Minor mitral regurgitation

Blood Pressure – Blood Pressure

CABG – coronary artery bypass grafting

AN – aortic insufficiency

AR – aortic regurgitation

DAK – bicuspid aortic valve

DLA – pulmonary artery pressure

X – artificial heart valve

IE – Infectious Endocarditis

CBAA – catheter balloon aortic valvuloplasty

KDR – the final diastolic size

KPS – valvular heart diseases

DAC – end-systolic size

LV – left ventricle

LP – left atrium

MK – mitral valve

PMK – mitral valve replacement

MN – mitral insufficiency

INR – international normalized attitude

MR – mitral regurgitation

NMK – mitral valve insufficiency

PAK – aortic valve replacement

RV – right ventricle

MVP – mitral valve prolapse

SI – heart index

TIAK – transcatheter aortic valve implantation

TTEchoKG – transthoracic echocardiography

PV – ejection fraction

FC – functional class

AF – atrial fibrillation

PE Echocardiography – transesophageal echocardiography

NYHA – New York Heart Association

AR 2D – two-dimensional echocardiography

VMTR – intrauterine growth inhibition

HHTV – activated partial thromboplastin time

GKM – hypertrophic cardiomyopathy

DMZhP – ventricular septal defect

ZhE – ventricular extrasystole

ZK – closed commissurotomy

KBMB – catheter balloon mitral valvuloplasty

KMBV – catheter mitral balloon valvulotomy

Mitro – mitral foramen

MCP – mitral valve replacement

LMWH – low molecular weight heparin

UFH – unfractionated heparin

OK – open commissurotomy

PMO – the area of ​​the mitral foramen

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

SVT – supraventricular tachycardia

SR – operation to preserve (save) the chords

SULA – stenosis of the mouth of the pulmonary artery

FMBV – percutaneous mitral balloon valvulotomy

MVG – mean mitral valve pressure gradient

MVR – mitral valve replacement

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

Terms and definitions

Valvular heart defects – violation
cardiac activity due to morphological and / or
functional changes in one or more of its valves.
Changes in valves can be in the form of stenosis, insufficiency or their

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

Appendix B. Patient Information

the choice of surgical tactics and treatment optimization the most important task
is the identification of risk factors and prediction of the outcome of the operation.
Operational risk can be assessed quickly enough – formulas for
death risk assessments are available on the Society of
Thoracic Surgeons (www.sts.

You have a heart operation. The more you will know about your
heart, the easier it is to cope with the difficulties of the postoperative period.

We suggest you get acquainted with the basic concepts of anatomy
heart and surgical operations, features of the postoperative
period, and also recommend a physical rehabilitation program in the first
12 months after surgery.

The heart of a healthy person is a powerful, continuously working organ,
provides blood flow throughout the body, and also quickly adapts to
his ever-changing needs. Heart beats in one minute
from 60 to 80 times, with physical activity, the rhythm accelerates, and then through
the heart flows more blood than at rest.

The heart consists of 4 chambers –
two atria and two ventricles, on the border between which are
valves that allow blood to flow in one direction. Muscular
a partition wall divides the heart into right and left halves. To the right
the atrium receives blood from the upper and lower parts of the body and through
the tricuspid valve enters the right ventricle, which pushes
her into the lungs through the valve of the pulmonary artery.

Blood enriched in the lungs
oxygen. Arterial blood returns to the left atrium and through
the mitral valve enters the left ventricle, which, contracting,
pumps blood into arteries, blood supply organs and tissues. Giving back
oxygen and taking carbon dioxide, the blood becomes venous and through the veins
returns to the right atrium.

Four heart valves – mitral, aortic, tricuspid,
pulmonary valve – pass blood in one direction and
interfere with its reverse current. Healthy valve has thin uniform

Pathological changes in the valves can be either congenital or
acquired as a result of rheumatism, infection, coronary disease
hearts with age. Stenosis may develop – narrowing of the opening, or
valve insufficiency when the flaps close tightly. Wherein
load on the heart increases. Over time, people begin to bother
palpitations, chest pain, lack of air, weakness, fast
fatigue, swelling on the legs, fainting.

