Valve replacement Z95.9

The first heart valve replacement was developed independently of each other in the early 1950s by Charles Hufnagel and J. Morre Campbell. It was a so-called ball valve. After it could be shown that implanting the valve into the descending aorta in dogs with aortic valve insufficiency significantly improved abnormal hemodynamics, Hufnagel first implanted it into the descending aorta in 1952 in a person with aortic valve insufficiency (Hombach 2001).

However, surgical measures on the heart valves under direct vision were only possible after the introduction of extracorporeal circulation by Gibbson in 1953. Initially, however, these operations were limited to purely repair measures of the defective valve.

The first replacement of a heart valve was performed in 1960 by Starr, Edwards, Harken and Braunwald (Pinger 2019). This was a mechanical valve, the Starr-Edwards prosthesis, named after its developers. This marked the beginning of the era of prosthetic heart valve replacement (Hombach 2001).

s. a. aortic valve stenosis, aortic valve insufficiency, mitral valve stenosis, mitral valve insufficiency, pulmonary valve stenosis, pulmonary valve insufficiency, tricuspid valve stenosis, tricuspid valve insufficiency

A heart valve replacement is an artificial heart valve made of biological or mechanical material that replaces the natural heart valve.

The indication for surgical valve replacement therapy is then given,

• if the patient's symptoms no longer allow conservative therapy
• if postponing the surgical measure could cause irreversible damage to the myocardium or other organs (e.g. through embolization) or threaten pulmonary hypertension (Herold 2018).

Heart valve replacement can be mechanical or biological material. The biological material is further differentiated between:

• Xenograft (animal material)
• Allograft or homograft (human material; but recipient and donor are not identical)
• Autograft (also human material; however, recipient and donor are identical)

Mechanical flaps. Mechanical dampers include:

• Ball Cage

These include the Starr-Edwards and Smeloff cutters, both of which are no longer implanted today.

• Disc cage

This includes the Kay- Shiley; it is also no longer used

• Folding disc

These are so-called mechanical prostheses of the 2nd generation such as Björk- Shiley, Medtronic Hall, Lillehei- Kaster, Omniscience/ Omnicarbon, Sorin Allcarbon

• Double wing

These include the 3rd generation prostheses, which have improved hemodynamics and lower thrombogenicity. These include St. Jude Medical, Duromedics, On- X, Carbomedics, Sorin Bicarbon, ATS (Pinger 2019).

The advantage of mechanical valves is their long durability (e.g. more than 40 years are described for a functional rigid Edwards prosthesis). The incidence of dysfunction requiring surgery is only about 0.03 / 100 patient years.

Patients usually complain suddenly about:

• severe dyspnoea
• thoracic pain
• disturbed consciousness
• ventricular arrhythmias
• pulmonary congestion
• Shock symptoms

Here, a quick diagnosis is required, e.g. auscultation (no longer indicates a click of the prosthesis), followed immediately by fluoroscopy or an echo. In case of dysfunction, immediate surgical intervention is required. See below for details (Pinger 2019).

The disadvantages of mechanical valves are:

• high risk of thromboembolism (0.5 - 2.5 % / year, depending on the location of the valve)
• required long-term anticoagulation
• All valve prostheses have a transvalvular gradient, which corresponds to at least a moderate stenosis and can increase under load (Niebauer 2015)
• Risk of haemolysis with LDH increase, haptoglobin decrease and reticulocyte increase. Pronounced hemolysis can lead to a drop in hemoglobin levels (Bob 2001) (Herold 2018)

One indication for mechanical valves are:

• the patient statistically still has a longer life expectancy
• for other reasons, anticoagulation is already required
• already existing renal insufficiency (Herold 2018)

Biological valves: The majority of bioprostheses are heterologous porcine prostheses, which are specially prepared and - to a lesser extent - bovine bioprostheses, which consist of bovine pericardium. Both are also known as xenografts.

