Mitral papillary dysfunction with degree 1 regurgitation

Mitral valve – left atrio-ventricular valve

Valve prosthetics – replacing the native valve with a prosthesis that performs its function.

Mitral regurgitation – the return of blood to the ventricular systole in the left atrium as a result of a violation of the integrity of the mitral clkpan

Valve reconstruction – restoration of valve function without replacement

Mitral regurgitation (MR) – return of blood to systole
ventricles into the cavity of the left atrium as a result of a violation
mitral clkpan integrity

The word “regurgitation” comes from the Latin gurgitare – “flood” – and the prefix re-, denoting the opposite action, that is, it assumes the opposite direction to the normal direction. In this case, the reverse flow of blood.

Causes of congenital tricuspid regurgitation

The most common causes of this congenital pathology are:

  • underdevelopment of valve leaflets;
  • abnormal development (number) of valve leaflets;
  • connective tissue dysplasia;
  • Ehlers-Danlos syndrome;
  • Marfan syndrome;
  • Ebstein anomaly.

Tricuspid regurgitation in the fetus in isolation is very rare, usually it is combined with other heart defects. This valve insufficiency may be part of the mitral-aortic-tricuspid defect.

List of Abbreviations

AR 2D – two-dimensional echocardiography

CABG – coronary artery bypass grafting

AN – aortic insufficiency

AR – aortic regurgitation

VMTR – intrauterine growth inhibition

HHTV – activated partial thromboplastin time

GKM – hypertrophic cardiomyopathy

DAK – bicuspid aortic valve

DLA – pulmonary artery pressure

DMZhP – ventricular septal defect

ZhE – ventricular extrasystole

X – artificial heart valve

IE – Infectious Endocarditis

KAG – coronary angiography

CBAA – catheter balloon aortic valvuloplasty

KBMB – catheter balloon mitral valvuloplasty

KDR – the final diastolic size

KMBV – catheter mitral balloon valvulotomy

KPS – valvular heart diseases

CSR – final systolic volume

DAC – end-systolic size

LV – left ventricle

LP – left atrium

MK – mitral valve

MCP – mitral valve replacement

MN – mitral insufficiency

INR – international normalized attitude

MR – mitral regurgitation

LMWH – low molecular weight heparin

NMK – mitral valve insufficiency

UFH – unfractionated heparin

OK – open commissurotomy

PAK – aortic valve replacement

MVP – mitral valve prolapse

PMK – mitral valve replacement

PMO – the area of ​​the mitral foramen

POMK – the area of ​​the opening of the mitral valve

SVT – supraventricular tachycardia

SI – heart index

SR – operation to preserve (save) the chords

SULA – stenosis of the mouth of the pulmonary artery

TN – triskupidny insufficiency

TTEchoKG – transthoracic echocardiography

PV – ejection fraction

AF – atrial fibrillation

FU – shortening fraction

FMBV – percutaneous mitral balloon valvulotomy

PE Echocardiography – transesophageal echocardiography

MVG – mean mitral valve pressure gradient

MVR – mitral valve replacement

NYHA – New York Heart Association

1. Carabello BA. Mitral regurgitation: basic pathophysiologic principles, part 1. Mod Concepts Cardiovasc Dis 1988; 57: 53–8.

Causes of acquired tricuspid regurgitation

Regurgitation of the tricuspid valve acquired is much more common than congenital. It is primary and secondary. The primary causes of this pathology include rheumatism, drug addiction, carcinoid syndrome.

  1. Rheumatism is the most common cause of this pathology. In 20% of cases, it is recurrent rheumatic endocarditis that leads to deformation (thickening and shortening) of the valve cusps, and tendon filaments change in the same way. Very often, stenosis of the right atrioventricular opening joins this pathology. This combination is called a combined tricuspid defect.
  2. Rupture of the papillary muscles can also lead to tricuspid regurgitation. Such breaks occur with myocardial infarction or may be traumatic.
  3. Carcinoid syndrome can also lead to this pathology. It occurs in certain types of oncology, for example, cancer of the small intestine, ovaries or lungs.
  4. Taking heavy drugs very often leads to infectious endocarditis, and it, in turn, can cause tricuspid regurgitation.
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The causes of secondary tricuspid insufficiency most often are the following diseases:

  • dilatation of the fibrous ring that occurs with dilated cardiomyopathy;
  • high degree of pulmonary hypertension;
  • weakness of the myocardium of the right ventricle, which occurs in the so-called pulmonary heart;
  • chronic heart failure;
  • myocarditis;
  • myocardial dystrophy.

