The contractility of the myocardium lzh satisfactory. Myocardial contractility

Identification of local disorders of LV contractility using two-dimensional echocardiography is important for the diagnosis of coronary artery disease. The study is usually carried out from the apical long-axis approach in the projection of two and four-chamber hearts, as well as from the left parasternal access to the true and short axes.

In accordance with the recommendations of the American Association of Echocardiography, the LV is conventionally divided into 16 segments located in the plane of three cross sections of the heart recorded from the left parasternal short-axis approach.

The image of 6 basal segments - anterior (A), anterior septal (AS), postero-septal (IS), posterior (I), posterolateral (IL) and anterolateral (AL) - is obtained by location at the level of the mitral valve leaflets (SAX MV), and the middle parts of the same 6 segments - at the level of the tapillary muscles (SAX PL). Images of the 4-apical segments - anterior (A), septal (S), posterior (I), and lateral (L) - are obtained by locating from a parasternal approach at the level of the apex of the heart (SAX AP).

The general idea of ​​the local contractility of these segments is well complemented by three longitudinal "sections" of the left ventricle, recorded from the parasternal approach along the long axis of the heart, as well as in the apical position of the four-chamber and two-chamber heart.

In each of these segments, the nature and amplitude of myocardial movement, as well as the degree of its systolic thickening, are assessed. There are 3 types of local disorders of the contractile function of the left ventricle, united by the concept of "asynergy":

1. Akinesia - the absence of contraction of a limited area of ​​​​the heart muscle.

2. Hypokinesia - a pronounced local decrease in the degree of contraction.

3. Dyskinesia - paradoxical expansion (bulging) of a limited area of ​​the heart muscle during systole.

The main causes of local disorders of LV myocardial contractility are:

1. Acute myocardial infarction (MI).

2. Postinfarction cardiosclerosis.

3. Transient painful and painless myocardial ischemia, including ischemia induced by functional exercise tests.

4. Permanent ischemia of the myocardium, which has still retained its viability (the so-called "hibernating myocardium").

5. Dilated and hypertrophic cardiomyopathy, which are often also accompanied by uneven damage to the LV myocardium.

6. Local disorders of intraventricular conduction (blockade, WPW syndrome, etc.).

7. Paradoxical movements of the IVS, for example, with volume overload of the pancreas or blockade of the legs of the bundle of His.

Two-dimensional echocardiogram recorded from the apical approach in the position of a four-chamber heart in a patient with transmural myocardial infarction and apical segment dyskinesia ("dynamic LV aneurysm"). Dyskinesia is determined only at the time of LV systole

Violations of local contractility of individual LV segments in patients with coronary artery disease are usually described on a five-point scale:

1 point - normal contractility;

2 points - moderate hypokinesia (a slight decrease in the amplitude of systolic movement and thickening in the study area);

3 points - severe hypokinesia;

4 points - akinesia (lack of movement and thickening of the myocardium);

5 points - dyskinesia (systolic movement of the myocardium of the studied segment occurs in the direction opposite to normal).

An important prognostic value is the calculation of the so-called local contractility index (LIS), which is the sum of the contractility score of each segment (2S) divided by the total number of LV segments studied (n):

High values ​​of this indicator in patients with MI or postinfarction cardiosclerosis are often associated with an increased risk of death.

ACQUIRED HEART DEFECTS

STENOSIS OF THE LEFT ATRIOVENTRICULAR HOLE (MITRAL STENOSIS)

Stenosis of the left atrioventricular orifice is characterized by partial fusion of the anterior and posterior leaflets of the mitral valve, a decrease in the area of ​​the mitral orifice, and obstruction of diastolic blood flow from the LA to the LV.

There are two characteristic echocardiographic signs of mitral stenosis detected by M-modal examination:

1) a significant decrease in the speed of diastolic cover of the anterior leaflet of the mitral valve;

2) unidirectional movement of the front and rear flaps of the valve. These signs are better detected by M-modal examination from the parasternal approach along the long axis of the heart.

Determination of the speed of diastolic closure of the anterior leaflet of the mitral valve in a healthy person (a) and in a patient with stenosis of the left atrioventricular orifice (6).

As a result of high pressure in the LA, the valve leaflets are constantly in the open position during diastole and, unlike the norm, do not close after early rapid filling of the LV. The blood flow from the left atrium acquires a constant (not interrupted) linear character. Therefore, on the echocardiogram, there is a flattening of the anterior leaflet movement curve and a decrease in the amplitude of the A wave corresponding to left atrial systole. The shape of the diastolic movement of the anterior leaflet of the mitral valve becomes U-shaped instead of M-shaped.

In a two-dimensional echocardiographic study from a parasternal approach along the long axis of the heart, the most characteristic sign of mitral stenosis, detected already at the initial stages of the disease, is a dome-shaped diastolic bulging of the anterior leaflet of the mitral valve into the LV cavity towards the IVS, which is called "sailing".

In the later stages of the disease, when the leaflets of the mitral valve thicken and become rigid, their "sailing" stops, but the leaflets of the valve during diastole are located at an angle to each other (normally they are parallel), forming a kind of conical shape of the mitral valve.

Scheme of diastolic opening of the mitral valve leaflets: a - normal (leaflets parallel to each other), b - funnel-shaped arrangement of the MV leaflets in the initial stages of mitral stenosis, accompanied by a dome-shaped diastolic bulging of the anterior leaflet into the LV cavity ("sailing"), c - conical shape of the MV on late stages of mitral stenosis (cusps are located at an angle to each other, rigid).


Parosing of the anterior leaflet of the mitral valve in mitral stenosis (two-dimensional echocardiogram of the true axis access). There is also an increase in the size of the left atrium.


Decrease in the dilstolic divergence of the valve leaflets and the area of ​​the mitral orifice in a two-dimensional study from the parasternal approach along the short axis: a - normal, b - mitral stenosis.

Doppler echocardiographic study of transmitral diastolic blood flow reveals several signs characteristic of mitral stenosis and associated mainly with a significant increase in the diastolic pressure gradient between the LA and LV and a slowdown in the decline of this gradient during LV filling. These signs include:

1) an increase in the maximum linear velocity of early transmitral blood flow up to 1.6-2.5 m.s1 (normally about 0.6 m.s1),

2) slowing down the decline in the rate of diastolic filling (flattening of the spectrogram),

3) significant turbulence in the movement of blood.

Dopplerograms of the transmitral blood flow in the norm (a) and in the mitral case (b).

To measure the area of ​​the left atrioventricular orifice, two methods are currently used. With a two-dimensional EchoCG from a parasternal approach along a short axis at the level of the tips of the valve leaflets, the area of ​​the hole is determined planimetrically, tracing the contours of the hole with the cursor at the moment of maximum diastolic opening of the valve leaflets.

More accurate data are obtained by Doppler study of the transmitral blood flow and determination of the diastolic gradient of the transmitral pressure. Normally, it is 3-4 mm Hg. As the degree of stenosis increases, so does the pressure gradient. To calculate the area of ​​the hole, measure the time during which the maximum gradient is halved. This is the so-called half-time of the pressure gradient (Th2) - The pressure gradient according to Doppler echocardiography is calculated using a simplified Bernoulli equation:

where DR is the pressure gradient on both sides of the obstruction (mm Hg) and V is the maximum

blood flow velocity of the distal obstruction (m s!).

This means that with a twofold decrease in AR, the maximum linear blood flow velocity decreases by 1.4 times (V2 = 1.4). Therefore, to measure the half-decay time of the pressure gradient (T1/2), it is sufficient to determine the time during which the maximum linear velocity of blood flow decreases by 1.4 times. It has been shown that if the area of ​​the left atrioventricular orifice is 1 cm2, the T1/2 time is 220 ms. From here, the hole area S can be determined by the formula:

When T1/2 is less than 220ms, the hole area is greater than 1cm2, conversely, if T1/2 is greater than 220ms, the hole area is less than 1cm2.

MITRAL VALVE INSUFFICIENCY

Insufficiency is the most common pathology of the mitral valve, the clinical manifestations of which (including auscultatory) are often mild or absent altogether.

There are 2 main forms of mitral regurgitation:

1. Organic insufficiency of the mitral valve with wrinkling and shortening of the valve leaflets, deposition of calcium in them and damage to the subvalvular structures (rheumatism, infective endocarditis, atherosclerosis, systemic diseases of the connective tissue).

2. Relative mitral insufficiency due to dysfunction of the valvular apparatus, in the absence of gross morphological changes in the valve leaflets.

The causes of relative mitral insufficiency are:

1) mitral valve prolapse;

2) IHD, including acute MI (papillary muscle infarction and other mechanisms of valvular dysfunction);

3) diseases of the left ventricle, accompanied by its pronounced dilatation and expansion of the fibrous ring of the valve and / or dysfunction of the valvular apparatus (arterial hypertension, aortic heart disease, cardiomyopathy, etc.);

4) rupture of tendon threads;

5) calcification of the papillary muscles and fibrous ring of the mitral valve.

Organic (a) and two variants of relative mitral valve insufficiency (b, c).

There are no direct echocardiographic signs of mitral insufficiency when using one and two-dimensional echocardiography. The only reliable sign of an organ - J ical mitral insufficiency - non-closure (separation) of the mitral valve cusps during ventricular systole - is extremely rare. Among the indirect echocardiographic signs of mitral insufficiency, reflecting the hemodynamic changes characteristic of this defect, include:

1) an increase in the size of the LP;

2) hyperkinesia of the posterior wall of the LA;

3) increase in total stroke volume (according to the Simpson method);

4) myocardial hypertrophy and dilatation of the LV cavity.