There is a need for valve repair surgery (reconstruction or plastic surgery) or replacement of a damaged valve (prosthetics).

Various models have been developed and are currently in use.
biological and mechanical valves of the heart. Mechanical valve
consists of a cuff in the form of a ring braided with synthetic fabric and
a locking element in the form of a disk or two half-disks.
Biological prostheses are made from various tissues of the animal

They can be completely donated (human,
pork), as well as prostheses constructed from animal tissue.
The advantage of mechanical prostheses is their durability.
The disadvantages of mechanical prostheses are the need for life
taking anticoagulants, as well as the possibility of their infection.

The preparation for the upcoming operation is important. Necessary
follow the doctor’s recommendations regarding medication, and
prepare your lungs for surgery.

Stop smoking as soon as possible! Smoking narrows the coronary
arteries, increases blood coagulation, promotes the accumulation of mucus in
bronchi, increases blood pressure and causes a heartbeat. All
the above can cause complications in the postoperative period.

1. Get out of bed should roll over on its side.

2. You need to get up from the chair by moving to its edge and putting your feet on the floor. Stand up, leaning on your feet.

3. Sit should be straight, both legs on the floor. Knees at hip level. Do not cross legs.

4. When lifting objects from the floor, do not bend in the lower back! Bend your knees, your back should be straight.

Depending on the condition, you will undergo early rehabilitation measures: a physiotherapist
prescribe inhalation therapy for better coughing, and a specialist
in physiotherapy exercises will conduct a course of massage and physiotherapy.
Physical activity is selected strictly individually for each
the patient.

– prevention and treatment of early postoperative complications;

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– improving the functions of the respiratory system;

– adaptation of the heart to the conditions of the new hemodynamics;

– improvement of the patient’s psychoemotional state.

Discharging from the hospital, you will receive the recommendations of the attending physician
regarding medication, degree of activity, diet. Your
recovery depends on how accurately you perform them.

If you have a mechanical valve implanted, then your doctor will
prescribed medications such as anticoagulants (usually
Warfarin or Phenindione) to prevent the formation of
blood clots on the valves of the prosthesis or cavity of the heart. Inadequate
anticoagulant therapy (insufficient or excessive dose
anticoagulant) can lead to serious complications: prosthetic thrombosis,
stroke, bleeding. Anticoagulants are prescribed for life!

Biological valves do not require lifelong administration of anticoagulants
and are usually prescribed within the first 3-6 months after surgery.

Anticoagulants prolong the period during which your
blood coagulates. The action of anticoagulants should be thorough
controlled by a blood test called prothrombin
time (Quick time) and an indicator of international normalized
ratio (INR). The dose of anticoagulant is selected individually for
retention of prothrombin time or INR within certain

Typically, INRs need to be maintained at 2,5-3,5. A drug
usually taken once a day at the same time if it
warfarin or 2-3 times a day in case of using phenindione. Important
take it strictly in accordance with the doctor’s prescription.

The doctor will also tell you how often it is necessary to control MNO. Anticoagulant treatment limits the body’s natural ability
stop bleeding. For this reason you should be especially
careful with activities that may cause cuts
or hemorrhages.

Anticoagulants can have a damaging effect on the fetus, therefore
women planning a pregnancy should discuss with their doctor
changes in anticoagulant therapy.

Before any medical procedure, inform your doctor that you
take anticoagulants. On the eve of the procedure, control is required
blood coagulability. When performing “small” surgical interventions,
performed on an outpatient basis (treatment of a tooth, ingrown nail and
etc.) there is no need to cancel the anticoagulant if the INR indicator
is in the range of 2,0 -3.0.

