Mitral valve stenosis I05.0

In 1954, Ferencz et al. for the first time compiled a larger number of patients with congenital mitral valve stenosis (MS). By then, 34 cases had been found, 8 of these patients had isolated mitral stenosis and 26 of these patients had additional heart defects (Beuren 1966).

A stenosis results in an adhesions of the heart valve. The resulting restriction of mobility leads to a reduction of the valve opening area and thus to an obstruction of the forward blood flow (Herold 2018).

Congenital MS is a very rare form of heart malformation. Until 1954, only 34 cases had been described in the literature (Beuren 1966).

The acquired form, however, is one of the most common acquired valve defects (Zechmann 2019). About 2/3 of patients with rheumatoid mitral stenosis are female (Lapp 2014).

Stenoses of the heart valves are primarily caused by:

• degenerative changes (in industrialized countries calcification is now the most common cause of stenosis in older people)
• inflammatory processes (such as rheumatic fever) and the resulting scarred adhesions and shrinkage (Herold 2018)

The most common cause of MS worldwide is rheumatic fever, the frequency of which Pinger (2019) puts at about 85 %.

Other causes can be (Pinger 2019):

• degenerative changes (about 12 %)
• as a result of a healed endocarditis in 0.6
• congenital (e.g. parachute deformity) in also 0.6
• very rare in carcinoid syndrome
• very rarely as a result of anorexic medication
• systemic lupus erythematosus
• rheumatoid arthritis (Kasper 2015)

Pathophysiology: In adults with healthy mitral valve the opening area is 4 - 5 cm². (Herald 2018). A gradual stenosis, which develops in MS, leads to a narrowing of the valve opening area (COPA) over years or decades. Hemodynamically effective is a valve opening area of < 1.5 - 2.0 cm2 (Pinger 2019).

The following factors play a role in pure mitral stenosis (Pinger 2019):

• Valve opening area
• reactive pulmonary hypertension
• the functional state of the myocardium
• possibly existing arrhythmias

The narrowing of the mitral valve leads to an increasing pressure load of the left atrium and consecutively to a dilatation and hypertrophy of the atrium. The pressure in the left atrium results from the left ventricular end-diastolic pressure (LVEDP) and the transmittoral pressure gradient. A pressure increase of:

• 18 mmHg leads to pulmonary overhydration
• 25 mmHg to interstitial edema
• 35 mmHg to an alveolar edema (Pinger 2019)

Since the transmittal pressure gradient is a quadratic function of the transvalvular flow rate, a doubling of the flow rate leads to a quadrupling of the pressure gradient. The pressure gradient itself is essentially dependent on the heart rate or the duration of diastole, i.e. the shorter the diastolic filling period (DFP), the higher the pressure gradient.

Example: For a patient with a HEART of 1.0 qcm and a cardiac output of 5 l /min:

• At a heart rate of 72/min the diastolic filling period is 0.58 s and the mean pressure gradient is between 8 - 10 mmHg.
• At a heart rate of 100/min, the diastolic filling period is 0.32 s and the mean pressure gradient is between approx. 17 mmHg.

For this reason, an existing mitral valve stenosis often only becomes symptomatic as soon as tachycardic atrial fibrillation occurs, as this leads to a loss of atrial contractions with a simultaneous shortening of the diastolic period.

The increase in pressure in the left atrium leads to pulmonary hypertension, the severity of which is variable. We differentiate between three different mechanisms:

passive pressure

anatomical-morphological due to media hypertrophy and intimafibrosis

functional- reflective by vasoconstriction

Due to the increased pulmonary arterial pressure (PA pressure), the right ventricle is strained. The resulting right ventricular failure with consecutive reduction of cardiac output can be so pronounced that pulmonary congestion (and thus dyspnoea) is reduced. The clinical picture is then dominated by right ventricular failure with low output syndrome or backward failure.

The course of the disease is not only caused by reactive vascular constriction, in the further course of the disease there is a reduction in capillary permeability and an increase in lymphatic drainage, which provides protection against the development of pulmonary oedema (Pinger 2019).