In addition, biological valves can be produced from cadaveric material (fascia mater, dura mater) as allograft - also called homograft - or consist of the body's own material as so-called autograft (Herold 2018). One differentiates between:

• prostheses with stent scaffolding such as Medtronic Mosaic, Medtronic Hancock II, SJM Epic [Biocor], Carpentier Edwards Perimount, Sorin Mitroflow
• stentless prostheses such as Medtronic Freestyle, Edwards prima plus, Sorin freedoms, SJM Toronto SPV
• and the so-called autologous bioprostheses, which consist of the patient's own material (Pinger 2019).

The advantage of the biological valve is:

• due to the low thrombogenicity, the patient does not need anticoagulation (Herold 2018)

The disadvantages of the biological valve are:

• the valves have a low durability (about 50% of patients require a second operation after 15 years; there is a clear dependence on the age of the patient at implantation: the younger the patient, the faster and more often the valve failure occurs [Pinger 2019])
• Progressive calcification of the valve with restriction of valve mobility and KÖF

Particularly affected are patients with renal insufficiency, z. n. endocarditis, with large prostheses, patients with existing calcium metabolism disorders, prostheses in mitral function (Herold 2018).

Indications for biological valves are:

• Patients > 75 years or with < 10 years life expectancy
• Patients who must not receive anticoagulation
• Re-operation due to thromboembolism complications of the previously inserted mechanical valve
• Patients with tricuspid stenosis without evidence of additional insufficiency (Herold 2018).

Allograft or autograft prosthesis

The allograft prostheses are made of cadaveric material (e.g. fascia mater, dura mater), the autograft prostheses of the patient's own material (e.g. use of the pulmonary valve to replace the aortic valve; the missing pulmonary valve is replaced by a pulmonary or aortic allograft; the procedure is called Ross-op) (Herold 2018).

The advantage of both procedures is:

• low thrombogenicity.

The disadvantages of the procedures are:

• the implantation is more difficult
• there is a possibility of degeneration
• the availability is limited

An indication is given:

• in patients with endocarditis which has not yet progressed
• for women who want to have children
• in younger patients (Herold 2018)

Catheter-assisted aortic valve replacement (TAVI = transcatheter aortic valve implantation)

The TAVI is a biological valve prosthesis that is implanted transfemorally or transapically by means of a catheter (Pinger 2019). The implantation is performed with the help of a balloon catheter (also called balloon-expandable) or through a valve folded into the lumen of the catheter (also called self-expandable).

After unfolding, the valves are immediately functional. During deployment, the native valve is pressed into the aortic wall and remains there (Herold 2018). The first catheter-assisted aortic valve replacement was implanted in 2002 (Pinger 2019).

Indication:

TAVI was initially used only in inoperable patients or in patients at high risk of surgery. In the meantime, studies have been published which show comparable results with the usual surgical implantation. For the transfemoral approach even a survival advantage has been shown. Since then, patients at intermediate risk also receive the valve through a TAVI (Herold 2018).

Absolute contraindications:

• there is no cardiac surgery in the house
• TAVI is not confirmed by the "heart team
• an improvement in the quality of life is not to be expected due to comorbidities
• the life expectancy is < 1 year
• there are other valve diseases that can only be treated surgically
• the size of the annulus is < 18 mm or > 29 mm
• there is a thrombus in the left ventricle
• mobile thrombi are present in the aortic arch or the aorta
• currently existing active endocarditis
• increased risk of coronary obstruction (e.g. in narrow sinus aortae, short distance between annulus and coronary ostia, asymmetric calcification of the valves)
• the vascular access is inadequate (in case of access via A. femoralis or A. subclavia) (Pinger 2019).

Complications:

• high grade AV block (10 % - 15 %)
• Paravalvular leakage (7 %)
• Acute renal failure (3 %)
• Apoplexy (2 %)

severe complications such as

• Annulus rupture
• Ventricular rupture
• the necessity of conversion to open surgery is < 1% (Herold 2018)

Antithrombotic therapy:

Postinterventional antithrombotic therapy is currently the subject of ongoing studies. Currently, dual antiplatelet therapy (ASA plus clopidogrel) is used, followed by ASA monotherapy (Herold 2018). According to ACC / AHA 2014, there is currently a recommendation level IIb for dual platelet inhibition. Patients should receive continuous ASA therapy and additionally clopidogrel in the first 6 months after surgery.