The most reliable method for detecting mitral regurgitation is a Doppler study. The study is carried out from the apical access of a four-chamber or two-chamber heart in a pulsed-wave mode, which allows you to sequentially move the control (strobe) volume at different distances from the mitral valve cusps, starting from the place of their closure and further towards the upper and side wall of the LA. Thus, a jet of regurgitation is searched for, which is well detected on Doppler echocardiograms in the form of a characteristic spectrum directed downward from the base zero line. The density of the spectrum of mitral regurgitation and the depth of its penetration into the left atrium are directly proportional to the degree of mitral regurgitation.

At the 1st degree of mitral regurgitation, the latter is detected immediately behind the MV cusps, at the 2nd degree - extends 20 mm from the cusps deep into the LA, at the 3rd degree - approximately to the middle of the LA and at the 4th degree - reaches the opposite wall of the atrium .

It should be remembered that minor regurgitation, which is recorded immediately behind the mitral valve leaflets, can be detected in approximately 40-50% of healthy people.

Mapping of the Doppler signal in a patient with mitral insufficiency: a - mapping scheme (black dots indicate the sequential movement of the control volume), b - Dopplerogram of the transmitral blood flow, recorded at the level of the outlet section of the LA. Blood regurgitation from the LV to the LA is marked with arrows.

The color Doppler scanning method is the most informative and clear in identifying mitral regurgitation.

The blood stream, which returns to the LA during systole, is colored light blue in color scanning from the apical access. The magnitude and volume of this flow of regurgitation depends on the degree of mitral insufficiency.

At a minimal degree, the regurgitant flow has a small diameter at the level of the leaflets of the left atrioventricular valve and does not reach the opposite LA wall. Its volume does not exceed 20% of the total volume of the atrium.

With moderate mitral regurgitation, the reverse systolic blood flow at the level of the valve leaflets becomes wider, and reaches the opposite wall of the LA, occupying about 50-60% of the volume of the atrium.

A severe degree of mitral insufficiency is characterized by a significant diameter of the regurgitant blood flow already at the level of the mitral valve cusps. The reverse flow of blood occupies almost the entire volume of the atrium and sometimes even enters the mouth of the pulmonary veins.


a - minimal degree (regurgitant blood flow has a small diameter at the level of the MV cusps and does not reach the opposite wall of the LI), 6 - moderate degree (regurgitant blood flow reaches the opposite wall of the LA), c - severe mitral valve insufficiency (regurgitant blood flow reaches the opposite wall LP and occupies almost the entire volume of the atrium).

AORTIC STENOSE

Diagnostic criteria for aortic stenosis in M-modal examination is a decrease in the degree of divergence of the aortic valve leaflets during LV systole, as well as thickening and heterogeneity of the structure of the valve leaflets.

Normally, the movement of the aortic valve leaflets is recorded in the form of a kind of "box" during systole and in the form of a straight line during diastole, and the systolic opening of the aortic valve leaflets usually exceeds 12-18 mm. With a severe degree of stenosis, the opening of the valves becomes less than 8 mm. The divergence of the valves within 8-12 mm may correspond to varying degrees of aortic stenosis.

a - systolic opening of the aortic valve (AV) leaflets in a healthy person,

b - systolic opening of the valves of the aortic valve in a patient with aortic stenosis.

At the same time, it should be borne in mind that this indicator, determined in the M-modal study, is not among the reliable and reliable criteria for the severity of stenosis, since it largely depends on the magnitude of the VR.

A two-dimensional B-mode study from the parasternal access of the true axis of the heart allows you to identify more reliable signs of aortic stenosis:

1. Systolic deflection of the valve leaflets towards the aorta (an echocardiographic symptom similar to the "parousing" of the mitral valve leaflets in stenosis of the left atrioventricular orifice) or the location of the leaflets at an angle to each other. These two signs indicate incomplete opening of the aortic valve during LV systole.

2. Pronounced hypertrophy of the LV myocardium in the absence of significant dilation of its cavity, as a result of which the EDV and ESV of the LV do not differ much from the norm for a long time, but there is a significant increase in the thickness of the IVS and the posterior wall of the LV. Only in advanced cases of aortic stenosis, when myogenic dilatation of the LV develops or mitralization of the defect occurs, an increase in the size of the LV is determined on the echocardiogram.

3. Post-stenotic expansion of the aorta, due to a significant increase in the linear velocity of blood flow through the narrowed aortic opening.

4. Severe calcification of the aortic valve leaflets and the aortic root, which is accompanied by an increase in the intensity of echo signals from the valve leaflets, as well as the appearance in the aortic lumen of many intense echo signals parallel to the walls of the vessel.

Two-dimensional echocardiogram recorded from the parasternal access of the true axis of the heart in a patient with aortic stenosis (6). Noticeable thickening of the AV leaflets, their incomplete opening in systole, significant post-stenotic expansion of the aorta, and marked hypertrophy of the posterior wall of the LV and IVS.

Diagram of a Doppler study of the transaortic blood flow (a) and a Dopplerogram (b) of a patient with aortic stenosis (apical position of the true LV axis)

.

Calculation of the aortic valve area using Doppler and two-dimensional jocardiographic study (scheme): a - planimetric determination of the area of ​​the transverse vein of the LV outflow tract, b - Doppler determination of the linear velocity of the systolic blood flow in the LV outflow tract and in the aorta (above the site of narrowing).

AORTIC INSUFFICIENCY

The main sign of aortic regurgitation in one-dimensional echocardiography (M-mode) is diastolic trembling of the anterior leaflet of the mitral valve, which occurs under the action of a reverse turbulent blood flow from the aorta to the left ventricle.

Changes in the one-dimensional echocardiogram in aortic insufficiency: a - a diagram explaining the possible mechanism of diastolic trembling of the anterior leaflet of the MV, b - one-dimensional echocardiogram in aortic insufficiency (diastolic trembling of the anterior leaflet of the mitral valve and IVS is noticeable)

Another sign - non-closure of the aortic valve leaflets in diastole - is not detected so often. An indirect sign of severe aortic insufficiency is also early closure of the mitral valve leaflets as a result of a significant increase in LV pressure.

Two-dimensional echocardiography in aortic insufficiency is somewhat inferior in informativeness to M-modal study due to lower temporal resolution and the impossibility in many cases to register diastolic trembling of the anterior leaflet of the mitral valve. Echocardiography usually reveals a significant expansion of the left ventricle.

Doppler echocardiography, especially color Doppler scanning, is the most informative in diagnosing aortic insufficiency and determining its severity.

Aortic diastolic regurgitation when using the apical or left parasternal position of the Doppler color scan appears as a motley stream originating from the aortic valve and penetrating the LV. This pathological regurgitant diastolic blood flow must be distinguished from normal physiological blood flow in diastole from the LA to the LV through the left atrioventricular orifice. In contrast to the transmitral diastolic blood flow, the regurgitant blood stream from the aorta comes from the aortic valve and appears at the very beginning of diastole, immediately after the closure of the aortic valve cusps (II sound). Normal diastolic blood flow through the mitral valve occurs a little later, only after the end of the LV isovolumic relaxation phase.

Doppler echocardiographic signs of aortic insufficiency.

Quantification of the degree of aortic insufficiency is based on the measurement of the half-life (T1 / 2) of the diastolic pressure gradient between the aorta and the left ventricle. The rate of regurgitation of blood flow is determined by the pressure gradient between the aorta and the left ventricle. The faster this speed decreases, the faster the pressure between the aorta and the ventricle equalizes, and the more pronounced aortic insufficiency (there are inverse relationships with mitral stenosis). If the half-life of the pressure gradient (T1/2) is less than 200 ms, severe aortic regurgitation is present. With T1 / 2 values ​​greater than 400 ms, we are talking about a small degree of aortic insufficiency.

Determination of the degree of aortic insufficiency according to the Doppler study of regurgitant diastole and blood flow through the aortic valve. Т1/2

is the half-life of the diastolic pressure gradient in the aorta and left ventricle.

THREE-LEAVEL VALVE INSUFFICIENCY

Tricuspid valve insufficiency often develops secondarily, against the background of pancreatic decompensation due to pulmonary hypertension (cor pulmonale, mitcal stenosis, primary pulmonary hypertension, etc.). Therefore, organic changes in the leaflets of the valve itself, as a rule, are absent. With M-modal and two-dimensional echocardiography, indirect signs of a defect can be detected - dilatation and hypertrophy of the pancreas and right ventricle, corresponding to the volume overload of these parts of the heart. In addition, a two-dimensional study reveals paradoxical movements of the IVS and systolic pulsation of the inferior vena cava. Direct and reliable signs of tricuspid regurgitation can only be detected with a Doppler study. Depending on the degree of insufficiency, a jet of tricuspid regurgitation is detected in the right atrium at various depths. Sometimes it reaches the inferior vena cava and the hepatic veins. At the same time, it should be remembered that in 60-80% of healthy individuals, a slight regurgitation of blood from the pancreas to the RA is also detected, however, the maximum rate of reverse blood flow does not exceed 1 m-s1.


Dopplerogram of tricuspid insufficiency: a - scheme of Doppler scanning from the apical position of the four-chamber heart, b - Dopplerogram of tricuspid regurgitation (marked with arrows).