In the first 3 - 4 decades, patients are usually still symptom-free (Pinger 2019). After that - depending on the severity of the disease - different symptoms appear (Herold 2018).

Once severe symptoms have occurred, the disease rapidly develops progressively and leads to death after 2 - 5 years (Kasper 2015). Due to the increase in pressure in the left atrium, the following symptoms may occur:

• Atrial fibrillation with absolute arrhythmia (reducing the performance of the heart by about 20%); permanent atrial fibrillation often marks the turning point in the course of the disease (Kasper 2015)
• Occurrence of thrombi in the left atrium (occurs in about 40% of cases).
• Emboli in the brain, extremities, and kidneys triggered by thrombi (occur in about 20% of cases - Herold 2018)

As a result of pulmonary congestion/pulmonary hypertension, the following symptoms may develop:

• Dyspnea, especially on exertion
• in the further course resting dyspnoea up to orthopnoea (Pinger 2019)
• nocturnal cough (so-called asthma cardiale).

A decrease in dyspnoea does not necessarily indicate a general improvement in symptoms, as the developing right heart failure with a subsequent reduction in cardiac output reduces pulmonary congestion (and thus dyspnoea). The clinical picture is then dominated by right heart failure with low output syndrome or reverse failure (Pinger 2019)

• Hemoptysis (rupture of broncho-venous vessels occurs due to increased pulmonary arterial pressure; however, these hemoptyses rarely end lethally [Kasper 2015]).
• Hemoptysis with coughing up of "cardiac defect cells" (pulmonary macrophages containing hemosiderin) in the sputum (Herold 2018)

As a result of right heart failure, the following symptoms may occur:

• Visible venous congestion in the neck and under the tongue due to increased venous pressure.
• Congestive liver
• Congestive kidneys
• Proteinuria
• Edema in the dependent parts of the body (Herold 2018).

Due to the decreased cardiac output, there may be:

• general reduction in performance
• Peripheral cyanosis (so-called facies mitralis with reddish-cyanotic cheeks; Herold 2018).

Due to the dilated left ventricle may occur:

• Hoarseness (due to compression of the recurrent laryngeal nerve )
• Dysphagia (Pinger 2019)

X-ray: The following changes can be seen in the X-ray of the thorax:

With enlargement of the left atrium, there are:

• in the p.a. possibly a double contour at the right edge of the heart
• a displaced cardiac waist due to the prominent left cardiac ear
• a spreading of the bifurcation of the trachea
• and in the left lateral image
• after contrast swallowing, an arcuate impression of the esophagus (due to the constriction of the posterior heart space at the level of the atria) (Herold 2018).

The eventual mitral configuration of the heart (also called "standing ovoid") results from:

• Hypertrophy of the right ventricle
• enlargement of the left atrium
• In the presence of pulmonary hypertension, by dilatation of the pulmonary artery (Herold 2018).

Possible existing signs of pulmonary congestion:

• the pulmonary veins in the hilar region are widened
• in interstitial pulmonary edema, so-called Kerley B- lines are found, preferably in the middle and lower fields (these are dense, fine, horizontally running lines that are formed by widening of the interlobar septa and lymphatics due to the edema fluid as soon as the mean pressure in the left atrium exceeds 20 mmHg at rest [Kasper 2015])
• A so-called milk glass drawing is found in alveolar pulmonary edema
• Possibly existing signs of hypertrophy of the right ventricle with
• constriction of the retrosternal cardiac anterior space in the lateral view
• In hypertrophy of the right ventricle, the left cardiac border may be formed by the right ventricle in the p.a. image
• Calcifications of the mitral valve may be detectable
• There is often a redistribution of blood flow to the lungs from basal to apical (Pinger 2019)

Cardio- MRI: In MRI, a planimetric determination of the COE is possible in principle, but this is overestimated by about 5% compared to the determination by catheter, and overestimated by about 8% compared to the determination by echocardiography (Pinger 2019). In addition, the pressure gradient across the valve can be determined here (Herold 2018).