Dosage recommendation (Bocksch 2012):

• on the day before surgery ASS 500 mg / Clopidogrel 600 mg
• during TAVI Heparin 70- 100 I.U./ kgKG, maximum 10.000 I.U. (ACT 300 - 350)
• Follow-up treatment with 100 mg ASS / d and 75 mg / d clopidogrel (Pinger 2019)

Oral anticoagulation should be reserved exclusively for patients with preoperative indications (e.g. atrial fibrillation) (Herold 2018).

After valve replacement, complications occur in about 50% of all patients within the first 10 years. We differentiate between early and late complications.

Early complications include:

• Infections
• Prosthetic endocarditis (occurs in 7-15% of cases within the first 15 years; has a very poor prognosis and a high mortality [Pinger 2019])
• Bleeding
• Arrhythmias
• Heart failure
• Perioperative lung, kidney, liver, or multiorgan failure.

[Herold 2018)

Late complications include:

• Thromboembolism
• Prosthetic endocarditis
• Bleeding under anticoagulation
• Complications of prostheses:
  • Tears in the sheath of valve cages
  • existing disproportion of valve to body size (also called patient/ prosthesis mismatch = PPM)
  • tear-out of prosthesis wings
  • defects of ball prostheses
• Heart failure later in life due to:
  • valve dysfunction
  • occurring hypertension and / or CHD
  • pre-existing myocardial damage (the pre-existing condition of the left ventricle essentially determines the long-term prognosis, especially in the case of pre-existing valvular insufficiency)

(Herold 2018)

Causes of prosthetic valve insufficiency may include:

• mechanical dysfunction (very rare, e.g., due to leaflet rupture)
• inability to close (due to thrombosis, vegetation, pannus, etc.)
• paravalvular leak / periprosthetic dehiscence (e.g. due to endocarditis, suture insufficiency, etc.)
• Degeneration of the valve (in bioprostheses).

(Pinger 2019)

Causes of prosthetic stenosis can be:

• mechanical dysfunction (very rarely occurring)
• degenerative changes (in bioprostheses)
• stenosis due to thrombus, pannus, endocarditic vegetation

(Pinger 2019)

Specific problems after valve replacement:

1. artificial valve thrombi.

The incidence of valve thrombi is under coagulation for

• the aortic valve prosthesis at 0.9 - 1.2 events / 1,000 patient-years
• The mitral valve at 2.1 - 3.4 events / 1,000 patient-years.

(Pinger 2019)

• most frequently, however, with prostheses of the tricuspid valve (exact figures are not available; patients with tricuspid stenosis receive almost exclusively biological valves because of the risk of thrombosis)
• Incidence depends on prosthesis type, rarely occurs with St. Jude Medical

(Herold 2018)

Valve insufficiency and / or stenosis with cardiac decompensation may develop as a consequence of valve thrombosis (Pinger 2019).

Clinical Symptoms:

A worsening of the clinical condition is found, signs of acute heart failure may occur, sudden cardiac arrhythmias are possible or emboli occur.

Therapy:

Prompt reoperation; lysis therapy may be required.

(Herold 2018)

In a study of 110 patients, lysis yielded success in 71% of cases. Mortality was 12% (due to both therapy failure and therapy complications [Pinger 2019].

According to Huang's 2013 expert recommendation, which included 662 operated and 756 lysed patients, thrombolysis should be the first-line therapy for right-sided thrombi. He recommended surgery only if lysis was unsuccessful.

For left-sided thrombi, Huang considers lysis to be the first-line therapy in patients

• with an absolute contraindication to surgery
• with NYHA I / II
• with comorbidities who are at high risk for surgery
• patients who refuse surgery
• with only small thrombus (< 0.8 cm² ) and no history of apoplectic insult

In turn, surgical treatment is the first choice in the following patients:

• in whom replacement of the valve prosthesis is necessary anyway
• with impaired blood flow to the coronary arteries
• with contraindication to lysis therapy
• if pannus formation contributes significantly to the obstruction
• after unsuccessful lysis therapy

Surgical intervention should initially be preferred in patients with:

• with NYHA III / IV
• thrombus size > 0.8 cm²

(Huang 2013)

2. thromboembolism

Thromboembolism occurs preferentially with the use of mechanical prosthetic valves and then predominantly in those in the mitral position, less frequently in the aortic position. The incidence is 2%-3% per patient year. Thromboembolism rarely occurs with homograft valves.

