended to avoid any isometric load (muscle tension without changing the muscle length, e.g. long, rigid sitting or standing) (Kasper 2015).

Operative valve replacement therapy or valve reconstruction:

Surgical measures available are valve replacement therapy and valve reconstruction. The operative mortality of valve reconstruction is with approx. 1 % - 2 % lower than that of valve replacement therapy, which is approx. 4 % - 6 %. Furthermore, postoperatively there is a better left ventricular function after valve reconstruction (Pinger 2019).

The individual mortality risk for valve replacement therapy can be calculated with the help of a score and has a very wide range of 0.2 % and 53 % (Amber 2005).

The ESC guidelines of 2015 therefore recommend - if possible - valve reconstruction with ring, with partial ring or without ring in minimally invasive endoscopic surgery or conventional surgery. However, if mitral valve replacement is required, either a mechanical or a biological valve can be used (Herold 2018).

Indications:

• Acute mitral valve insufficiency: Acute mitral valve insufficiency requires immediate surgical intervention (Herold 2018).
• Chronic mitral valve insufficiency: In chronic mitral valve insufficiency, a different approach is recommended depending on the genesis of the valve insufficiency:
• Primary MI: In this group of patients, surgical intervention has shown very good results. Therefore, surgery is also indicated in asymptomatic patients with pulmonary hypertension, recent atrial fibrillation and non-hypercontractile ventricular function, provided the valve is well reconstructible.
• For symptomatic patients:
  • Level of recommendation I: for left ventricular ejection fraction (LVEF) of ≥ 30 %
  • Level of recommendation IIa: for LVEF of < 30 %, if capable of reconstruction (Herold 2018)
• For asymptomatic patients:
  • Level of recommendation I: LVEF of ≤ 60 % and / or a left ventricular enddiastolic diameter (EVESD) ≥ 45
  • Level of recommendation IIa: in paroxysmal or newly developed atrial fibrillation and when the systolic pulmonary arterial pressure at rest is > 50 mmHg
  • Level of recommendation IIb: if the volume of the left atrium is > 60 ml/m2 or if the systolic pulmo-arterial pressure at load is > 60 mmHg and the valve is well reconstructed

Secondary MI: In this patient group the indication for surgery is controversially discussed. It is recommended as an accompanying measure in patients with planned aortocoronary bypass or as a symptomatic measure, provided that left ventricular function is not yet severely impaired. It has been shown in recent studies that in secondary MI, valve reconstruction is likely to be considered equivalent to valve replacement.

Contraindications: Relative contraindications for surgical valve replacement therapy or valve reconstruction exist in

• LVEF < 20 %, as the surgical risk is higher than the expected benefit (Herold 2018)

Postoperatively, patients require oral anticoagulation. This is required for life after implantation of a mechanical heart valve and at least 3 months postoperatively if a biological valve is used. If initial Quick or INR values are within the normal range, the following dosage can be started in adults:

• Marcumar 3 mg 2 x 1 tbl/d in the first 3 days, afterwards dose adjustment according to the result of the INR value.
• Alternatively, the preparation Falithrom 3 mg can be given in the same dosage.
• Foods rich in vitamin K (e.g. broccoli, cabbage, spinach, etc.) do not have to be avoided during the therapy, but they should not be taken in excess and distributed over the week. For more details see thrombosis prophylaxis

Antibiotics: Patients with valve reconstruction or prosthetic heart valve have a significantly increased risk of endocarditis. The post-procedural bacteremia frequency after tooth extractions in gingivitis, for example, is up to 90%. For this reason, postoperative endocarditis prophylaxis is necessary for certain procedures. The standard therapy is administered as a single dose approx. 30-60 minutes before the procedure, e.g. amoxicillin or ampicillin 2 g orally or i.v., or in the case of penicillin allergy clindamycin 600 mg also orally or i.v. (Pinger 2019).

For further details see Endocarditis prophylaxis

Basically, it can be said that in valve insufficiency, the resulting volume load, which leads to eccentric hypertrophy, has a more favourable prognosis compared to a pressure load with concentric hypertrophy (Herold 2018).

Life expectancy in patients with mild MI can be almost equal to that of a healthy person (Herold 2018).

In asymptomatic patients the prognosis depends on the ERO (Effective Regurgitant Orifice) and the regurgitation volume.

The 5-year mortality from cardiac cause is:

• with ERO < 20 mm² of 3
• for ERO between 20 - 39 mm2 of 20
• for ERO > 39 mm2 from 36

(ping 2019)

In patients with a flail leaflet MI, it has been shown that early surgery has a significantly better prognosis than delayed surgery:

• the 10-year mortality from cardiac cause is 8 % versus 28 %
• congestive heart failure 27% versus 59

(ping 2019)

Natural course:

Basically, the life expectancy of patients with mitral valve insufficiency depends on the disease causing the MI.

In primary mitral valve insufficiency and asymptomatic course, the 5-year survival rate without surgery is 80% and the 10-year survival rate is 60% (Herold 2018).

Although the ejection fraction remains normal for a longer period of time, an advanced stage of the disease is reached with the onset of reduced contractility and there is a risk that the ventricular function will not be able to recover despite the subsequent surgery.

In the case of functional or secondary mitral valve insufficiency, the prognosis is significantly less favourable without surgical measures. Depending on the severity of the ventricular dysfunction, the mortality rate is between 70 % - 30 %.

(Herold 2018)

Follow-up:

Depending on the severity of the disease, follow-up should be carried out every 6 - 12 months so that the indication for surgery can be established in good time. The following examinations are recommended:

• clinical examination
• ECG
• Echocardiography
• chest x-ray

(Herald 2018)

Pinger (Pinger 2019) still differentiates in the frequency of follow-up between asymptomatic patients with moderate MI and good left ventricular function. He recommends that the general check-ups be performed annually, but echocardiography only every 2 years. In asymptomatic patients with severe MI and good left ventricular function, he recommends that the general check-ups be carried out every six months and the echocardiography only every year.

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