Echocardiography: Echocardiography can be performed transthoracically and transesophageally (TEE). TEE is the cornerstone of diagnosis and may be sufficient as the sole modality of examination if the sound quality is good. Even with poor TEE quality, at least a sufficient diagnosis is usually possible (Pinger 2019). TEE can usually be used to decide whether the stenosis is suitable for percutaneous mitral valve balloon valvuloplasty (see below) (Kasper 2015). The following measurements or assessments are possible:

• Quantification of the degree of stenosis by:
  • Measurement of the mean gradient
  • Planimetry of the valve opening area
  • Calculation of the valve opening area from the Doppler profile
  • Measurement of the left atrium (enlarged for values > 40 mm)
  • Measurement of the (reduced) left ventricle
  • assessment of the function of both ventricles
• possible involvement of other valves should be excluded!
• estimation of the pressure conditions in the small circulation as well as in the right ventricle
• TEE allows detection of possible thrombi in the atrium
• in the color duplex a possible reflux with simultaneous valve insufficiency can be detected
• Provided that the mitral valve is fibrosed and / or calcified, we find.
  • a reduced separation
  • parallel multiple echoes in m-mode at the anterior mitral leaflet.

Otherwise, the following changes may occur:

• the posterior mitral leaflet shows a parallel motion
• EF slope is flattened (normal > 70 mm/s, in MS < 35 mm/s)
• Doming of the mitral valve (possible with fusion of the commissures and preserved mobility of the leaflets [Weihs 2015]).
• In color Doppler, the so-called candle flame phenomenon (Pinger 2019).

The so-called Wilkins score can be determined in TEE to estimate whether the MS is suitable for percutaneous balloon valvuloplasty. Here, valve mobility, leaflet thickening, valve holding apparatus, and degree of calcification are determined (Mewis 2006).

Valve mobility:

• Score 1:
  • very mobile valve, there may be an isolated restriction of movement at the edges of the valve
• Score 2:
  • the middle and base parts of the valve leaflets are normally mobile
• Score 3:
  • diastolic forward motion of the mitral valve is preserved mainly at the base of the valve
• Score 4:
  • in diastole there is no or only a slight mobility of the valve.

Thickening of the valve:

• Score 1:
  • thickness of the valve normal (4 - 5 mm)
• Score 2:
  • clearly visible thickening in the area of the valve edges (5 - 8 mm)
• Score 3:
  • clearly visible thickening of the entire mitral valve leaflet (5 - 8 mm))
• Score 4:
  • clearly visible thickening in the area of the entire valve (8 - 10 mm)

thickening of the valve retaining apparatus (in this case there is involvement of the chordae by subvalvular thickening)

• Score 1:
  • there is a minimal thickening of the chordae immediately below the valve
• Score 2:
  • the thickening covers up to 1/3 of the total length of the chordae
• Score 3:
  • the thickening reaches the distal third of the chordae
• Score 4:
  • there is a pronounced thickening and shortening of the chordae up to the papillary muscles

Degree of calcification of the valve:

• Score 1:
  • there is a singular, circumscribed calcification of the valve
• Score 2:
  • there are multiple calcification zones, but these are limited to the edges of the valve
• Score 3:
  • the calcification also reaches the middle parts of the mitral leaflet
• Score 4:
  • there is a pronounced calcification that encompasses almost the entire mitral leaflet (Pinger 2019).

Assessment:

• With a score < 8, balloon valvuloplasty is possible and good acute and long-term results can be expected.
• With a score > 12, the mitral valve is not suitable for balloon valvuloplasty (Pinger 2019).

Left heart catheterization and coronary angiography.

Nowadays, left heart catheterization should still be performed if there is a significant discrepancy between the clinical symptoms and the examination findings of noninvasive techniques (Kasper 2015).