Clinical Symptoms:

Depending on the vascular territory affected (e.g., brain, extremities, intestinal vessels), ischemia is found with corresponding symptoms

(Herold 2018)

Prophylaxis:

The ACC / AHA 2014 recommends oral coagulation with Vit. K- antagonists.

Recommendation grade I:

• for mechanical aortic valve replacement (both double leaflet prosthesis and modern tilt disc prosthesis) without risk of embolism: oral anticoagulation with INR- target value 2.5
• in case of mechanical aortic valve replacement with existing risks for embolism (e.g. atrial fibrillation, left ventricular dysfunction, post-thromboembolism, hypercoagulability) or in case of older mechanical aortic valve replacement (e.g. ball-and-cage prosthesis): oral anticoagulation with INR target value 3.0
• in case of mechanical mitral valve replacement: oral anticoagulation with INR target value 3.0

Recommendation grade IIa:

• For biological mitral valve replacement or reconstruction of the mitral valve:

for the first 3 months postoperatively oral anticoagulation with INR-target 2,5

Recommendation grade IIb:

• Patients with bioprosthesis as aortic valve replacement should receive oral anticoagulation with INR- target value 2.5 for the first 3 months postoperatively

Oral coagulation with 100 mg ASA / d:

Recommendation grade I:

• In addition to oral anticoagulation with Vit. K antagonists, ALL patients with mechanical prosthesis should receive ASA.

Grade of recommendation IIa:

• all patients with bioprosthesis as aortic valve replacement or mitral valve replacement should receive ASS- continuous therapy

Grade of recommendation IIb:

• Patients with TAVI (transcatheter aortic valve implantation) should receive ASA continuous therapy and also clopidogrel in the first 6 months postoperatively;

See below for dosage recommendation.

(Pinger 2019)

Direct anticoagulants such as apixaban, edoxaban, dibagratan, rivaroxaban are contraindicated for anticoagulation in patients with artificial valves (Herold 2018).

3. prosthetic endocarditis

Prosthetic endocarditis occurs preferentially with both mechanical and biologic replacement valves. It is found less frequently only with homograft valves.

The risk of prosthetic endocarditis is about 7-15% in 15 years. The prognosis is always very serious, mortality high (Pinger 2019).

A distinction is made between early and late endocarditis.

Early endocarditis occurs within the first postoperative year and generally reflects perioperative contamination . The causative organisms are usually staphylococci and gram-negative pathogens. Only rarely are fungi the causative agent (Herold 2018).

Late endocarditis occurs only in the second postoperative year. The pathogens are identical to those that can also cause endocarditis on native heart valves such as Streptococcus aureus, Streptococcus viridans, Staphylococcus epidermidis, enterococci, etc. (Herold 2018).

Clinical Symptoms:

• Fever
• previously absent valvular murmurs
• Altered opening or closing sounds

(Herold 2018)

Diagnostics:

• transesophageal echocardiography
• a blood culture should be taken immediately (before starting antibiotics)

(Herold 2018)

Therapy:

It is recommended to start with a maximum dose combination therapy of synergistic and additive antibiotics . The duration of treatment should not be less than 6 weeks (Suttrop 2004).

Prophylaxis:

To prevent late prosthetic endocarditis, high-risk patients (which include all patients with artificial heart valves) should receive antibiotics during procedures that lead to bacteremia. Suggested dosage:

• To administer antibiotic prophylaxis as a single dose 30-60 min before the procedure;
• if oral administration is possible, amoxicillin or ampicillin 2 g p. o. can be administered
• if oral administration is not possible, ampicillin or cefalexin 2 g i.v. is recommended
• in case of ampicillin or penicillin allergy, clindamycin 600 mg should be given orally
• if i.v. administration is necessary, clindamycin 600 mg i.v.