For major interventions (e.g., inguinal surgery
hernia, cholelithiasis) may require withdrawal of the anticoagulant.
In this case, in the hospital 3-5 days before surgery, an anticoagulant
is canceled and the patient is transferred to heparin or low molecular weight
anticoagulants (nadroparin, dalteparin, etc.). From 2-3 days after surgery, anticoagulant administration begins again.

The effect of drugs and food on anticoagulant therapy

Foods can significantly affect the effect.
anticoagulant, therefore it is necessary to limit the consumption of foods,
containing a significant amount of vitamin K. Products such as
green tea, herbal infusions should be excluded from the diet. Cabbage
(white, colored, Brussels, broccoli), spinach, greens
(parsley, etc.

Inform your healthcare provider about the medicines you
accept as the anticoagulant interacts with many
medicines, which leads to an increase and weakening of its action.
Aspirin, for example, should not be taken without consulting a doctor.

If the following symptoms appear, you should immediately consult a doctor and determine the INR:

  1. The appearance of hematomas on the skin (“bruises”).
  2. An admixture of blood in the urine.
  3. Bleeding from the nose or gums.
  4. Long periods.
  5. Blood stained or black stool.

It is very important to reduce the amount of salt consumed, as
even after a successful operation, there may be a delay
body fluids.

In addition to following certain rules when choosing food, take care of your weight.

Artificial Valve Infectious Endocarditis

Infectious endocarditis is an infectious and inflammatory disease,
which affects the heart valves, or artificial heart valve (prosthetic endocarditis).
Prosthetic endocarditis is caused by bacteria (or, less commonly, fungi), which
enter the bloodstream and settle on the synthetic cuff of a mechanical
prosthesis, which can cause a violation of its function.

Infection can enter the bloodstream due to various
dental (tooth extraction, prosthetics and even brushing),
gynecological (curettage of the uterus), urological
(cystoscopy) procedures, as well as due to suppuration of the skin.

In order to minimize the risk of contracting an infectious
endocarditis, all patients with artificial heart valves need
adhere to the following rule: on the eve and shortly after completion
any intervention that could result in blood circulation
infection (dental, gynecological, urological procedures and
etc.), antibiotics should be taken prophylactically. Discuss with your
your healthcare provider what antibiotic you should take before

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.

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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].

The most common causes of AR are idiopathic aortic expansion,
congenital malformations of the aortic valve (most often bicuspid
valve), sclerotic degeneration, rheumatism, infectious
endocarditis, systemic hypertension, myxomatous degeneration, stratification
ascending aorta and Marfan syndrome, less often – traumatic injuries
aortic valve, ankylosing spondylitis, syphilitic aortitis,
rheumatoid arthritis, deforming osteoarthrosis, giant cell aortitis,
Ellers – Danlos syndrome, Reiter syndrome, intermittent subaortic
stenosis and ventricular septal defect with aortic prolapse

Most of these causes lead to chronic AR with gradual
and hidden LV dilatation and with a long asymptomatic period [1].
Other causes, including infectious endocarditis, aortic dissection, and
trauma often leads to acute severe AR, which can cause
sudden catastrophic increase in LV filling pressure and decrease
cardiac output.

volume and final
LV diastolic pressure and pressure in the left atrium may
increase quickly and cause a sharp deterioration in health
the patient. Ventricular failure to rapid compensatory dilatation
cavity leads to a decrease in stroke volume. Tachycardia which
develops as a compensatory mechanism for maintaining cardiac
emission is often not enough for such compensation.

With severe AR, there is a high risk of developing pulmonary edema or cardiogenic
shock. The most noticeable hemodynamic changes in patients with
LV hypertrophy against arterial hypertension with a small LV cavity
and reduced preload reserve. As an example,
illustrating the latter situation, aortic dissection in
patients with arterial hypertension, infectious endocarditis in
patients with preexisting aortic stenosis (AS) and acute
regurgitation after balloon valvotomy or surgery
commissurotomy in congenital AS.