DIAGNOSIS OF PERICARDIAL LESIONS

Echocardiographic examination allows diagnosing various types of pericardial lesions:

1) dry pericarditis,

2) the presence of fluid in the pericardial cavity (exudative pericarditis, hydropericardium,

3) constrictive pericarditis.

Dry pericarditis is accompanied, as is known, by thickening of the pericardial layers and an increase in the echogenicity of the posterior pericardial layer, which is well detected in the M-modal study. The sensitivity of one-dimensional echocardiography in this case is higher than that of two-dimensional scanning.

Effusion in the pericardial cavity. If there is a pathological effusion in the pericardial cavity that exceeds the normal volume of serous fluid (about 30-50 ml), an echocardiogram reveals separation of the pericardial sheets with the formation of an echo-negative space behind the posterior wall of the LV, and diastolic separation of the pericardial sheets has diagnostic value. The movement of the parietal sheet of the pericardium decreases or disappears altogether, while the excursion of the epicardial surface of the heart increases (hyperkinesia of the epicardium), which serves as an indirect sign of the presence of fluid in the pericardial cavity.

Quantitative determination of the volume of effusion in the pericardial cavity using echocardiography is difficult, although it is believed that 1 cm of the echo-negative space between the sheets of the pericardium corresponds to 150-400 ml, and 3-4 cm corresponds to 500-1500 ml of fluid.

One-dimensional (a) and two-dimensional (6) echo cardiogram with effusion pleurisy. Thickening and moderate separation of the pericardial layers are noted.

Two-dimensional echocardiogram in a patient with a significant amount of effusion in the pericardial cavity (PE). The fluid is determined behind the posterior wall of the left ventricle, in the region of the apex of the heart and in front of the right ventricle.

Constrictive pericarditis is characterized by the fusion of the pericardial layers into a single conglomerate, followed by calcification and the formation of a dense, immovable capsule that surrounds the heart ("armored" heart) and impedes the process of diastolic relaxation and filling of the ventricles. Severe disorders of diastolic function underlie the formation and progression of heart failure.

With a one-dimensional or two-dimensional echocardiographic study, thickening and significant compaction of the sheets of the pericardium can be detected. The echo-negative space between the sheets is filled with an inhomogeneous layered mass, less echo-dense than the pericardium itself. There are also signs of impaired blood supply to the heart in diastole and myocardial contractility.

1. Early diastolic paradoxical movement of the IVS into the LV cavity with subsequent development of hypokinesia and akinesia of the IVS.

2. Flattening of the diastolic movement of the posterior LV wall (M-mode).

3. Reducing the size of the cavities of the ventricles.

4. Reducing the collapse of the inferior vena cava after a deep breath (normally, the collapse of the inferior vena cava is about 50% of its diameter).

5. Decrease in SV, ejection fraction and other indicators of systolic function.

Doppler study of the transmitral blood flow reveals a significant dependence of the LV diastolic filling rate on the phases of respiration: it increases during expiration and decreases during inspiration.

Changes during respiration in the amplitude of the Doppler signal of the transmitral diastolic blood flow in a patient with constrictive pericarditis: a - scheme of ultrasonic Doppler scanning, b - Dopplerogram of the diastolic blood flow (a significant decrease in the blood flow velocity is determined during inspiration)

CARDIOMYOPATHY

Cardiomyopathies (CM) are a group of myocardial diseases of unknown etiology, the most characteristic features of which are cardiomegaly and progressive heart failure.

There are 3 forms of CMP:

1) hypertrophic cardiomyopathy,

2) dilated CMP,

3) restrictive ILC.

Hypertrophic cardiomyopathy (HCM) is characterized by

1) severe LV myocardial hypertrophy,

2) a decrease in the volume of its cavity

3) violation of the diastolic function of the left ventricle.

The most common form is asymmetric HCM with predominant hypertrophy of the upper, middle or lower third of the IVS, the thickness of which can be 1.5-3.0 times the thickness of the posterior LV wall.

Of interest is the ultrasound diagnostics of the so-called obstructive form of HCM with asymmetric lesion of the IVS and LV outflow obstruction (“subaortic subvalvular stenosis”). Echocardiographic features of this form of HCM are:

1. Asymmetric thickening of the IVS and limitation of its mobility.

2. Anterior systolic movement of the mitral valve leaflets.

3. Covering the aortic valve in the middle of systole.

4. The appearance of a dynamic pressure gradient in the LV outflow tract.

5. High linear velocity of blood flow in the LV outflow tract.

6. Gierkinesia of the posterior wall of the left ventricle.

7. Mitral regurgitation and dilatation of the left atrium.


Echocardiographic features of hypertrophic cardiomyopathy

: a - scheme of asymmetric IVS hypertrophy, b - two-dimensional echocardiogram from the parasternal access of the true axis of the heart. A pronounced thickening of the IVS is determined.

Anterior systolic movement of the mitral valve leaflet in a patient with hypertrophic cardiomyopathy: a - diagram explaining the possible mechanism of anterior systolic movement, b - one-dimensional echocardiogram, which clearly shows the systolic movement of the anterior MV leaflet (marked with red arrows) and a significant thickening of the IVS and posterior LV wall.

Dopplerogram shape of systolic blood flow in the outflow tract of the left ventricle in a patient with hypertrophic cardiomyopathy, reflecting the appearance of a dynamic pressure gradient in the outflow tract and aorta, caused by aortic valve occlusion in the middle of systole. An increase in the maximum linear velocity of blood flow (Vmax) is also noticeable.

Dilated cardiomyopathy (DCM) characterized by diffuse damage to the heart muscle and is accompanied by

1) a significant increase in the cavities of the heart,

2) mild myocardial hypertrophy,

3) a sharp decrease in systolic and diastolic function,

4) a tendency to rapid progression of signs of heart failure, the development of parietal thrombi and thromboembolic complications.

The most characteristic echocardiographic signs of DCM are significant dilatation of the left ventricle with normal or reduced thickness of its walls and a decrease in EF (below 30-20%). Often there is an expansion of other chambers of the heart (RV, LA). As a rule, total hypokinesia of the LV walls develops, as well as a significant decrease in blood flow velocity in the ascending aorta and LV outflow tract and in the LA (Doppler mode). Intracardiac parietal thrombi are often visualized.


Two-dimensional (a) and one-dimensional echocardiography (b) in a patient with dilated cardiomyopathy. Significant dilatation of the left ventricle is determined, as well as the right ventricle and atria with normal thickness of their walls.

Restrictive cardiomyopathy. The concept of restrictive cardiomyonatia (RCMP) combines two diseases: endocardial fibrosis and Loeffler's eosinophilic fibroplastic endocarditis. Both diseases are characterized by:

1) significant thickening of the endocardium,

2) myocardial hypertrophy of both ventricles,

3) obliteration of the cavities of the left ventricle and pancreas,

4) severe diastolic ventricular dysfunction with relatively preserved systolic function.

With one-dimensional, two-dimensional and Doppler echocardiography in RCMP, you can find:

1. Thickening of the endocardium with a decrease in the size of the cavities of the ventricles.

2. Various variants of the paradoxical movement of the IVS.

3. Prolapse of the mitral and tricuspid valves.

4. Pronounced diastolic dysfunction of the ventricular myocardium of the restrictive type with an increase in the maximum rate of early diastolic filling (Peak E) and a decrease in the duration of isovolumic relaxation of the myocardium (IVRT) and the deceleration time of early diastolic filling (DT).

5. Relative insufficiency of the mitral and tricuspid valves.

6. The presence of intracardiac parietal thrombi.


Changes detected on a two-dimensional echocardiogram (a) and dopplerogram of the transmitral blood flow (b) in a patient with restrictive cardiomyopathy. There is a noticeable thickening of the IVS and the posterior wall of the left ventricle, a decrease in the cavities of the ventricles, and an increase in the size of the left atrium. Dopplerogram shows signs of restrictive LV diastolic dysfunction (a significant increase in the E/A ratio, a decrease in the duration of IVRT and DT).


Two-dimensional echocardiograms (a, b) recorded from the apical position of the four-chamber heart in a patient with a parietal thrombus in the cavity of the left ventricle (in the region of the apex).

Main literature

1. N. Schiller, M.A. Osipov Clinical echocardiography. 2nd edition, Practice 2005. 344p.

2. Mitkov V. V., Sandrikov V. A. Clinical guide to ultrasound diagnostics in 5 volumes. M.: Vidar. 1998; 5: 360 s.

3. Feigenbaum X. Ultrasonic diagnostics. M.: Medicine. 1999;416s.

additional literature

1.M.K.Rybakova, M.E. Alekhin, V.V. Mitkov. A practical guide to ultrasound diagnostics. Echocardiography. Vidar, Moscow 2008. 512 p.

2. A. Kalinin, M.N. Alekhine. Assessment of the state of the atrial myocardium in the mode of two-dimensional greyscale deformation in patients with arterial hypertension with slight left ventricular hypertrophy. Journal "Cardiology" №8, 2010.

3. Yu.N. Belenkov. Remodeling of the left ventricle; A complex approach. Heart failure. 2002, Vol.3, No.4, 163s.

4. A.V. Grachev. Mass of the left ventricular myocardium in patients with arterial hypertension with different echocardiographic types of geometry of the left ventricle of the heart. Journal "Cardiology" No. 3, 2000.

5. Yu.A. Vasyuk, A.A.Kazina Peculiarities of systolic function and remodeling in patients with arterial hypertension. Heart failure #2, 2003.