(Herold 2018)

For more details, see endocarditis prophylaxis.

4. paravalvular leaks

Paravalvular leaks occur preferentially in the early postoperative phase on valves that have been sutured into heavily calcified valve rings. In a later phase, they usually occur in the setting of endocarditis(Herold 2018).

After aortic valve replacement, they are found in approximately 2%-10% and after mitral valve prosthesis in 7%-17% (Pinger 2019).

Paravalvular leak leads to hemolysis and regurgitation during its course (Pinger 2019).

Clinical Symptoms:

Most patients remain asymptomatic. Clinical effects of severe hemolytic anemia or signs of heart failure due to volume loading are found in only about 1%-5% (Pinger 2019).

Diagnostics;

On auscultation, reflux sounds are found at the affected valve. Laboratory chemistry indicates hemolysis (LDH, haptoglobin, reticulocytosis). A proximal zone of convergence may be present on echocardiography.

(Pinger 2019)

Therapy:

The standard therapy has been reoperation. Depending on the extent of the leak, direct suture or patch- plastic are used. The 30-day major adverse cardiatic events (MACE) is 8.7%.

Increasingly, however, percutaneous catheter-based closure systems are also being used. The mortality rate of 1.4 % - 2 % is lower than with the previous surgical procedure. Long-term data are currently lacking.

(Pinger 2019)

5. hemolysis

Mechanically induced hemolysis occurs preferentially in older valve models. It is insignificant in otherwise well-functioning prosthetic valves and is manifested only by a small increase in LDH (Herold2018).

Hemolysis is caused by high flow velocities and abnormal shear forces. A distinction is made between mild hemolysis (LDH 220 - 400 U/l). It can occur even with an intact valve.

In the case of moderate hemolysis, an LDH increase of 400 - 800 U/l is found.

From an LDH > 400 U/l, a dysfunction, such as (thrombosis, dehiscence, etc.) should be excluded.

(Pinger 2019)

As soon as valve dysfunction occurs, hemolysis increases and laboratory chemistries are detectable:

• marked LDH- elevation
• HBDH increased
• Drop in haptoglobin (is no longer measurable at all in the case of severe hemolysis)
• Hemopexin may decrease (but usually only in severe hemolysis).
• Reticulocytes are elevated
• Indirect bilirubin is also elevated
• Evidence of fragmentocytosis
• Hb-value normal or decreased (as long as the Hb-value is normal, it is a compensated hemolysis. Only when the Hb- value is decreased is it referred to as decompensated hemolysis, which is also known as hemolytic anemia).

(Herold 2018

Diagnostics:

• echocardiography should be performed to exclude prosthetic dysfunction (Herold 2018).

Therapy:

Therapy depends on the cause of hemolysis.

Conservative treatment can be used:

• Beta-blockers (reduce the flow velocity).
• Substitution of iron
• Administration of erythropoietin

(Pinger 2019)

In case of severe hemolysis, surgical revision may be necessary. A Euroscore calculator can be used on the Internet to estimate early postoperative mortality.

(Herold 2018)

The preoperatively passed condition of the left ventricle essentially determines the long-term prognosis, especially in cases of previously passed valve insufficiency (Herold 2018).

Performance after heart valve replacement:

Patients after mitral valve replacement or multiple valve replacement should be advised against higher physical exertion due to the persistent obstruction. Patients undergoing aortic valve replacement with persistent myocardial dysfunction should also avoid strenuous exercise.

(pinger 2019)

Course after mitral valve replacement:

Very few patients are free of symptoms postoperatively. The NYHA class passed preoperatively usually improves by 1 step (Pinger 2019).

Course after aortic valve replacement:

After aortic valve replacement, the postoperative exercise tolerance corresponds to about 80% of the age norm, whereby the variability is usually less in a previously passed stenosis than in a preoperatively passed insufficiency. On average, about 43 % improves by 1 NYHA class and 46 % by 2 NYHA classes.

(Pinger 2019)

Long term prognosis:

Even if a normal life expectancy can be assumed for individual subtypes, the long-term prognosis is generally burdened after valve replacement.