Patients may also have symptoms.
myocardial ischemia. Since the final diastolic pressure of the left ventricle
approaching diastolic pressure in the aorta and coronary arteries,
myocardial perfusion of the subendocardium is reduced. LV dilatation and
thinning of the LV wall due to increased afterload combined with
tachycardia leads to an increase in myocardial oxygen demand.
Therefore, in acute severe AR, ischemia and complications often develop
which can lead to sudden death.

In response to volume overload in chronic AR in the left ventricle, a series of
compensatory mechanisms, including an increase in the final
diastolic volume and compliance of the LV chamber, which leads to
increase in volume without increasing LV filling pressure and combination
eccentric and concentric hypertrophy.

Increased stroke volume
achieved by the normal operation of each contractile unit along
increased circumference [2,3]. Thus, LV contractile function
remains normal, and expulsion phase indicators such as fractions
emission and shortening fraction remain within acceptable limits. However
an increase in the LV cavity and the associated increase in systolic
near-wall stress, in turn, lead to an increase
LV afterload, which causes further hypertrophy [2, 4].

Thus, the AR creates the conditions for a combination of volume overload and
pressure overload [5]. As the disease progresses, an increase
preload reserve and compensatory hypertrophy make it possible
ventricle maintain normal discharge despite increase
afterload [6,7]. Most patients remain asymptomatic on
during the compensation phase, which may continue for many
decades 7.

Decreased myocardial contractility may also exacerbate the situation. Often
at this stage of the development of the disease, patients experience shortness of breath;
decreased coronary reserve in a hypertrophic myocardium may
lead to angina pectoris. However, patients may remain
asymptomatic until severe LV dysfunction develops.

LV systolic dysfunction (most often defined as a decrease
ejection fraction below normal at rest) is associated mainly with growth
afterload and may be reversible in the initial stages after
aortic valve replacement (PAA) [10–20]. Gradually as
dilatation, LV takes on a spherical shape.

Most studies have shown that LV systolic function and
final systolic size are the most important determinants
LV survival and postoperative function in patients subject to PAA
in chronic AR.

1.3 Ep >According to many experts, in the world there are no full-fledged
information about the prevalence of valvular heart defects, in connection with which
a global epidemiological study is needed.

The prevalence of mitral regurgitation in combination with MK prolapse, according to J. Chikwe, is 2–6% in the population

According to many experts, in the world there are no full-fledged
information about the prevalence of valvular heart defects, in connection with which
a global epidemiological study is needed.
Separate studies give an idea of ​​the prevalence of
other vices. In the Cardiovascular Health Study population study,
including 5621 people over 65 years old, damage to the aortic valve
(leaflet thickening, calcifications) detected in 29%, at the same time using
Doppler echocardiography aortic insufficiency or stenosis (gradient
pressure gt; 25 mmHg Art.

) – in 2% (Stewart BF, 1997). In 2009 in
Russia was recorded 178 623 cases of valvular pathology in
patients with chronic rheumatic heart disease. Despite the fact that
rheumatism is still one of the leading factors in the formation
valvular defects in the Russian Federation, the proportion of patients with
called degenerative lesions of the heart valves, (myxomatosis,
dysplastic processes, calcification) in 2014 reached 46.6% of the total
the number of operations for acquired heart defects.

2.1 Complaints and medical history

An anamnesis is crucial for evaluating a patient with chronic MR.

  • A thorough initial assessment of physical tolerance is recommended.
    the burden of identifying minor changes in symptoms with
    subsequent inspections.

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

  • At the stage of diagnosis, it is recommended to collect anamnesis and complaints in all patients with suspected AR [8, 31-39].

