Tricuspid regurgitation

from Wikipedia, the free encyclopedia
Classification according to ICD-10
I07.1 Tricuspid regurgitation
I36.1 Tricuspid regurgitation non-rheumatic
ICD-10 online (WHO version 2019)

Tricuspid valve insufficiency , and tricuspid regurgitation called, is in the medicine the name of a leakage of the tricuspid valve of the heart , during the ejection phase ( systole ) to a backflow of blood from the right ventricle into the right atrium and the vena cava (→ structure of the heart leads) .

Mild forms of tricuspid regurgitation are discovered quite often during an ultrasound scan of the heart ( echocardiography ) and are usually harmless. Severe forms require precise clarification.

Most tricuspid regurgitation is the result of overstretching the retaining ring ( annulus fibrosus ) of the tricuspid valve or excessive pressure in the right ventricle; the valve itself would still function adequately. This is known as secondary valve regurgitation. In addition, tricuspid regurgitation occurs as a single congenital heart defect or occurs with other congenital heart defects or as a consequence of other congenital diseases of the connective tissue .

A distinction must be made between acute tricuspid regurgitation (for example, as part of a pulmonary embolism ) and chronic insufficiency (for example, as part of primary pulmonary hypertension ).

Epidemiology

Although it is one of the most common valve defects in humans, exact frequency information is not available because the diagnosis depends very much on the accuracy of the heart examination or the valve disease is only a consequence of other diseases and is then no longer explicitly mentioned.

In athletes and young people, a low level of tricuspid regurgitation with no disease value can often be demonstrated. This is probably due to an enlargement of the heart during exercise and to an expansion of the tricuspid valve ring. If the leaflets are pulled apart as part of this expansion, the flap closure is no longer complete.

Pathophysiology

The tricuspid valve works like a valve between the right atrium and the right ventricle of the heart. It opens during the filling phase of the ventricle ( diastole ) and thus enables blood to flow in from the atrium. At the beginning of the ejection phase ( systole ), the sudden increase in pressure in the ventricle closes the valve and thus “seals” the atrium. In this way there is only a pressure of about 4 mmHg in the atrium  , while at the same time the systolic pressure of about 25 mmHg in the ventricle drives the blood on its usual route into the pulmonary artery .

In the case of mild tricuspid regurgitation, these physiological processes are only slightly changed. Neither the size of the leak ( regurgitation opening ) nor the amount of blood flowing back (regurgitation volume, pendulum volume, backflow volume) reach significant proportions, so that the pressures in the right atrium and in the vena cava remain as normal as the pumping capacity of the heart.

In severe tricuspid regurgitation, however, the regurgitation opening is more than 40 mm² and the regurgitation volume is more than 60  ml , which can lead to serious and sometimes life-threatening changes.

In the acute stage, with the right ventricle and right atrium of normal size, there is a considerable increase in pressure in the atrium and thus also in the vena cava. This can be up to 50 mmHg, which, if the vena cava is normal, leads to immediate liver congestion and venous congestion in the neck veins. In addition, the predominant return flow of blood can result in poor ejection capacity into the pulmonary artery and thus in poor blood flow to all organs.

If the acute stage is over or if the tricuspid valve insufficiency develops over a longer period of time, a number of adaptation processes ( compensation mechanisms ) occur chronically in the heart and in the upstream veins. First of all, the sustained pressure and volume load on the atrium leads to its enlargement ( dilatation, dilatio cordis ), whereby the atrial volume can often increase three to fourfold within months and years. Over time, this dilation also reduces the pressure-increasing effect of the regurgitation volume in the vena cava and the liver. In addition, the volume load also causes the right ventricle to enlarge, which now has to promote the regurgitation volume in addition to the amount of blood actually required with each heartbeat. On the one hand, this dilatation can also increase the stroke volume via the Frank Starling mechanism , but on the other hand it leads into a vicious circle if, with the expansion of the ventricle, the geometry of the valve is also disturbed and its insufficiency is increased in this way.

Classification and nomenclature

There is no uniform classification of tricuspid insufficiency : The insufficiency is referred to as organic (or valvular ) if changes in the valve itself have been identified as the cause. Functional (secondary) insufficiency, on the other hand, is the result of changes in the surrounding structures, mainly the right ventricle and right atrium.