Mitral regurgitation in a child

  • Mitral valve prolapse can be different depending on the degree of deflection of the valves and on the degree of reverse blood flow through the valve (regurgitation).
  • Regurgitation itself during pregnancy is not considered a ban on pregnancy or childbirth, but only when the valve performs its main function – providing unilateral blood flow.
  • For children, the proper diet and the functioning of the heart and circulatory system play an important role, but disruptions are quite common. Most often, valve defects with insufficiency and return of blood in childhood are predetermined by genetic developmental abnormalities.
  • Severe regurgitation, if there is an irregular heart structure, appears almost immediately after birth with symptoms of respiratory failure, blue skin, insufficiency in the right ventricle.
  • Often, significant malfunctions can lead to death, so each mother must take care of herself before pregnancy and be monitored by an ultrasound specialist in time when carrying a child.

Congenital tricuspid regurgitation in infants in 25% of cases is manifested as supraventricular tachycardia or atrial fibrillation, and later severe heart failure may occur.

In older children, even with minimal exertion, shortness of breath and a strong heartbeat appear. A child may complain of heart pain. Dyspeptic disorders (nausea, vomiting, flatulence) and pain or a feeling of heaviness in the right hypochondrium may occur. If there is stagnation in the great circulation, peripheral edema, ascites, hydrothorax, or hepatomegaly appear. All these are very serious conditions.

Symptoms of the disease in adults

If this pathology is acquired at a later age, then at the initial stage a person may not even suspect about it. Minor tricuspid regurgitation is manifested only in some patients by pulsation of the cervical veins. The patient does not note other symptoms. Regurgitation of the tricuspid valve of the 1st degree may not manifest itself in any way.

With more severe valve insufficiency, significant swelling of the jugular veins is observed. In this case, if you put a palm to the right jugular vein, you can feel its trembling. In severe cases, this pathology leads to dysfunction of the right ventricle, atrial fibrillation, or may cause heart failure.

The combination of mitral and tricuspid insufficiency

Often, mitral and tricuspid regurgitation are diagnosed simultaneously in one patient. The cardiologist, after a detailed examination and obtaining test results, will decide on the treatment tactics of such a patient. If valve insufficiency is not very pronounced, it is possible that no treatment will be needed, but it will be necessary to periodically monitor your cardiologist and undergo the necessary examinations.

If the cause of valve insufficiency is established, then therapeutic treatment will be prescribed to eliminate the provocative disease. In the absence of positive dynamics, surgical treatment of regurgitation is indicated. This usually happens with severe and severe disease.

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Patients who have undergone surgical treatment for valve insufficiency are usually prescribed indirect anticoagulants.

1.2 Etiology and pathogenesis

Common causes of organic MR include MVP syndrome, rheumatism, ischemic heart disease,
infectious endocarditis, certain medications and diseases
connective tissue. Secondary or relative MR may arise from
for expansion of the fibrous ring due to dilatation of the left ventricle. IN
some cases (separation of the tendon chord, rupture of the papillary muscle
or infectious endocarditis) MR can be acute and severe. However
possible gradual development of MR over a long period
time. The clinical manifestations of MR are very diverse.

Acute severe mitral regurgitation

In acute severe MR, a sudden overload of the left
atria and left ventricle. Acute volume overload increases
LV preload, moderately increasing its total stroke volume [1]. However
lack of compensatory eccentric hypertrophy (which does not
manages to develop) effective stroke volume and cardiac output
are decreasing.

At the same time, untrained left atrium and left
ventricle cannot adapt to the volume of regurgitation that
causes a large backflow in the left atrium and leads to edema
lung. Effective emission (even percussion) is reduced. In severe MR
urgent need to reconstruct or prosthetics MK.

