Heart valve defectI38

An acquired heart valve defect is defined as the changes that occur in one or more heart valves during the course of a lifetime (Anschütz 1974). These can appear as random findings, but can also cause severe haemodynamic changes.

In heart valve defects, we differentiate between stenosis and insufficiency.

• Stenosis: In this type of stenosis the heart valves become stuck together. 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 / Anschütz 1974).
• Insufficiency: Insufficiency leads to scarred shrinkage of the valves. This ultimately leads to the inability to close the valves. The insufficiency can occur both in the acute stage of the disease and in its chronic course (Herold 2018).

Both the stenosis and the insufficiency can develop separately or in combination (so-called combined cardiac vitium [Herold 2018 / Anschütz 1974]).

One, several or all heart valves may be affected in one and the same patient (Herold 2018).

In the majority of cases of acquired vitreous disease, the valves of the left heart are affected, since they are exposed to greater mechanical stress (the absolute pressure and also the pressure gradient on the left exceed the pressure on the right [Herold 2018]).

Acquired valve defects of the right heart are rather rare. They can occur, for example, through pacemaker probes or ICD probes after passage of the tricuspid valve or in the context of bacterial endocarditis (e.g. in i.v. drug addicts). The acquired vitilia of the right heart are mainly functional insufficiencies (Herold 2018).

The most common valve disease in Europe and North America is aortic stenosis. It occurs in about 4% of the over 75-year-olds (Pinger 2019).

Isolated hemodynamically effective tricuspid valve defects account for only about 4 % - 5 % of acquired heart valve defects and are therefore extremely rare (Hanrath 2006).

Rheumatic fever plays a major role in the development of acquired heart disease in developing countries. However, here too there are great differences from country to country. The prevalence of school-age children ranges from 1.0 per 100,000 (in Costa Rica) to 150 per 100,000 (in China). Worldwide there are about 15 - 20 million people with rheumatic heart disease. The annual rate of new cases is 300,000 and the mortality rate is about 233,000 patients. The highest mortality rate is found in Southeast Asia with 7.6 of 100,000 patients (Kasper 2015).

Rheumatic heart attacks (usually of the mitral or aortic valve) have become significantly less common in industrialized countries thanks to antibiotic therapy and prophylaxis. On the other hand, there has been an increase in degenerative valve diseases due to higher life expectancy (Erdmann 2006).

There has been an increase in the prevalence of both women and men in recent years. Relevant changes in the heart valves of the left heart are found in approx. 12 % - 13 % of those over 75 years of age (Kasper 2015).

The majority of acquired valve diseases are valvular heart defects in which the valve apparatus is primarily altered (Erdmann 2006). They show a variety of causes:

• infectious
• ischemic
• immunological
• degenerative
• traumatic

Rare causes include the following triggers:

• Tumours (carcinoid syndrome)
• Storage diseases
• Collagen diseases (e.g. scleroderma, systemic lupus etc.)
• rheumatoid arthritis
• ankylosing spondylitis
• hereditary connective tissue diseases (Marfan syndrome is the most common cause of valve lesions)
• among others (Erdmann 2006)

Stenoses 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 insufficiency can also be caused by degenerative or inflammatory processes. The following play a special role here::

• coronary heart disease
• cardiomyopathies (both primary and secondary)
• congenital anomalies (Herold 2018)

Functional pulmonary insufficiency can occur, for example, in the context of severe pulmonary hypertension due to overstretching of the valve attachment ring.

Functional tricuspid insufficiency, in turn, can lead to overstretching of the valve attachment ring, e.g. in severe right heart failure with right ventricular hyperextension (Herold 2018)

The clinical symptoms of the Vitien depend on the type of cardiac load and are discussed under the respective valve vitium. See below:

• Aortic Stenosis
• Aortic Insufficiency
• Mitral Stenosis
• Mitral regurgitation
• Pulmonary stenosis (almost always congenital valve defect; acquired pulmonary stenosis is a rarity [Krakow 2005])
• Pulmonary insufficiency
• tricuspid stenosis (the isolated stenosis is rare, usually there is a combined vitium [Krakow 2005])
• tricuspid insufficiency (isolated insufficiency is rare, mostly combined vitium [Krakow 2005])

Auscultation: During auscultation, the typical sounds for the respective valve defect occur. As these depend on the type of valve defect, they are discussed in the respective clinical picture.

Echocardiography: In case of stenosis a pressure gradient can be determined echocardiographically. The following applies to the aortic and pulmonary valves:

• - The pressure gradient depends on the pumping function of the ventricle as well as on the valve opening area.
• The severity of the stenosis is classified as low, medium or high depending on the valve opening area and the gradients across the valve (Herold 2018).

Color duplex: In case of valve insufficiency, the reflux can be directly visualized and quantified in color duplex (Herold 2018)

Lävocardiography: Also in lävocardiography the extent of an insufficiency can be determined and assigned to one of the 3 degrees of severity (low / medium / high) (Herold 2018).

Coronary angiography: A coronary angiography is indicated if coronary heart disease is also suspected. This often occurs together with vitium (e.g. in about 35% of patients with aortic stenosis [Bonzel 2009]).

The gradient in stenoses can - in addition to echocardiography - also be calculated using coronary angiography (Herold 2018).

The treatment of valve diseases can be performed both internally and surgically (Herold 2018). Before a decision on therapy is made, a detailed diagnosis is always necessary to clarify the:

• etiology
• Acute or chronic development of the vitamin
• Degree of severity of the valve alteration
• Severity of ventricular dilation and dysfunction
• Presence of dysrhythmia
• Presence of pulmonary hypertension (Herold 2018)

The possibilities of an internal treatment consist of:

- Treatment of any existing heart failure (see d.)

- Endocarditis prophylaxis, see below (see endocarditis prophylaxis)

- Thromboembolism prophylaxis after implantation of a mechanical valve (Herold 2018)

Surgical replacement of the defective heart valve (see also valve replacement).

Preoperatively, it should be decided individually whether coronary angiography is necessary to exclude a coronary artery disease, as this could then be treated during the upcoming operation (Herold 2018).

In general, it can be said that the volume load has the more favourable prognosis in case of valve insufficiency. The pressure load caused by stenosis of the valves is much more stressful for the heart and therefore has a less favourable prognosis (Herold 2018).

Patients with valve reconstruction or prosthetic heart valves have a significantly increased risk of endocarditis. The post-procedural bacteremia frequency after tooth extractions in gingivitis, for example, is up to 90%. Therefore, preoperative 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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2. Bonzel T et al (2009) Guideline heart catheter. Steinkopff Publishing House 54- 57
3. Erdmann E et al (2006) Clinical Cardiology: Diseases of the heart, circulation and the vessels near the heart. Springer Publishing House 703- 741
4. Herold G et al (2018) Internal Medicine. Herold Publishing House 164- 165
5. Kasper D L et al (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 1528- 1552
6. Kasper D L et al (2015) Harrison's Internal Medicine. Georg Thieme Publishing House 1863- 1891
7. Krakow I et al (2005) The Cardiac Catheter Book: Diagnostic and interventional catheter techniques. Georg Thieme Publisher 145, 215
8. Pinger S (2019) Repetitorium Kardiologie: For clinic, practice, specialist examination. German medical publisher. 275- 361