A slight leak in the valve, which has no disease value, can be determined with the help of sensitive examination methods in up to 90% of all adults with healthy heart. It is often referred to as physiological tricuspid regurgitation or minimal tricuspid regurgitation .

“Real” tricuspid insufficiency is usually divided into degrees of severity, with a distinction nowadays usually three (mild, moderate and severe) and occasionally four (grade I to grade IV) manifestations.

causes

Solitary congenital tricuspid regurgitation is rare. Mostly there is tricuspid regurgitation in the context of other combined heart defects.

The secondary is more common

Any volume or pressure load on the right heart can sooner or later lead to tricuspid regurgitation.

A bacterial and non-bacterial endocarditis can valve tissue and thus lead to destruction or scarring shrinkage of a tricuspid regurgitation. In contrast to endocarditis of the valves of the left heart, people with frequent bacteremia and immune deficiencies are particularly susceptible to bacterial colonization of the tricuspid valve (e.g. drug addicts with intravenous drug supply, dialysis patients , alcoholics).

A special case is the occurrence of slight tricuspid regurgitation after an electrode has been inserted from the right atrium into the right ventricle as part of a pacemaker implantation .

Clinical picture

Symptoms and clinical signs

Lighter forms are not noticed by the person concerned. The typical symptoms of severe tricuspid regurgitation are leg edema, hepatic and neck vein congestion. Cardiac arrhythmias, which occur more frequently in tricuspid regurgitation, can manifest themselves in the form of palpitations or palpitations .

The most important and groundbreaking finding during the physical examination is a high-frequency band-shaped systolic heart murmur , which can usually be heard loudest above the epigastric angle through auscultation . The volume of the noise often changes with the inhalation and exhalation (the increase in volume when inhaling deeply is called the Rivero-Carvallo sign). A jugular vein congestion and edema can also be detected. It is not uncommon to feel an enlarged liver and sometimes an ascites ( water in the abdomen ). Typical pulsations of the neck veins that are visible and palpable during inspection and also liver pulsations that can be seen in the epigastrium and palpation are typical.

In the percussion, the enlargement of the right atrium can be determined by widening the attenuation to the right and the enlargement of the right ventricle by widening the attenuation to the top left.

In children and adolescents, symptoms of the disease are no different from symptoms in adulthood. In young children and newborns, the symptoms of developmental delay or stagnation in growth should be emphasized: Despite sufficient food intake, the weight does not increase in children with significant tricuspid regurgitation, and the expected increase in size does not occur. Otherwise, the severity of valve insufficiency also correlates with the severity of the symptoms in children.

Technical findings

In addition to the physical examination, nowadays only an ultrasound examination of the heart ( echocardiography , abbreviation TTE) is usually required to assess tricuspid regurgitation . Further examination procedures are only required in special cases or before a planned operation to exclude concomitant diseases. The diagnosis of tricuspid regurgitation in children does not differ from that in adults. In the TEE ( swallowing echo ), weakness in the tricuspid valve is usually less recognizable.

Echocardiography

Echocardiography is indispensable as a standard procedure: it allows the diagnosis to be confirmed and the severity to be determined, as well as an assessment of the course. The color Doppler echocardiography shows an existing tricuspid regurgitation as a (mostly blue ) color cloud in the right atrium, which is referred to as the insufficiency jet . The width and extent of this color cloud already allow a rough estimate of the severity of the insufficiency. In addition, the underlying mechanism (ring dilatation, incomplete valve closure, endocarditis) and the location of any valve changes can sometimes be documented. According to the guidelines of the European Society for Cardiology ESC, criteria for high-grade tricuspid regurgitation include: the width of the insufficiency jet (vena contracta) ≥ 7 mm, an EROA ("effective regurgitant orifice area") ≥ 40 mm², dilatations of the right ventricle , right atrium and inferior vena cava as well as dilated hepatic veins.

From the maximum speed of the regurgitation jet, the pressure gradient over the valve and thus the systolic pulmonary artery pressure can be estimated, which can be useful for assessing high pressure in the pulmonary artery.

The size and pumping function of the right and left ventricles can also be reliably determined with the help of echocardiography. These important parameters of the heart function are important for the assessment of severe tricuspid regurgitation.