6. A.V. Preobrazhensky, B.A. Sidorenko, M.N. Alekhin et al. Left ventricular hypertrophy in hypertension. Part 1. Criteria for the diagnosis of left ventricular hypertrophy and its prevalence. "Cardiology" No. 10, 2003, 104 p.

If, with an increase in the load, the volume of blood circulation does not increase, they speak of a decrease in myocardial contractility.

Causes of reduced contractility

The contractility of the myocardium decreases when metabolic processes in the heart are disturbed. The reason for the decrease in contractility is the physical overstrain of a person for a long period of time. If the oxygen supply is disturbed during physical activity, not only the supply of oxygen to cardiomyocytes decreases, but also the substances from which energy is synthesized, so the heart works for some time due to the internal energy reserves of the cells. When they are exhausted, irreversible damage to cardiomyocytes occurs, and the ability of the myocardium to contract is significantly reduced.

Also, a decrease in myocardial contractility can occur:

  • with severe brain injury;
  • with acute myocardial infarction;
  • during heart surgery
  • with myocardial ischemia;
  • due to severe toxic effects on the myocardium.

Reduced contractility of the myocardium can be with beriberi, due to degenerative changes in the myocardium with myocarditis, with cardiosclerosis. Also, a violation of contractility can develop with increased metabolism in the body with hyperthyroidism.

Low myocardial contractility underlies a number of disorders that lead to the development of heart failure. Heart failure leads to a gradual decline in a person's quality of life and can cause death. The first alarming symptoms of heart failure are weakness and fatigue. The patient is constantly worried about swelling, the person begins to quickly gain weight (especially in the abdomen and thighs). Breathing becomes more frequent, attacks of suffocation may occur in the middle of the night.

Violation of contractility is characterized by a not so strong increase in the force of myocardial contraction in response to an increase in venous blood flow. As a result, the left ventricle does not empty completely. The degree of decrease in myocardial contractility can only be assessed indirectly.

Diagnostics

A decrease in myocardial contractility is detected using ECG, daily ECG monitoring, echocardiography, fractal analysis of heart rate and functional tests. EchoCG in the study of myocardial contractility allows you to measure the volume of the left ventricle in systole and diastole, so you can calculate the minute volume of blood. A biochemical blood test and physiological testing, as well as blood pressure measurement, are also carried out.

To assess the contractility of the myocardium, the effective cardiac output is calculated. An important indicator of the state of the heart is the minute volume of blood.

Treatment

To improve the contractility of the myocardium, drugs are prescribed that improve blood microcirculation and medicinal substances that regulate the metabolism in the heart. To correct impaired myocardial contractility, patients are prescribed dobutamine (in children under 3 years old, this drug can cause tachycardia, which disappears when the administration of this drug is stopped). With the development of impaired contractility due to burns, dobutamine is used in combination with catecholamines (dopamine, epinephrine). In the event of a metabolic disorder due to excessive physical exertion, athletes use the following drugs:

  • phosphocreatine;
  • asparkam, panangin, potassium orotate;
  • riboxin;
  • Essentiale, essential phospholipids;
  • bee pollen and royal jelly;
  • antioxidants;
  • sedatives (for insomnia or nervous overexcitation);
  • iron preparations (with a reduced level of hemoglobin).

It is possible to improve the contractility of the myocardium by limiting the physical and mental activity of the patient. In most cases, it is sufficient to prohibit heavy physical exertion and prescribe a 2-3 hour rest in bed for the patient. In order for the function of the heart to recover, it is necessary to identify and treat the underlying disease. In severe cases, bed rest for 2-3 days may help.

Detection of a decrease in myocardial contractility in the early stages and its timely correction in most cases allows you to restore the intensity of contractility and the patient's ability to work.

Positron emission tomography

Positron emission tomography (PET) is a relatively new and highly informative non-invasive method for studying the metabolism of the heart muscle, oxygen uptake and coronary perfusion. The method is based on recording the radiation activity of the heart after the introduction of special radioactive labels, which are included in certain metabolic processes (glycolysis, oxidative phosphorylation of glucose, β-oxidation of fatty acids, etc.), imitating the “behavior” of the main metabolic substrates (glucose, fatty acids, etc.).

In patients with coronary artery disease, the PET method allows non-invasive study of regional myocardial blood flow, glucose and fatty acid metabolism, and oxygen uptake. PET has proven to be an indispensable diagnostic method myocardial viability. For example, when a violation of local LV contractility (hypokinesia, akinesia) is caused by a hibernating or stunned myocardium that has retained its viability, PET can register the metabolic activity of this area of ​​the heart muscle (Fig. 5.32), while in the presence of a scar, such activity is not detected.

Echocardiography in patients with coronary artery disease provides important information about morphological and functional changes in the heart. Echocardiography (EchoCG) is used to diagnose:

  • violations of local LV contractility due to a decrease in perfusion of individual segments of the LV during exercise tests ( stress echocardiography);
  • viability of ischemic myocardium (diagnosis of "hibernating" and "stunned" myocardium);
  • post-infarction (large-focal) cardiosclerosis and LV aneurysm (acute and chronic);
  • the presence of an intracardiac thrombus;
  • the presence of systolic and diastolic LV dysfunction;
  • signs of stagnation in the veins of the systemic circulation and (indirectly) - the magnitude of the CVP;
  • signs of pulmonary arterial hypertension;
  • compensatory hypertrophy of the ventricular myocardium;
  • dysfunction of the valvular apparatus (prolapse of the mitral valve, detachment of chords and papillary muscles, etc.);
  • change in some morphometric parameters (thickness of the walls of the ventricles and the size of the chambers of the heart);
  • violation of the nature of blood flow in large CA (some modern methods of echocardiography).

Obtaining such extensive information is possible only with the integrated use of the three main modes of echocardiography: one-dimensional (M-mode), two-dimensional (B-mode) and Doppler mode.

Assessment of systolic and diastolic function of the left ventricle

LV systolic function. The main hemodynamic parameters reflecting LV systolic function are EF, VR, MO, SI, as well as end-systolic (ESV) and end-diastolic (EDV) LV volumes. These indicators are obtained when studying in two-dimensional and Doppler modes according to the method described in detail in Chapter 2.

As shown above, the earliest marker of LV systolic dysfunction is reduction in ejection fraction (EF) up to 40-45% and below (Table 2.8), which is usually combined with an increase in CSR and CWW, i.e. with LV dilatation and its volume overload. In this case, one should keep in mind the strong dependence of EF on the magnitude of pre- and afterload: EF can decrease with hypovolemia (shock, acute blood loss, etc.), a decrease in blood flow to the right heart, as well as with a rapid and sharp rise in blood pressure.

In table. 2.7 (Chapter 2) presented the normal values ​​of some echocardiographic indicators of global LV systolic function. Recall that moderately severe LV systolic dysfunction is accompanied by a decrease in EF to 40–45% or lower, an increase in ESV and EDV (i.e., the presence of moderate LV dilatation) and the preservation of normal CI values ​​for some time (2.2–2.7 l / min / m 2). At pronounced LV systolic dysfunction, there is a further drop in the value of EF, an even greater increase in EDV and ESV (pronounced myogenic dilatation of the LV) and a decrease in SI to 2.2 l / min / m 2 and below.

LV diastolic function. LV diastolic function is assessed according to the results of the study transmitral diastolic blood flow in pulsed Doppler mode (see Chapter 2 for details). Determine: 1) the maximum speed of the early peak of diastolic filling (V max Peak E); 2) the maximum rate of transmitral blood flow during left atrial systole (V max Peak A); 3) area under the curve (rate integral) of early diastolic filling (MV VTI Peak E) and 4) area under the curve of late diastolic filling (MV VTI Peak A); 5) the ratio of the maximum speeds (or speed integrals) of early and late filling (E/A); 6) LV isovolumic relaxation time - IVRT (measured with simultaneous recording of aortic and transmitral blood flow in a constant-wave mode from the apical access); 7) deceleration time of early diastolic filling (DT).

The most common causes of LV diastolic dysfunction in CAD patients with stable angina are:

  • atherosclerotic (diffuse) and postinfarction cardiosclerosis;
  • chronic myocardial ischemia, including “hibernating” or “stunned” LV myocardium;
  • compensatory myocardial hypertrophy, especially pronounced in patients with concomitant hypertension.

In most cases, there are signs of LV diastolic dysfunction. according to the type of “delayed relaxation”, which is characterized by a decrease in the rate of early diastolic filling of the ventricle and a redistribution of diastolic filling in favor of the atrial component. At the same time, a significant part of the diastolic blood flow is carried out during the active systole of the LA. Dopplerograms of the transmitral blood flow reveal a decrease in the amplitude of the E peak and an increase in the height of the A peak (Fig. 2.57). The E/A ratio is reduced to 1.0 and below. At the same time, an increase in the time of LV isovolumic relaxation (IVRT) up to 90-100 ms or more and the time of deceleration of early diastolic filling (DT) - up to 220 ms or more are determined.

More pronounced changes in LV diastolic function ( "restrictive" type) are characterized by a significant acceleration of early diastolic ventricular filling (Peak E) with a simultaneous decrease in blood flow velocity during atrial systole (Peak A). As a result, the E/A ratio increases to 1.6–1.8 or more. These changes are accompanied by a shortening of the isovolumic relaxation phase (IVRT) to values ​​less than 80 ms and the deceleration time of early diastolic filling (DT) less than 150 ms. Recall that the “restrictive” type of diastolic dysfunction, as a rule, is observed in congestive heart failure or immediately precedes it, indicating an increase in filling pressure and LV end pressure.