After aortic valve replacement, 40% of the causes of death are caused by the prosthesis itself or the resulting complications. For mitral valve replacement, the figure is even between 40 % and 60 %.

10-year survival after:

Aortic valve replacement for stenosis: 52 % - 68 %

in case of insufficiency: 59

Mitral valve replacement for stenosis: 65

with insufficiency: 53 %

There are no significant differences between the individual mechanical prostheses in terms of long-term prognosis. Homografts are not superior to other bioprostheses.

The op- mortality is

Aortic valve replacement: 17 %

Aortic valve replacement plus ACVB: 24

Mitral valve replacement: 22 %

Mitral valve replacement plus ACVB: 37 %

Dialysis patients have the highest op mortality and the worst long-term prognosis after valve replacement, although there is no difference between mechanical or biological valves over the long term.

Mortality is 46 % after 1 year and 85 % after 5 years.

(Pinger 2019)

An initial echocardiographic check should be performed before the patient is discharged. A further control is recommended after 6 - 12 weeks.

Thereafter, regular examinations should be performed 1 x per year.

(Vahanian 2012)

Medical history:

During history taking, the following new onset changes should be asked:

• intermittent fever
• Fatigue
• Performance slump
• dyspnea (especially at night)
• Stenocardia
• Palpitations
• Hyperhidrosis
• Edema
• Dizziness
• Syncope

Inspection and palpation:

• peripheral edema
• Neck vein congestion
• Pulmonary congestion

(Pinger 2019)

• Hepatomegaly
• Ascites
• Tachycardia (e.g., in anemia, fever, heart failure, endocarditis, volume deficiency, etc.)

(Herold 2018)

Auscultation:

• Opening and closing click.

In bioprostheses and also in homografts, no specific sound phenomena are usually found. In mechanical prostheses, however, an opening and closing click is predominantly heard, with the closing click being louder than the opening click.

• the heart sounds become softer (any softening of the opening and closing click may be an indication of artificial valve thrombosis)
• watch for pleuropericardial rubbing (may occur in postpericardiotomy syndrome in the early postoperative period)
• any new systolic or diastolic murmur (may indicate valve malfunction)
• Tachycardia
• Atrial fibrillation

(Herold 2018)

• with prosthetic valves in the aortic position, a systolicmurmur is often found
• with valve prostheses in mitral position the systolic is found exclusively with the older ball-and-cage prostheses
• on the other hand, with valve prostheses in mitral position sometimes a diastolicis found
• in case of a valve replacement in aortic position a diastolic is always suspicious for an insufficiency of the valves
• if no valve closure sound is audible with a mechanical valve, there is always a suspicion of prosthetic valve thrombosis

(Pinger 2019)

Echocardiography:

An initial echocardiographic check should be performed before the patient is discharged. A further echocardiographic check is recommended after 6 - 12 weeks.

Contrary to the usual practice in Germany, after implantation of a mechanical valve prosthesis, further echocardiographic examinations are not necessary - apart from the echocardiographic control 6 - 12 weeks postoperatively - if the course is uncomplicated.

If a biological valve is implanted, annual echo examinations should be performed 10 years after surgery. Before that, they are not necessary from a medical point of view (Pinger 2019).

During echocardiography, special focus should be placed on any

• Pleural effusions
• Pericardial effusion (in the early postoperative period in postpericardiotomy syndrome; in later stages, signs of heart failure)
• Presence of calcification or buildup.

(Pinger 2019)

• Evidence of any valvular or paravalvular leaks.
• Vegetations (in the presence of bacterial endocarditis).

(Herold 2018)

Otherwise, should be described:

• Movement pattern of the valve
• Flow profiles
• Gradients
• Valve opening areas
• function and size of the ventricles

(Herold 2018)

There is V. a. significant stenosis at the following thresholds:

for aortic valve prosthesis

• max. flow velocity > 4 m/s
• mean pressure gradient > 35 mmHg
• DVI < 0.25
• EOA < 0.8 cm²
• AT > 100 ms
• PHT

with mitral valve prosthesis

• max. flow velocity > 2.5 m/s
• mean pressure gradient > 10 mmHg
• DVI
• EOA < 1 cm²
• AT
• PHT > 200 ms

(Pinger 2019)

X-ray:

In the presence of heart failure, a chest x-ray should always be performed.