Coronary angiography is no longer an indispensable diagnostic measure in MS according to the recommendation of the AHA / ACC 2014 in modern times: " It must be emphasized that there is no longer a "routine" cardiac catheterization" (Pinger 2019).

Preoperatively, coronary angiography should only be performed if:

• coronary artery disease is still present (Kasper 2015)
• Patients are at increased risk of CHD, including men > 40 years and postmenopausal women (Pinger 2019)
• There is reduced left ventricular function (Pinger 2019).

Manometrically, this can be determined:

• the PC pressure curve
• the pressure in the pulmonary arteries
• the gradient across the valve
• the calculation of the valve opening area

The pressure increase in the left atrium depends on the following factors:

• severity of MS (and thus on the valve opening area, which is calculated according to the so-called Gorlin formula)
• Diastolic duration
• Cardiac output (Lapp 2010)

The following changes may be present in cardiac catheterization with existing MS:

Laevocardiography: In the vast majority of cases, the left ventricle is normal in size and well-contractile. Otherwise, regional hypokinesia of the apical and posterobasal wall segments may significantly limit left ventricular function.

Left atrial pressure curve/pulmonary capillary pressure in:

• low-grade mitral valve stenosis:
  • In low-grade MS, the only sign of increased left atrial contraction often found is an increased a-wave in the left atrial or pulmonary capillary pressure curve.
• high grade mitral valve stenosis:
  • a markedly increased mean pressure in the left atrium (> 20 mmHg)
  • as long as a sinus rhythm is present, the emphasis of the a-wave is maintained
  • a well pronounced x- valley
  • the v-wave shows a sluggish decline to the y-valley (due to delayed filling of the left ventricle during diastole)
  • as soon as atrial fibrillation occurs, the a-wave is absent and the x-valley is much less pronounced
  • if there is concomitant mitral regurgitation, the x-valley is completely abolished and there is an accentuated and exaggerated v- wave (Lapp 2010).
• Pulmonary artery pressure / pulmonary vascular resistance
• Normally, the mean pulmonary artery pressure is about 5 - 10 mmHg higher than the mean pulmonary capillary pressure and the diastolic pulmonary artery pressure is the same. In the case of MS, the diastolic pulmonary artery pressure is higher than the pulmonary capillary mean pressure because there is an increase in resistance in the pulmonary circulation due to the structural changes. In severe MS, up to 10-fold elevated values can occur (> 1,500 dyn x s x cm -5 )
• (Lapp 2010)

Right ventricular and right atrial pressure.

• Pulmonary hypertension results in an increase in systolic right ventricular pressure, which in extreme cases can lead to pressure imbalance between the right and left ventricles. The end-diastolic pressure in the right ventricle also increases due to this pressure load. As long as sinus rhythm is present, the a-wave of the atrial pressure curve is elevated as a sign of increased atrial contraction. As soon as an arrhythmia with atrial fibrillation occurs, the atrial mean pressure increases as a sign of right heart failure. If there is concomitant tricuspid regurgitation, the increased right atrial mean pressure results in a high v- wave, an increase in the y- valley, and a flattening of the x- valley (Lapp 2010).

Auscultation

Auscultation should preferably be performed in the left lateral position.

In MS we differentiate between 4 sound phenomena:

murmuring 1st heart sound

Found in 90% of patients. (Pinger 2019).

In an early stage of the disease, the 1st heart sound may be slightly delayed (Kasper 2015).

Mitral Orifice Tone (MET).

The PM of the MET is located in the 4th ICR left parasternal (Pinger 2019). It is best heard in expiration (Kasper 2015).

The tympanic 1st heart sound and also the MET are produced at the moment when the ventricular pressure exceeds or falls below the pressure in the left atrium by a loud flip of the mitral leaflets. Both sounds may also be absent in cases of congealed mitral leaflets (due to fibrosis, calcification) (Herold 2018).

The mitral valve opens earlier, the higher the degree of stenosis and, accordingly, the shorter the interval between with closure of the aortic valve (A2) and MET.