Assessment of violations of regional contractility of the left ventricle

Identification of local disorders of LV contractility using two-dimensional echocardiography is important for the diagnosis of coronary artery disease. The study is usually carried out from the apical approach along the long axis in the projection of the two- and four-chamber heart, as well as from the left parasternal approach along the long and short axis.

In accordance with the recommendations of the American Association of Echocardiography, the LV is conditionally divided into 16 segments located in the plane of three cross sections of the heart, recorded from the left parasternal short-axis approach (Fig. 5.33). Picture 6 basal segments- anterior (A), anterior septal (AS), posterior septal (IS), posterior (I), posterolateral (IL) and anterolateral (AL) - obtained when located at the level of the mitral valve leaflets (SAX MV), and middle parts the same 6 segments - at the level of papillary muscles (SAX PL). Images 4 apical segments- anterior (A), septal (S), posterior (I) and lateral (L), - obtained by location from parasternal access at the level of the apex of the heart (SAX AP).

The general idea of ​​the local contractility of these segments is well complemented by three longitudinal “slices” of the left ventricle registered from parasternal access along the long axis of the heart (Fig. 5.34), as well as in the apical position of the four-chamber and two-chamber heart (Fig. 5.35).

In each of these segments, the nature and amplitude of myocardial movement, as well as the degree of its systolic thickening, are assessed. There are 3 types of local disorders of the contractile function of the left ventricle, united by the concept “asynergy”(Fig. 5.36):

1. Akinesia - lack of contraction of a limited area of ​​the heart muscle.

2. Hypokinesia- pronounced local decrease in the degree of contraction.

3.Dyskinesia- paradoxical expansion (bulging) of a limited area of ​​the heart muscle during systole.

The causes of local disorders of LV myocardial contractility in patients with IHD are:

  • acute myocardial infarction (MI);
  • postinfarction cardiosclerosis;
  • transient pain and painless myocardial ischemia, including ischemia induced by functional stress tests;
  • permanent ischemia of the myocardium, which has still retained its viability (“hibernating myocardium”).

It should also be remembered that local violations of LV contractility can be detected not only in IHD. The reasons for such violations can be:

  • dilated and hypertrophic cardiomyopathy, which are often also accompanied by uneven damage to the LV myocardium;
  • local disorders of intraventricular conduction (blockade of the legs and branches of the His bundle, WPW syndrome, etc.) of any origin;
  • diseases characterized by volume overload of the pancreas (due to paradoxical movements of the IVS).

The most pronounced violations of local myocardial contractility are detected in acute myocardial infarction and LV aneurysm. Examples of these disorders are given in Chapter 6. Patients with stable exertional angina who have had a previous MI may show echocardiographic evidence of a large or (rarely) small focal postinfarction cardiosclerosis.

Thus, in large-focal and transmural post-infarction cardiosclerosis, two-dimensional and even one-dimensional echocardiography, as a rule, makes it possible to identify local zones of hypokinesia or akinesia(Fig. 5.37, a, b). Small-focal cardiosclerosis or transient myocardial ischemia are characterized by the appearance of zones hypokinesia LV, which are more often detected with anterior septal localization of ischemic damage and less often with its posterior localization. Often, signs of small-focal (intramural) postinfarction cardiosclerosis are not detected during echocardiographic examination.

Violations of local contractility of individual LV segments in patients with coronary artery disease are usually described on a five-point scale:

1 point - normal contractility;

2 points - moderate hypokinesia (a slight decrease in the amplitude of systolic movement and thickening in the study area);

3 points - severe hypokinesia;

4 points - akinesia (lack of movement and thickening of the myocardium);

5 points - dyskinesia (systolic movement of the myocardium of the studied segment occurs in the direction opposite to normal).

For such an assessment, in addition to the traditional visual control, frame-by-frame viewing of images recorded on a VCR is used.

An important prognostic value is the calculation of the so-called local contractility index (LIS), which is the sum of each segment contractility score (SS) divided by the total number of LV segments examined (n):

High values ​​of this indicator in patients with MI or postinfarction cardiosclerosis are often associated with an increased risk of death.

It should be remembered that with echocardiography, it is far from always possible to achieve sufficiently good visualization of all 16 segments. In these cases, only those parts of the LV myocardium that are well identified by two-dimensional echocardiography are taken into account. Often in clinical practice they are limited to assessing local contractility 6 LV segments: 1) interventricular septum (its upper and lower parts); 2) tops; 3) anterior-basal segment; 4) lateral segment; 5) posterior diaphragmatic (lower) segment; 6) posterior basal segment.

Stress echocardiography. In chronic forms of coronary artery disease, the study of local LV myocardial contractility at rest is far from always informative. The possibilities of the ultrasound method of research are significantly expanded when using the method of stress echocardiography - registration of violations of local myocardial contractility using two-dimensional echocardiography during exercise.

More often, dynamic physical activity is used (treadmill or bicycle ergometry in a sitting or lying position), tests with dipyridamole, dobutamine, or transesophageal electrical stimulation of the heart (TEAS). The methods of conducting stress tests and the criteria for terminating the test do not differ from those used in classical electrocardiography. Two-dimensional echocardiograms are recorded in the horizontal position of the patient before the start of the study and immediately after the end of the load (within 60–90 s).

To detect violations of local myocardial contractility, special computer programs are used to assess the degree of change in myocardial movement and its thickening during exercise (“stress”) in 16 (or other number) previously visualized LV segments. The results of the study practically do not depend on the type of load, although TPES and dipyridamole or dobutamine tests are more convenient, since all studies are carried out in the horizontal position of the patient.

The sensitivity and specificity of stress echocardiography in the diagnosis of coronary artery disease reaches 80–90%. The main disadvantage of this method is that the results of the study significantly depend on the qualifications of a specialist who manually sets the boundaries of the endocardium, which are subsequently used to automatically calculate the local contractility of individual segments.

Myocardial viability study. Echocardiography, along with 201 T1 myocardial scintigraphy and positron emission tomography, has recently been widely used to diagnose the viability of "hibernating" or "stunned" myocardium. For this purpose, a dobutamine test is usually used. Since even small doses of dobutamine have a pronounced positive inotropic effect, the contractility of the viable myocardium, as a rule, increases, which is accompanied by a temporary decrease or disappearance of echocardiographic signs of local hypokinesia. These data are the basis for the diagnosis of "hibernating" or "stunned" myocardium, which is of great prognostic value, in particular, for determining indications for surgical treatment patients with coronary artery disease. It should, however, be borne in mind that at higher doses of dobutamine, the signs of myocardial ischemia are aggravated and contractility decreases again. Thus, when conducting a dobutamine test, one can meet with a two-phase reaction of the contractile myocardium to the introduction of a positive inotropic agent.

Coronary angiography (CAG) is a method of X-ray examination of the coronary arteries of the heart (CA) using selective filling of the coronary vessels with a contrast agent. Being the “gold standard” in the diagnosis of coronary artery disease, coronary angiography makes it possible to determine the nature, location and degree of atherosclerotic narrowing of the coronary artery, the extent of the pathological process, the state of collateral circulation, and also to identify some congenital malformations of the coronary vessels, for example, abnormal coronary outlet or coronary arteriovenous fistula. In addition, when performing CAG, as a rule, they produce left ventriculography, which makes it possible to evaluate a number of important hemodynamic parameters (see above). The data obtained during CAG are very important when choosing a method for surgical correction of obstructive coronary lesions.

Indications and contraindications

Indications. In accordance with the recommendations of the European Society of Cardiology (1997), the most common indications for planned CAG are clarification of the nature, degree and localization of coronary artery lesions and assessment of LV contractility disorders (according to left ventriculography) in patients with coronary artery disease subject to surgical treatment, including:

  • patients with chronic forms of coronary artery disease (stable angina pectoris III–IV FC) with the ineffectiveness of conservative antianginal therapy;
  • patients with stable angina pectoris of I–II FC, who underwent MI;
  • patients with post-infarction aneurysm and progressive, predominantly left ventricular, heart failure;
  • patients with stable angina pectoris with bundle branch block in combination with signs of myocardial ischemia according to myocardial scintigraphy;
  • patients with coronary artery disease in combination with aortic heart disease requiring surgical correction;
  • patients with obliterating atherosclerosis of the arteries of the lower extremities referred for surgical treatment;
  • patients with coronary artery disease with severe cardiac arrhythmias requiring clarification of the genesis and surgical correction.

In some cases, planned CAG is also indicated for verification of the diagnosis of coronary artery disease in patients with pain in the heart and some other symptoms, the genesis of which could not be established using non-invasive research methods, including ECG 12, functional stress tests, daily Holter ECG monitoring, etc. However, in these cases, the doctor referring such a patient to a specialized institution for CAG should be especially careful and take into account many factors that determine the appropriateness of this study and the risk of its complications.

Indications for holding emergency CAG in patients with acute coronary syndrome are presented in chapter 6 of this manual.

Contraindications. Carrying out CAG is contraindicated:

  • in the presence of fever;
  • in severe diseases of parenchymal organs;
  • with severe total (left and right ventricular) heart failure;
  • with acute disorders of cerebral circulation;
  • with severe ventricular arrhythmias.

There are mainly two CAG techniques currently in use. Most commonly used Judkins technique, in which a special catheter is inserted by percutaneous puncture into the femoral artery, and then retrograde into the aorta (Fig. 5.38). 5–10 ml of a radiopaque substance are injected into the mouth of the right and left CA, and X-ray film or video filming is carried out in several projections, which makes it possible to obtain dynamic images of the coronary bed. In cases where the patient has occlusion of both femoral arteries, use the Sones technique in which a catheter is inserted into the exposed brachial artery.