Other procedures

Other examination procedures are required to identify possible causes and complications or to prepare for surgery immediately. For example, an ECG and, if necessary, a long-term ECG can be helpful for diagnosing accompanying cardiac arrhythmias and an X-ray of the thoracic organs for the question of possible pulmonary congestion.

In the right heart catheter examination , the pressure conditions in the right half of the heart and in the pulmonary artery are diagnosed and quantified, but the examination is only necessary for special questions.

The sonographic examination of the abdominal cavity shows possible liver congestion, regurgitation in the hepatic veins and ascites formation as a result of the valve disease.

course

The course of tricuspid regurgitation is extremely variable and can only rarely be foreseen. Even severe tricuspid regurgitation can remain completely "stable" (unchanged) for many years, and this is even the rule for minor insufficiencies. Regular check-ups, for example at annual intervals, can provide information about the individual progress. Particular attention is paid to the severity of the insufficiency, the size and pumping function of the right ventricle and other signs of an impending overload of the heart in order to recognize impending deterioration at an early stage. These “progress parameters” are important pointers for optimal therapy planning .

therapy

Basically, all patients with “real” (not just “physiological”) tricuspid regurgitation have an increased risk of developing bacterial endocarditis . The indication to carry out endocarditis prophylaxis in patients with tricuspid valve regurgitation was withdrawn in the ESC guidelines for therapy and prophylaxis of endocarditis from 2015.

Therapy is not required for mild tricuspid regurgitation.

In childhood, regular check-ups by means of echocardiography at intervals of 6 to 12 months are indicated.

Medical therapy

In severe tricuspid regurgitation with signs of heart failure , therapy is based on the principles of heart failure therapy. Whether long-term drug therapy with ACE inhibitors improves the prognosis even in symptom-free patients without heart failure is still controversial. If cardiac arrhythmias are present at the same time , the use of antiarrhythmics may be necessary.

Depending on the size of the right atrium, the use of can anticoagulants such as phenprocoumon or warfarin for prevention of thrombus formation within the (extended) and the right atrium of the most congested vein be required.

In acute severe tricuspid regurgitation, treatment usually has to be carried out in the intensive care unit .

In children, the mild forms of tricuspid regurgitation are also treated with medication. The start of drug therapy depends on the severity itself and the course of the echocardiographic controls. The primary therapeutic goal is to reduce the afterload. As in adults, mainly ACE inhibitors are used; in addition, diuretics are used.

Operative therapy

Surgical therapy for tricuspid regurgitation is rarely performed. Either

forecast

Due to the very different course of tricuspid regurgitation, the prognosis of the patients is also very different. Today it is assumed that people with mild insufficiency without any other heart disease have a normal life expectancy.

In severe chronic tricuspid regurgitation, liver cirrhosis can occur as part of the constant liver congestion. (Cirrhosis cardiaque)

Sudden deaths are rare in patients with tricuspid regurgitation. Secondary pulmonary embolism can sometimes be identified as the cause.

See also

literature

  • Reinhard Larsen: Anesthesia and intensive medicine in cardiac, thoracic and vascular surgery. (1st edition 1986) 5th edition. Springer, Berlin / Heidelberg / New York et al. 1999, ISBN 3-540-65024-5 , pp. 268-270 ( tricuspid insufficiency ).
  • Klaus Holldack, Klaus Gahl: Auscultation and percussion. Inspection and palpation. Thieme, Stuttgart 1955; 10th, revised edition, ibid 1986, ISBN 3-13-352410-0 , pp. 173-175.

Individual evidence

  1. ↑ Eduardo Bossone, Melvyn Rubenfire, David S Bach, Mark Ricciardi, William F Armstrong: Range of tricuspid regurgitation velocity at rest and during exercise in normal adult men: implications for the diagnosis of pulmonary hypertension. In: Journal of the American College of Cardiology. 33, 1999, pp. 1662-1666, doi : 10.1016 / S0735-1097 (99) 00055-8 .
  2. ↑ Valvular Heart Disease (management of). In: www.escardio.org. Retrieved November 22, 2016 .
  3. ↑ Infective Endocarditis (Guidelines on Prevention, Diagnosis and Treatment of). In: www.escardio.org. Retrieved November 22, 2016 .