At values of A2 - MET < 0.08 s, severe MS is to be expected (Pinger 2019).

Diastolic decrescendo murmur.

The PM is over the cardiac apex in left-sided position. The murmur is low frequency and auscultable after the MET. A prolonged murmur (with long diastolic duration) indicates higher grade stenosis (Pinger 2019).

Presystolic crescendo murmur.

This murmur is found exclusively in sinus rhythm. The diastolic decrescendo murmur described above transitions to the presystolic crescendo murmur (Herold 2018).

Graham- Steell murmur

In severe MS with pulmonary hypertension, the following additional murmur phenomena are found : Graham- Steell- murmur. This murmur phenomenon is heard immediately after the amplified pulmonary segment of the 2nd heart sound. It arises from relative pulmonary valve regurgitation (Herold 2018) and is auscultable as a 2nd ICR on the left as a short, decrescent early diastolic (Pinger 2019). It increases in strength inspiratory and is thus distinguishable from the murmur of aortic valve regurgitation 1(Kasper 2015).

• pulmonary ejection click
• split 2nd heart sound with accentuated pulmonary segment
• possibly 3rd heart sound

In severe right heart failure, the mitral stenosis murmur and ME may be heard only very softly (Pinger 2019).

ECG: The following changes may appear on the ECG:

• P- sinistroatrial or also called P- mitral (P > 0.11 sec. in Abl- II, double-peaked P- wave with emphasis on the 2nd peak).
• Atrial fibrillation with absolute arrhythmia (Herold 2018) in about 40% (Pinger 2019).

With onset of pulmonary hypertension, there is:

• Change of the position type towards the steep to right type.
• Sokolow- Lyon index as a sign of right heart hypertrophy ( RV1 +SV5/6 > 1.05 mV).
• P in lead II high and peaked
• P may be positive in V1 (Kasper 2015).

Other imaging techniques (see there).

• Atrial myxoma (are the most common benign tumors of the heart; often incidental finding [Herting 2014]).
• Cor triatriatum (rare congenital heart defect with membrane in the left atrium that can lead to obstruction of venous pulmonary outflow [Krasemann 2007])
• Lutembacher- syndrome (rare defect with congenital atrial septal defect [ASD] and acquired mitral stenosis [Sy 2011]).
• Atrial septal defects
• Mitral regurgitation (in this case, a diastolic over the cardiac apex can also be auscultated; however, further examination findings are indicative)
• Aortic valve insufficiency (a mesodiastolic murmur can be heard above the apex of the heart; however, further examination findings are indicative in this case as well)
• Tricuspid stenosis (rarely occurs in isolation; in this case the diastolic m urmur increases inspiratory and in the jugular venous pressure curve the y- depression is delayed Kasper 2015)

Possible complications in the course of the disease can be:

• arterial embolisms
• Pulmonary oedema
• bacterial endocarditis

There are three different therapeutic methods for the treatment of MS: conservative therapy, balloon valvuloplasty and surgical treatment.

The indication for surgical-interventional therapy is given in case of existing symptoms and a CDF ≤ 1.5 cm2. However, there is otherwise no evidence for the optimal timing of invasive therapeutic procedures. It has probably been shown that existing pulmonary hypertension significantly increases the risk of surgery (Pinger 2019).

Conservative therapy: Patients with heart failure may receive the following medications:

• Diuretics (thiazide, spironolactone or a loop diuretic).
• Digitalis exclusively in case of atrial fibrillation
• ACE inhibitors and ATII blockers are contraindicated.
• Salt restriction is recommended in existing heart failure (Kasper 2015)
• Reduction of physical exertion (Pinger 2019).

Atrial fibrillation: In case of new onset of atrial fibrillation, if there is a MS not intended for BVP or surgical intervention, pharmacological or electrical cardioversion should be performed. The patient must have been anticoagulated for at least 3 weeks in the therapeutic range for this. If cardioversion is required sooner, heparinization and exclusion of thrombi in the left atrium by transesophageal echocardiography are recommended (Kasper 2015).