Among the most difficult complications that may occur during CAG include: 1) rhythm disturbances, including ventricular tachycardia and ventricular fibrillation; 2) development of acute MI; 3) sudden death.

When analyzing coronarograms, several signs are evaluated that quite fully characterize changes in the coronary bed in IHD (Yu.S. Petrosyan and L.S. Zingerman).

1. Anatomical type of blood supply to the heart: right, left, balanced (uniform).

2. Localization of lesions: a) LCA trunk; b) LAD LCA; c) OV LCA; d) anterior diagonal branch of the LCA; e) PCA; f) marginal branch of the RCA and other branches of the CA.

3. The prevalence of the lesion: a) localized form (in the proximal, middle or distal third of the coronary artery); b) diffuse lesion.

4. The degree of narrowing of the lumen:

a. I degree - by 50%;

b. II degree - from 50 to 75%;

in. III degree - more than 75%;

d. IV degree - occlusion of the CA.

The left anatomical type is characterized by the predominance of blood supply due to the LCA. The latter is involved in the vascularization of the entire LA and LV, the entire IVS, the posterior wall of the right ventricle, most of the posterior wall of the pancreas, and part of the anterior wall of the pancreas adjacent to the IVS. In this type, the RCA supplies blood only to a part of the anterior wall of the pancreas, as well as to the anterior and lateral walls of the RA.

At right type a large part of the heart (all RAs, most of the anterior and entire posterior wall of the pancreas, posterior 2/3 of the IVS, posterior wall of the LV and LA, apex of the heart) is supplied by the RCA and its branches. The LCA in this type supplies blood to the anterior and lateral walls of the left ventricle, the anterior third of the IVS, and the anterior and lateral walls of the left ventricle.

More often (about 80-85% of cases) there are various options balanced (uniform) type of blood supply heart, in which the LCA supplies blood to the entire LA, the anterior, lateral and most of the posterior wall of the LV, the anterior 2/3 of the IVS and a small part of the anterior wall of the RV adjacent to the IVS. The RCA is involved in the vascularization of the entire RA, most of the anterior and entire posterior wall of the pancreas, the posterior third of the IVS, and a small part of the posterior wall of the LV.

During selective CAG, a contrast agent is sequentially injected into the RCA (Fig. 5.39) and into the LCA (Fig. 5.40), which makes it possible to obtain a picture of the coronary blood supply separately for the RCA and LCA basins. In patients with coronary artery disease, according to CAG, atherosclerotic narrowing of 2-3 CAs is most often detected - LAD, OB and RCA. The defeat of these vessels has a very important diagnostic and prognostic value, since it is accompanied by the occurrence of ischemic damage to significant areas of the myocardium (Fig. 5.41).

Myocardial contractility

The human heart has a huge potential, it can increase the volume of blood circulation up to 5-6 times. This is achieved by increasing heart rate or blood volume. It is the contractility of the myocardium that allows the heart to adapt with maximum accuracy to the state of a person, pump more blood with increasing loads, and accordingly supply all organs with the right amount of nutrients, ensuring their correct uninterrupted operation.

Sometimes, assessing myocardial contractility, doctors note that the heart, even under heavy loads, does not increase its activity or does it in insufficient volume. In such cases, the health and functioning of the organ should be given special attention, excluding the development of diseases such as hypoxia, ischemia.

If the contractility of the myocardium of the left ventricle is reduced

A decrease in myocardial contractility can occur for various reasons. The first is a large overload. For example, if an athlete for a long time exposes himself to excessive physical exertion that exhausts the body, over time, a decrease in the contractile function of the myocardium may be found in him. This is due to insufficient supply of oxygen and nutrients to the heart muscle, respectively, the inability to synthesize the proper amount of energy. For some time, the contractility will be preserved through the use of available internal energy resources. But, after a certain period of time, the possibilities will be completely exhausted, malfunctions in the work of the heart will begin to manifest themselves more clearly, symptoms characteristic of them will appear. Then you will need an additional examination, taking energy medicines that stimulate the work of the heart and metabolic processes in it.

There is a decrease in myocardial contractility in the presence of a number of diseases, such as:

  • brain injury;
  • acute myocardial infarction;
  • ischemic disease;
  • surgical intervention;
  • toxic effect on the heart muscle.

It is also reduced if a person suffers from atherosclerosis, cardiosclerosis. The cause may be vitamin deficiency, myocarditis. If we talk about beriberi, then the problem is solved quite simply, you just need to restore proper and balanced nutrition, providing the heart and the whole body with important nutrients. When a serious illness became the reason for the decrease in the contractility of the heart, the situation becomes more serious and requires increased attention.

It's important to know! Violation of local myocardial contractility entails not only a deterioration in the patient's well-being, but also the development of heart failure. It, in turn, can provoke the appearance of serious heart diseases, often leading to death. Signs of the disease will be: asthma attacks, swelling, weakness. Rapid breathing may be observed.

How to determine reduced myocardial contractility

In order to be able to get the maximum information about the state of your health, you need to undergo a full examination. Usually, reduced or satisfactory myocardial contractility is detected after ECG and echocardiography. If the results of the electrocardiogram make you think, do not allow you to immediately make an accurate diagnosis, a person is recommended to conduct Holter monitoring. It consists in the constant recording of indicators of the work of the heart using a portable electrocardiograph attached to clothing. So you can get a more accurate picture of the state of health, make a final conclusion.

Ultrasound of the heart is also considered a fairly informative method of examination in this case. It helps to more accurately assess the condition of a person, as well as the functional features of the heart, to identify violations, if any.

Additionally, a biochemical blood test is prescribed. Systematic monitoring of blood pressure is carried out. Physiological testing may be recommended.

How is reduced contractility treated?

First of all, the patient is limited in emotional and physical stress. They provoke an increase in the heart's need for oxygen and nutrients, but if the global contractility of the left ventricular myocardium is impaired, the heart will not be able to perform its function, and the risk of complications will increase. Be sure to prescribe drug therapy, which consists of vitamin preparations and agents that improve metabolic processes in the heart muscle, supporting the performance of the heart. The following medications will help to cope with satisfactory contractility of the myocardium of the left ventricle:

Note! If the patient cannot independently protect himself from stressful situations, he will be prescribed sedatives. The simplest are tincture of valerian, motherwort.

If the cause of the violation was a heart or vascular disease, it will be treated first of all. Only then, after re-diagnosis, electrocardiography, will they make a conclusion about the success of therapy.

What is myocardial contractility normokinesis

When a doctor examines a patient's heart, he necessarily compares the proper indicators of his work (normokinesis) and the data obtained after the diagnosis. If you are interested in the question of determining the normokinesis of myocardial contractility - what it is, only a doctor can explain. This is not about a constant figure, which is considered the norm, but about the ratio of the patient's condition (physical, emotional) and indicators of the contractility of the heart muscle at the moment.

After determining the violations, the task will be to identify the causes of their occurrence, after which we can talk about successful treatment that can bring the working parameters of the heart back to normal.

The ability of the myocardium to contract (inotropic function) provides the main purpose of the heart - pumping blood. It is maintained due to normal metabolic processes in the myocardium, sufficient supply of nutrients and oxygen. If one of these links fails or the nervous, hormonal regulation of contractions, the conduction of electrical impulses is disturbed, then contractility decreases, leading to heart failure.

Read in this article

What does a decrease, an increase in myocardial contractility mean?

With insufficient energy supply to the myocardium or metabolic disorders, the body tries to compensate for them through two main processes - an increase in the frequency and strength of heart contractions. Therefore, the initial stages of heart disease can occur with increased contractility. This increases the ejection of blood from the ventricles.



Increased heart rate

The possibility of increasing the strength of contractions is primarily provided by myocardial hypertrophy. In muscle cells, protein formation increases, the rate of oxidative processes increases. The growth of the mass of the heart noticeably outstrips the growth of arteries and nerve fibers. The result of this is an insufficient supply of impulses to the hypertrophied myocardium, and poor blood supply further exacerbates ischemic disorders.

After the exhaustion of the processes of self-maintenance of blood circulation, the heart muscle weakens, its ability to respond to an increase in physical activity decreases, so there is an insufficiency of the pumping function. Over time, against the background of complete decompensation, symptoms of reduced contractility appear even at rest.

The function is preserved - an indicator of the norm?

Not always the degree of circulatory insufficiency is manifested only by a decrease in cardiac output. In clinical practice, there are cases of progression of heart disease with a normal indicator of contractility, as well as a sharp decrease in inotropic function in individuals with erased manifestations.

The reason for this phenomenon is believed to be that even with a significant violation of contractility, the ventricle can continue to maintain an almost normal volume of blood entering the arteries. This is due to the Frank-Starling law: with increased extensibility of muscle fibers, the strength of their contractions increases. That is, with an increase in the filling of the ventricles with blood in the relaxation phase, they contract more strongly during the systole period.

Thus, changes in myocardial contractility cannot be considered in isolation, since they do not fully reflect the degree of pathological changes occurring in the heart.

Reasons for changing state

A decrease in the strength of heart contractions may occur as a result of coronary disease, especially with a previous myocardial infarction. Almost 70% of all cases of circulatory failure are associated with this disease. In addition to ischemia, a change in the state of the heart leads to:

  • or on the background of rheumatism;
  • cardiomyopathy with expansion of cavities ();
  • diabetes.