This will show the size of the heart and any pulmonary congestion.

If there is a suspicion of dysfunction of the mechanical prosthesis and there is echocardiographic uncertainty, X-ray fluoroscopy is recommended. This will provide more detailed information on

• assessment of opening and closing movements
• abnormal tilting movements (pathological for aortic prosthesis > 8 degrees, for mitral valve prosthesis > 10 degrees)
• possible missing parts of the prosthesis after embolization

(Pinger 2019)

CT:

CT may well be an option in individual cases. In a small study by Symersky (2009), it was shown that obstruction not previously detectable by echocardiography or fluoroscopy could be detected by CT in 8 of 13 patients.

MRI:

MRI is not required for follow-up after valve replacement. If MRI must be performed for other reasons, this examination is possible with one exception: MRI must not be performed for the Pre 6000 rigid Edwards prosthesis (Pinger 2019).

ECG:

In the ECG can be detectable:

• stress of the atria and ventricles
• Excitation regression disorders
• Block images
• Arrhythmias

(Herold 2018)

Laboratory:

Special attention should be paid to:

• Inflammatory parameters (e.g. leukocytes, ESR, CRP, etc.)
• If bacterial endocarditis is suspected, blood cultures should be taken immediately.
• Indications of anemia (blood count, iron, ferritin)
• evidence of hemolysis (bilirubin, fragmentocytes, haptoglobin, HBDH, LDH, etc.)
• If therapy with anticoagulants is given, coagulation monitoring should be performed

(Herold 2018)

Home Monitoring:

After alloprosthetic valve replacement, appropriate patients can be trained in:

• INR- self-determination with the so-called CoaguChek- device (the frequency of severe bleeding complications can be demonstrably reduced)
• Control of valve function by fully automated frequency analysis of valve sound (this allows early detection of valve dysfunction).

(Herold 2018)

1. Amber G et al (2005) Generic, simple risk stratification model for heart valve surgery. Circulation (112) Lippincott Williams and Wilkins American 224 - 231
2. Bob A. et al (2001) Internal Medicine Special Edition. MLP Dual Series. Georg Thieme Publisher 71
3. Bocksch W et al (2012) Antithrombotic therapy during and after implantation of aortic valves (TAVI). Cardio up (3) Georg Thieme Publisher 188 - 192
4. Herold G et al (2018) Internal Medicine. Herold Verlag 165 - 179, 181- 183
5. Hombach (2001) Interventional Cardiology, Angiology and Cardiovascular Surgery: Technology, Clinical, Therapy. Schattauer publishing house 257
6. Huang G et al (2013) Treatment of Obstructive Thrombosed Prosthetic Heart Valve. Journal of the American College of Cardiology (19) 1732 - 1736
7. Karathanos A et al (2019) Pulmonary valve disease: interventional and surgical treatment options. Actuel Cardiol (2) 139 - 144
8. Kasper D L et al (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 1528- 1534, 1539 - 1543, 1548 , 1550
9. Kasper D L et al (2015) Harrison's Internal Medicine. Georg Thieme Publishing House 1863 - 1883, 1884 - 1886, 1887 - 1888, 1875 - 1879
10. Niebauer J (2015) Sports Cardiology. Springer Publishing House 254
11. Pinger S (2019) Repetitorium Kardiologie: For clinic, practice, specialist examination. German medical publisher. 286 – 298, 308 – 335 , 336 – 341, 342 – 361, 397 – 399,
12. Symersky P et al (2009) Comparison of multidetector-row computed tomography to echocardiography and fluoroscopy for evaluation of patients with mechanical prosthetic valve obstruction. Am J Cardiol (104) 1128 - 1134
13. Suttorp N et al (2004) Infectious diseases: understand, recognise, treat. Georg Thieme Publisher 337 - 339
14. Vahanian A et al (2012) ESC Pocket Guidelines Heart Valve Disease. German Society for Cardiology - Cardiovascular Research 38, 39, 41