The chances of success of cardioversion are low in the case of

• high-grade MS
• marked dilatation of the left ventricle
• atrial fibrillation lasting longer than 1 year

However, if sinus rhythm is re-established after cardioversion, in the majority of cases this cannot be maintained in the longer term (Kasper 2015).

Coumarins: If arterial embolism or pulmonary embolism occurs in the course of MS, coumarins with a target INR of 2- 3 must be administered for at least 1 year. In case of atrial fibrillation, continuous administration of coumarin is recommended (Kasper 2015). Dosage recommendation:

For Quick or INR- values that are initially in 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 (Herold 2918).

For further details see Thrombosis prophylaxis.

The coumarin derivative warfarin is controversially discussed in patients in sinus rhythm with dilated left atrium > 5.5 cm and spontaneous contrast (Kasper 2015).

New oral anticoagulants are currently not approved for patients with significant valvular disease (Kasper 2015) and are not indicated in at least moderate MS according to ESC- guideline Heart Failure 2016 (Pinger 2019).

In case of embolic recurrence under ongoing marcoumarization, an INR- value of 2.3 - 3.5 should be aimed for or, as an alternative, an additional administration of ASA 80 - 100 mg / d (Pinger 2019).

Catheter procedures

One of the catheter procedures is balloon valvuloplasty = BVP (also used synonymously as mitral valvuloplasty = MVP or percutaneous mitral commissurotomy = PMC [percutaneous mitral commissurotomy] or BMV [balloon mitral valvotomy]). As early as around 1929, Cutler and Beck succeeded in dilating a stenosed mitral valve with their fingers (Roskamm 2013). After the development of balloon catheters, the so-called balloon valvuloplasty has been performed since the mid-1980s (Pinger 2019). With the help of the so-called Wilkins score, echocardiography can be used to assess whether the MS is even a candidate for percutaneous balloon valvuloplasty. Here, the valve mobility, the leaflet thickening, the valve retaining apparatus and the degree of calcification are determined (Mewis 2006).

(For classification and details of the Wilkins score, see above under "Echocardiography").

Indication: The indication for percutaneous balloon valvuloplasty is according to ACC / AHA 2014:

Indication class I

• symptomatic patients with severe MS (COF > 1.5 cm²) and favorable valve morphology without existing contraindications

Indication class IIa

• asymptomatic patients with very severe MS (COF < 1.0 cm²) and favourable valve morphology without existing contraindications

Indication class IIb

• NYHA class III - IV patients with severe MS (COF < 1.5 cm²) and suboptimal valve morphology who are at high risk for valve surgery or unsuitable for valve surgery.
• asymptomatic patients with severe MS (COF < 1.5 cm²) and new onset atrial fibrillation and favorable valve morphology without existing contraindications
• Symptomatic patients with MS and a COF of > 1.5 cm² , in whom the (PAM) pulmonary arterial mean pressure is > 25 mmHg and the mean pressure gradient at the valve exceeds a value of > 15 mmHg under stress, provided that favorable valve morphology is present (Pinger 2019).

According to ESC 2012, the indication for percutaneous mitral valvuloplasty (also known as mitral valve dissection) is when the COF is < 1.5 cm²

Indication class I/B:

• This class includes symptomatic patients with favorable conditions for balloon valvuloplasty who do not have any of the following risk factors: advanced age, NYHA IV, ECHO score > 8, recent commissurotomy, severe pulmonary hypertension, valve calcification on fluoroscopy, very small CAF, AF (atrial fibrilation), or severe tricuspid regurgitation.

Indication class I/C:

• symptomatic patients with a contraindication to surgery or with a high risk of surgery

Indication class IIa/C:

• as initial therapy option in symptomatic patients with unfavourable anatomy but otherwise good clinical characteristics
• previously asymptomatic patients with favourable anatomy but at high risk of thromboembolism, post embolism, dense spontaneous echocontrast, systolic PA pressure > 50 mmHg at rest, recent atrial defibrillation or implantation of a paroxysmal atrial defibrillator, childbearing or need for major non-cardiac surgery (Pinger 2019).