Chronic asymptomatic mitral regurgitation

Patients with mild to moderate MR may remain
asymptomatic for a long time against the background of small hemodynamic
compensatory changes. However, MR with valve damage progresses to
due to increasing volume overload. MR progression depends on
degree of progression of the defect (organic lesion of the valve) or
an increase in the size of the mitral ring [7].

As soon as mr becomes
severe, eccentric LV hypertrophy develops, in which
new sarcomeres appear, increasing the length of individual myocardial
fibers [1]. An increase in the final LV diastolic volume is
compensatory, makes it possible to increase the total stroke volume, which, in
in turn, allows you to restore effective cardiac output [8].

It should be noted that in the compensatory phase, the increased
preload and reduced or normal afterload (decreases
regurgitation load on the left atrium) facilitate the release of LV, which
results in a large total stroke volume and normal effective
shock volume.

The compensatory phase of MR can last for many years. However
prolonged volume overload can ultimately lead to
LV contractile dysfunction, which contributes to an increase in the final
systolic volume. This can lead to further dilatation of the LV and
increase the pressure of its filling. Hemodynamic changes that have occurred
lead to a decrease in effective ejection and pulmonary congestion.

Numerous studies show that progression
symptoms with the appearance of LV dysfunction in patients with chronic severe
MR develops over a period of 6–10 years [11,12]. However the number of cases
sudden death of asymptomatic patients with normal LV function widely
varies in these studies. In the group of patients with severe MR
due to pathologically mobile posterior leaflet MK for 10 years
90% of patients died or were operated on for MK. Mortality in

patients with severe MR caused by threshing valves is
6-7% annually. The highest risk of death is in patients with a fraction.
LV ejection of less than 0,60 or with symptoms of FC III – IV according to NYHA; less risk –
in asymptomatic patients and / or with normal LV function [13]. Heavy
the course of the disease is accompanied by worse reconstruction results or
prosthetics MK [13].

2.4. Instrumental diagnostics.

  • An ECG and chest x-ray are recommended.
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Level of persuasion C (level of evidence-2a).

Comment. To assess heart rate and clarify the condition of the pulmonary circulation and identify pulmonary stasis.

  • Transthoracic echocardiography for baseline recommended
    (primary) assessment of the size and function of the left ventricle, pancreas and the size of the drug, pressure in
    pulmonary artery and MR severity to any patient who is suspected

The level of credibility C (level of confidence of evidence-1).

3.1 Conservative treatment

acute severe MR the role of drug therapy is limited and directed
primarily for the stabilization of hemodynamics in preparation for surgery
(increase effective emission and reduce pulmonary congestion).

  • The use of nitroprusside is recommended in normotensive patients.
    sodium and peripheral vasodilatatols individually selected

Level of persuasion C (level of evidence-2a).

3.2 Surgical treatment

1) reconstruction of the MK;

2) prosthetics MK with the preservation of part or all of the mitral apparatus;

3) prosthetics MK with the removal of the mitral apparatus.

  • MK surgery is recommended for symptomatic patients with acute and
    chronic severe MR and NYHA’s symptoms II, III, or IV FC
    the absence of severe LV dysfunction (ejection fraction less than 0,30) and / or
    final systolic size over 55 mm [17, 19]

Level of credibility B (level of evidence-1).

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Tatyana Jakowenko

Editor-in-chief of the Detonic online magazine, cardiologist Yakovenko-Plahotnaya Tatyana. Author of more than 950 scientific articles, including in foreign medical journals. He has been working as a cardiologist in a clinical hospital for over 12 years. He owns modern methods of diagnosis and treatment of cardiovascular diseases and implements them in his professional activities. For example, it uses methods of resuscitation of the heart, decoding of ECG, functional tests, cyclic ergometry and knows echocardiography very well.

For 10 years, she has been an active participant in numerous medical symposia and workshops for doctors - families, therapists and cardiologists. He has many publications on a healthy lifestyle, diagnosis and treatment of heart and vascular diseases.

He regularly monitors new publications of European and American cardiology journals, writes scientific articles, prepares reports at scientific conferences and participates in European cardiology congresses.