Level of credibility of recommendations I (level of reliability of evidence C)

1.5 Classification

Anatomical and functional classification of mitral regurgitation according to Carpentier

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Type I. Normal leaflet mobility

  • Ventricular ring dilatation
  • Leaf splitting
  • Sash defect

Type II Sash prolapse

  • Lack of chords
  • Elongation chords
  • Papillary muscle lengthening

IIIA. Normal papillary muscles

  • Union of commissions
  • Shortening chords
  • Valve change by type of Ebstein anomaly

IIIB. Anomaly of the papillary muscles

  • Parachute valve
  • Hammock valve
  • Agenesis, hypoplasia of the papillary muscles

There are also primary mitral
insufficiency – changes are associated with organic congenital or
acquired diseases of the mitral valve itself, and secondary (functional,
relative) —changes in the spatial-geometric relationship
mitral valve and left ventricle, as well as acute and chronic mitral regurgitation.

I degree – slight mitral regurgitation

II degree – moderate mitral regurgitation

III degree – pronounced mitral regurgitation

IV degree – severe mitral regurgitation

3.3 Postoperative therapy

  • Treatment of arterial hypertension (systolic blood pressure)gt; 140 mmHg) is recommended for patients with severe AR [73–75, 80, 82]. –
  • For patients who have a mechanical valve implanted, it is recommended
    taking warfarin ** for life under the control of international
    normalized ratio (INR) for the prevention of thromboembolic
    complications [22, 59].

Level of evidence of recommendations I (level of evidence evidence A)

  • It is recommended that INR is maintained at 2,5 in patients who
    implanted mechanical valve without risk factors
    thromboembolic complications and 3,0 in the presence of one or more factors
    [22, 59].

3.2 Surgical treatment

  • PAA is recommended for symptomatic patients with severe AR regardless of LV systolic function [15, 17-20, 32, 37-38]
  • PAA is recommended for asymptomatic patients with chronic severe AR and
    LV systolic dysfunction (ejection fraction not more than 50%) at rest
    [15, 17-20, 32, 37-38].
  • PAA is recommended for patients with chronic severe AR undergoing
    CABG or operations on the aorta, or on other heart valves [15, 17-20,
    32, 37-38].
  • PAA is recommended for asymptomatic patients with severe AR with
    normal systolic function (ejection fraction of more than 50%), but
    significant dilatation of the left ventricle (final diastolic size over 75 mm
    or final systolic size greater than 55 mm) [32, 37-38].

Confidence Level IIa (Evidence Level B)

  • Surgery on the ascending aorta is recommended, regardless of the degree of aortic insufficiency, to the following groups of patients:
  1. patients with Marfan syndrome with aortic root expansion and
    maximum diameter of the ascending aorta gt; 45 mm subject to factors
    risk 64.
    Confidence Level IIa (Evidence Level C)
  2. patients with Marfan syndrome with expansion of the aortic root and a maximum diameter of the ascending aortagt; 50 mm [63].
    Level of credibility of recommendations I (level of reliability of evidence C)
  3. patients with bicuspid aortic valve with root expansion
    aorta and the maximum diameter of the ascending aorta gt; 50 mm if available
    risk factors 68.
    Confidence Level IIa (Evidence Level C)
  4. patients with aortic root expansion and a maximum diameter of the ascending aorta gt; 55 mm 66.
    Conf >

    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).

    2.4. Instrumental diagnostics.

    • An ECG and chest x-ray are recommended.

    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).

    5.1 Dynamic surveillance

    • Recommended
      during dynamic observation of a patient with MR assess changes
      clinical status, function and size of the left ventricle, tolerance to physical

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

    5.1.1 Assessment of the condition of patients after aortic valve replacement:

    • After PAK, life-long patient monitoring is recommended.
      cardiologist. It is recommended that the following deadlines be observed.
      patient examinations:
    1. The first examination no later than 2-4 weeks after surgery [84];
    2. The second and third examinations after 6 and 12 months, respectively, from the moment of the first examination;
    3. Subsequent – 1 time per year in uncomplicated clinical course.
    • Antibacterial therapy is recommended to prevent exacerbation.
      rheumatic fever in patients with rheumatic AS [22, 59].

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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.