Advantages of the catheter procedure: major surgery can be avoided or delayed.

• the MEF is usually doubled by the procedure
• gradient is usually approximately halved by the procedure (Herold 2018).

Complications of PMC may include:

• Increase in mitral regurgitation.
• Development of atrial septal defect due to transatrial puncture.
• Perforation of the atrial septal defect- Perforation of the ventricle.
• Thromboembolism
• AV blockages (Herold 2018)

Contraindications:

• Existence of already higher grade mitral valve regurgitation.
• Atrial thrombi
• History of thromboembolism
• thickened atrial septum
• KÖF > 1,5 cm²
• necessity of ACVB surgery in case of existing CHD
• no fusion of the commissures
• severe or bi-commissural calcification (Pinger 2019).

Notes: PMC is found to have similar results as surgical mitral commissurotomy: 10-year survival rate is 80%-90% (Herold 2018). From this point of view, assuming a suitable anatomy, PMC is the therapy of choice (Kasper 2015). Pinger (2019) emphasizes that the results of PMC are better than those of closed commissurotomy, but without giving more details. The best postoperative results are found in sinus rhythm, young patients with low score values, minimal calcifications and without already concomitant mitral regurgitation (Herold 2018). Failure of the procedure is reported to be 1%-15%. Mortality from the procedure ranges from 1%-2%, sometimes < 1% (Pinger 2019).

Surgical therapy: Surgical measures are differentiated between an open and a closed mitral commissure rotomy and a surgical mitral valve replacement.

Closed mitral tissue rototomy:

For this surgical procedure, the use of a heart-lung machine is not necessary. The procedure is still performed in some developing countries. The prognosis of closed mitral commissure rotomy is better than that of purely conservative treatment (Pinger 2019).

Open mitral commissure rotomy:

Open mitral commissular rototomy is an established surgical procedure that competes with the percutaneous method. However, it is rarely used in Germany nowadays. The mortality rate is between 1 % - 3 %. The re-operation rate is 4 % - 7 % (occasionally even more) within the first 5 years. The complication-free 5-year survival is between 80 % and 90 % (Pinger 2019).

Surgical mitral valve replacement:

The first implantation of a FORTIS valve was performed in 2014, the first transapical implantation of a direct flow aortic valve prosthesis in mitral position in the following year (Pinger 2019). The indication for mitral valve replacement is when PCM is out of the question and patients with severe symptoms (NYHA III - IV) and a mitral opening area of < 1.5 cm² of minor symptoms (NYHA I - II) and a mitral opening area of < 1.0 cm² (Herold 2018) are concerned. The mortality rate in surgery is between 1 % - 8 % and in risk patients between 10 % - 20 % (Pinger 2019). It depends mainly on the age of the patient, on the left ventricular function, on a possible existing coronary artery disease and on additional concomitant diseases (Kasper 2015).

Postoperatively a more or less normalization of the small circulation at rest occurs. However, a pathological increase in PAM is still found under stress. There is an improvement by one NYHA class, the majority of the patients are found in NYHA class II. Only very rarely are patients completely free of symptoms after the operation. The prosthesis-related mortality rate is 2.5 % / year, the prosthesis-related complication rate is 5 % / year. The 10-year survival rate is 65.4 % (Pinger 2019).

The following check-ups should be carried out regularly:

• clinical examination
• Chest X-ray
• Echocardiography
• Ergometry

The time intervals depend on the severity of the disease (Herold 2018)

Pinger (2019) recommends the following echo controls:

• in mild MS every 3 - 5 years
• for moderate MS every 1 - 2 years
• in severe MS, annually

The pressure load caused by stenosis of the valves is much more stressful for the heart and therefore has the less favourable prognosis (Herold 2018).

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

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 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

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