The degree of decrease in inotropic function in such patients depends on the progression of the underlying disease. In addition to the main etiological factors, a decrease in the reserve capacity of the myocardium is facilitated by:

In such conditions, most often it is possible to almost completely restore the work of the heart, if the damaging factor is eliminated in time.

Manifestations of reduced myocardial contractility

With severe weakness of the heart muscle in the body, circulatory disorders occur and progress. They gradually affect the work of all internal organs, since blood nutrition and the excretion of metabolic products are significantly disrupted.



Classification of acute disorders of cerebral circulation

Changes in gas exchange

The slow movement of blood increases the absorption of oxygen from the capillaries by cells, increases. The accumulation of metabolic products leads to stimulation of the respiratory muscles. The body suffers from a lack of oxygen, as the circulatory system cannot meet its needs.

The clinical manifestations of starvation are shortness of breath and bluish coloration of the skin. Cyanosis can occur both due to stagnation in the lungs, and with increased oxygen uptake in the tissues.

Water retention and swelling

The reasons for the development of edematous syndrome with a decrease in the strength of heart contractions are:

  • slow blood flow and interstitial fluid retention;
  • reduced excretion of sodium;
  • protein metabolism disorder;
  • insufficient destruction of aldosterone in the liver.

Initially, fluid retention can be identified by an increase in body weight and a decrease in urine output.. Then, from hidden edema, they become visible, appear on the legs or sacral area, if the patient is in a supine position. As failure progresses, water accumulates in the abdominal cavity, pleura, and pericardial sac.

congestion

In the lung tissue, blood stasis manifests itself in the form of difficulty breathing, coughing, sputum with blood, asthma attacks, weakening of respiratory movements. In the systemic circulation, signs of stagnation are determined by an increase in the liver, which is accompanied by pain and heaviness in the right hypochondrium.

Violation of the intracardiac circulation occurs with relative valve insufficiency due to the expansion of the cavities of the heart. This provokes an increase in heart rate, overflow of the cervical veins. Stagnation of blood in the digestive organs causes nausea and loss of appetite, which in severe cases causes malnutrition (cachexia).

In the kidneys, the density of urine increases, its excretion decreases, the tubules become permeable to protein, erythrocytes. The nervous system reacts to circulatory failure with rapid fatigue, low tolerance for mental stress, insomnia at night and drowsiness during the day, emotional instability and depression.

Diagnosis of the contractility of the ventricles of the myocardium

To determine the strength of the myocardium, an indicator of the magnitude of the ejection fraction is used. It is calculated as the ratio between the amount of blood supplied to the aorta and the volume of the contents of the left ventricle in the relaxation phase. It is measured as a percentage, determined automatically during ultrasound, by the data processing program.

The norm is considered if the value is in the range of 55 - 60%. With insufficiency of contractility, it drops to 35 - 40%.

Increased cardiac output can be in athletes, as well as in the development of myocardial hypertrophy at the initial stage. In any case, the ejection fraction does not exceed 80%.

In addition to ultrasound, patients with suspected decreased contractility of the heart undergo:

  • blood tests - electrolytes, oxygen and carbon dioxide levels, acid-base balance, kidney and liver tests, lipid composition;
  • to determine myocardial hypertrophy and ischemia, standard diagnostics can be supplemented;
  • to identify defects, consequences of ischemic and hypertension disease;
  • X-ray of the chest organs - an increase in the cardiac shadow, stagnation in the lungs;
  • radioisotope ventriculography shows the capacity of the ventricles and their contractile capabilities.

If necessary, ultrasound of the liver and kidneys is also prescribed.

Watch the video about the methods of examining the heart:

Treatment in case of deviation

In case of acute circulatory failure or chronic decompensation, treatment is carried out in conditions of complete rest and bed rest. All other cases require limiting loads, reducing salt and fluid intake.

Drug therapy includes the following groups of drugs:

  • cardiac glycosides (Digoxin, Korglikon), they increase the strength of contractions, urine output, pumping function of the heart;
  • (Lisinopril, Kapoten, Prenesa) - lower the resistance of the arteries and dilate the veins (blood deposition), facilitate the work of the heart, increase cardiac output;
  • nitrates (, Kardiket) - improve coronary blood flow, relax the walls of veins and arteries;
  • diuretics (Veroshpiron, Lasix) - remove excess fluid and sodium;
  • beta-blockers (Carvedilol) - relieve tachycardia, increase the filling of the ventricles with blood;
  • anticoagulants (, Varfareks) - increase blood flow;
  • exchange activators in the myocardium (, Mildronate, Neoton,).

The contractility of the heart ensures the flow of blood to the internal organs and the removal of metabolic products from them. With the development of myocardial diseases, stress, inflammatory processes in the body, intoxication, the strength of contractions decreases. This leads to deviations in the work of internal organs, disruption of gas exchange, edema and stagnant processes.

To determine the degree of decrease in inotropic function, the ejection fraction index is used. It can be installed with an ultrasound of the heart. To improve the functioning of the myocardium, complex drug therapy is required.

Read also

There is hypertrophy of the left ventricle of the heart, mainly due to increased pressure. The reasons may even be hormonal. Signs and indications on the ECG are quite pronounced. It is moderate, concentric. Why is hypertrophy dangerous in adults and children? How to treat heart disease?

  • Pathology dilated cardiomyopathy is a dangerous disease that can cause sudden death. How is diagnosis and treatment carried out, what complications can occur in congestive dilated cardiomyopathy?
  • Under the influence of certain diseases, dilatation of the heart develops. It can be in the right and left sections, ventricles, myocardial cavities, chambers. Symptoms in adults and children are similar. Treatment is primarily directed at the disease that led to the dilation.
  • In cases of heart disease, including angina pectoris and others, Isoket is prescribed, the use of which is allowed in the form of sprays and droppers. Cardiac ischemia is also considered an indication, but there are many contraindications.


  • These properties include automatism (the ability to independently generate electricity), conductivity (the ability to transmit electrical impulses to nearby muscle fibers in the heart) and contractility - the ability to contract synchronously in response to electrical stimulation.

    In a more global concept, contractility is the ability of the heart muscle as a whole to contract in order to push blood into the large main arteries - into the aorta and into the pulmonary trunk. Usually they talk about the contractility of the myocardium of the left ventricle, since it is he who performs the greatest work of expelling blood, and this work is estimated by ejection fraction and stroke volume, that is, by the amount of blood that is ejected into the aorta with each cardiac cycle.

    Bioelectric bases of myocardial contractility

    heart beat cycle

    The contractility of the entire myocardium depends on the biochemical characteristics in each individual muscle fiber. Cardiomyocyte, like any cell, has a membrane and internal structures, mainly consisting of contractile proteins. These proteins (actin and myosin) can contract, but only if calcium ions enter the cell through the membrane. This is followed by a cascade of biochemical reactions, and as a result, protein molecules in the cell contract like springs, causing contraction of the cardiomyocyte itself. In turn, the entry of calcium into the cell through special ion channels is possible only in the case of repolarization and depolarization processes, that is, sodium and potassium ion currents through the membrane.

    With each incoming electrical impulse, the membrane of the cardiomyocyte is excited, and the current of ions into and out of the cell is activated. Such bioelectrical processes in the myocardium do not occur simultaneously in all parts of the heart, but in turn - first the atria are excited and contracted, then the ventricles themselves and the interventricular septum. The result of all processes is a synchronous, regular contraction of the heart with the ejection of a certain volume of blood into the aorta and further throughout the body. Thus, the myocardium performs its contractile function.

    Video: more about the biochemistry of myocardial contractility

    Why do you need to know about myocardial contractility?

    Cardiac contractility is the most important ability that indicates the health of the heart itself and the whole organism as a whole. In the case when a person has myocardial contractility within the normal range, he has nothing to worry about, since in the absence of cardiac complaints, it can be confidently stated that at the moment everything is in order with his cardiovascular system.

    If the doctor suspected and confirmed with the help of an examination that the patient has impaired or reduced myocardial contractility, he needs to be examined as soon as possible and start treatment if he has a serious myocardial disease. About what diseases can cause a violation of myocardial contractility, will be described below.

    Myocardial contractility according to ECG

    The contractility of the heart muscle can be assessed already during an electrocardiogram (ECG), since this research method allows you to register the electrical activity of the myocardium. With normal contractility, the heart rhythm on the cardiogram is sinus and regular, and the complexes reflecting the contractions of the atria and ventricles (PQRST) have the correct appearance, without changes in individual teeth. The nature of the PQRST complexes in different leads (standard or chest) is also assessed, and with changes in different leads, it is possible to judge the violation of contractility of the corresponding sections of the left ventricle (lower wall, high-lateral sections, anterior, septal, apical-lateral walls of the left ventricle). Due to the high information content and ease of conducting ECG is a routine research method that allows you to timely determine certain violations in the contractility of the heart muscle.

    Myocardial contractility by echocardiography

    EchoCG (echocardioscopy), or ultrasound of the heart, is the gold standard in the study of the heart and its contractility due to good visualization of cardiac structures. Myocardial contractility by ultrasound of the heart is assessed based on the quality of the reflection of ultrasonic waves, which are converted into a graphic image using special equipment.

    photo: assessment of myocardial contractility on echocardiography with exercise

    According to the ultrasound of the heart, the contractility of the myocardium of the left ventricle is mainly assessed. In order to find out whether the myocardium is reduced completely or partially, it is necessary to calculate a number of indicators. So, the total wall mobility index is calculated (based on the analysis of each segment of the LV wall) - WMSI. LV wall mobility is determined based on the percentage increase in LV wall thickness during cardiac contraction (during LV systole). The greater the thickness of the LV wall during systole, the better the contractility of this segment. Each segment, based on the thickness of the walls of the LV myocardium, is assigned a certain number of points - for normokinesis 1 point, for hypokinesia - 2 points, for severe hypokinesia (up to akinesia) - 3 points, for dyskinesia - 4 points, for aneurysm - 5 points. The total index is calculated as the ratio of the sum of points for the studied segments to the number of visualized segments.

    A total index equal to 1 is considered normal. That is, if the doctor “looked” three segments on ultrasound, and each of them had normal contractility (each segment has 1 point), then the total index = 1 (normal, and myocardial contractility is satisfactory ). If at least one of the three visualized segments has impaired contractility and is estimated at 2-3 points, then the total index = 5/3 = 1.66 (myocardial contractility is reduced). Thus, the total index should not be greater than 1.

    sections of the heart muscle on echocardiography

    In cases where the contractility of the myocardium according to the ultrasound of the heart is within the normal range, but the patient has a number of complaints from the heart (pain, shortness of breath, swelling, etc.), the patient is shown to conduct a stress-ECHO-KG, that is, an ultrasound of the heart performed after physical loads (walking on a treadmill - treadmill, bicycle ergometry, 6-minute walk test). In the case of myocardial pathology, contractility after exercise will be impaired.

    Normal contractility of the heart and violations of myocardial contractility

    Whether the patient has preserved the contractility of the heart muscle or not can be reliably judged only after an ultrasound of the heart. So, based on the calculation of the total index of wall mobility, as well as determining the thickness of the LV wall during systole, it is possible to identify the normal type of contractility or deviation from the norm. Thickening of the examined myocardial segments by more than 40% is considered normal. An increase in myocardial thickness by 10-30% indicates hypokinesia, and a thickening of less than 10% of the original thickness indicates severe hypokinesia.

    Based on this, the following concepts can be distinguished:

    • Normal type of contractility - all LV segments contract in full force, regularly and synchronously, myocardial contractility is preserved,
    • Hypokinesia - decreased local LV contractility,
    • Akinesia - the complete absence of contraction of this LV segment,
    • Dyskinesia - myocardial contraction in the studied segment is incorrect,
    • Aneurysm - "protrusion" of the LV wall, consists of scar tissue, the ability to contract is completely absent.

    In addition to this classification, there are violations of global or local contractility. In the first case, the myocardium of all parts of the heart is not able to contract with such force as to carry out a full cardiac output. In the event of a violation of local myocardial contractility, the activity of those segments that are directly affected by pathological processes and in which signs of dys-, hypo- or akinesia are visualized decreases.

    What diseases are associated with violations of myocardial contractility?

    graphs of changes in myocardial contractility in various situations

    Disturbances in global or local myocardial contractility can be caused by diseases that are characterized by the presence of inflammatory or necrotic processes in the heart muscle, as well as the formation of scar tissue instead of normal muscle fibers. The category of pathological processes that provoke a violation of local myocardial contractility includes the following:

    1. Myocardial hypoxia in ischemic heart disease,
    2. Necrosis (death) of cardiomyocytes in acute myocardial infarction,
    3. Scar formation in postinfarction cardiosclerosis and LV aneurysm,
    4. Acute myocarditis - inflammation of the heart muscle caused by infectious agents (bacteria, viruses, fungi) or autoimmune processes (systemic lupus erythematosus, rheumatoid arthritis, etc.),
    5. Postmyocardial cardiosclerosis,
    6. Dilated, hypertrophic and restrictive types of cardiomyopathy.

    In addition to the pathology of the heart muscle itself, pathological processes in the pericardial cavity (in the outer cardiac membrane, or in the heart bag), which prevent the myocardium from fully contracting and relaxing - pericarditis, cardiac tamponade, can lead to a violation of global myocardial contractility.

    In acute stroke, with brain injuries, a short-term decrease in the contractility of cardiomyocytes is also possible.

    Of the more harmless reasons for the decrease in myocardial contractility, beriberi, myocardial dystrophy (with general exhaustion of the body, with dystrophy, anemia), as well as acute infectious diseases can be noted.

    Are there clinical manifestations of impaired contractility?

    Changes in myocardial contractility are not isolated, and, as a rule, are accompanied by one or another pathology of the myocardium. Therefore, from the clinical symptoms of the patient, those that are characteristic of a particular pathology are noted. Thus, in acute myocardial infarction, intense pain in the region of the heart is noted, with myocarditis and cardiosclerosis - shortness of breath, and with increasing LV systolic dysfunction - edema. Often there are cardiac arrhythmias (more often atrial fibrillation and ventricular extrasystole), as well as syncope (fainting) conditions due to low cardiac output, and, as a result, low blood flow to the brain.

    Should contractility disorders be treated?

    Treatment of impaired contractility of the heart muscle is mandatory. However, when diagnosing such a condition, it is necessary to establish the cause that led to the violation of contractility, and treat this disease. Against the background of timely, adequate treatment of the causative disease, myocardial contractility returns to normal. For example, in the treatment of acute myocardial infarction, zones prone to akinesia or hypokinesia begin to normally perform their contractile function after 4-6 weeks from the moment the infarction develops.

    Are there possible consequences?

    If we talk about the consequences of this condition, then you should know that possible complications are due to the underlying disease. They can be represented by sudden cardiac death, pulmonary edema, cardiogenic shock in a heart attack, acute heart failure in myocarditis, etc. Regarding the prognosis of impaired local contractility, it should be noted that akinesia zones in the area of ​​necrosis worsen the prognosis in acute cardiac pathology and increase the risk of sudden heart death in the future. Timely treatment of the causative disease significantly improves the prognosis, and the survival of patients increases.

    What will tell the contractility of the myocardium

    The ability of the myocardium to contract (inotropic function) provides the main purpose of the heart - pumping blood. It is maintained due to normal metabolic processes in the myocardium, sufficient supply of nutrients and oxygen. If one of these links fails or the nervous, hormonal regulation of contractions, the conduction of electrical impulses is disturbed, then contractility decreases, leading to heart failure.

    What does a decrease, an increase in myocardial contractility mean?

    With insufficient energy supply to the myocardium or metabolic disorders, the body tries to compensate for them through two main processes - an increase in the frequency and strength of heart contractions. Therefore, the initial stages of heart disease can occur with increased contractility. This increases the ejection of blood from the ventricles.

    Increased heart rate

    The possibility of increasing the strength of contractions is primarily provided by myocardial hypertrophy. In muscle cells, protein formation increases, the rate of oxidative processes increases. The growth of the mass of the heart noticeably outstrips the growth of arteries and nerve fibers. The result of this is an insufficient supply of impulses to the hypertrophied myocardium, and poor blood supply further exacerbates ischemic disorders.

    After the exhaustion of the processes of self-maintenance of blood circulation, the heart muscle weakens, its ability to respond to an increase in physical activity decreases, so there is an insufficiency of the pumping function. Over time, against the background of complete decompensation, symptoms of reduced contractility appear even at rest.

    Learn more about the complications of myocardial infarction here.

    The function is preserved - an indicator of the norm?

    Not always the degree of circulatory insufficiency is manifested only by a decrease in cardiac output. In clinical practice, there are cases of progression of heart disease with a normal indicator of contractility, as well as a sharp decrease in inotropic function in individuals with erased manifestations.

    The reason for this phenomenon is believed to be that even with a significant violation of contractility, the ventricle can continue to maintain an almost normal volume of blood entering the arteries. This is due to the Frank-Starling law: with increased extensibility of muscle fibers, the strength of their contractions increases. That is, with an increase in the filling of the ventricles with blood in the relaxation phase, they contract more strongly during the systole period.

    Thus, changes in myocardial contractility cannot be considered in isolation, since they do not fully reflect the degree of pathological changes occurring in the heart.

    Reasons for changing state

    A decrease in the strength of heart contractions may occur as a result of coronary disease, especially with a previous myocardial infarction. Almost 70% of all cases of circulatory failure are associated with this disease. In addition to ischemia, a change in the state of the heart leads to:

    The degree of decrease in inotropic function in such patients depends on the progression of the underlying disease. In addition to the main etiological factors, a decrease in the reserve capacity of the myocardium is facilitated by:

    • physical and psychological overload, stress;
    • rhythm disturbance;
    • thrombosis or thromboembolism;
    • pneumonia;
    • viral infections;
    • anemia;
    • chronic alcoholism;
    • decreased kidney function;
    • excess thyroid hormones;
    • prolonged use of medications (hormonal, anti-inflammatory, increasing pressure), excessive fluid intake during infusion therapy;
    • fast weight gain;
    • myocarditis, rheumatism, bacterial endocarditis, fluid accumulation in the pericardial sac.

    In such conditions, most often it is possible to almost completely restore the work of the heart, if the damaging factor is eliminated in time.

    Manifestations of reduced myocardial contractility

    With severe weakness of the heart muscle in the body, circulatory disorders occur and progress. They gradually affect the work of all internal organs, since blood nutrition and the excretion of metabolic products are significantly disrupted.

    Classification of acute disorders of cerebral circulation

    Changes in gas exchange

    The slow movement of blood increases the absorption of oxygen from the capillaries by the cells, and the acidity of the blood increases. The accumulation of metabolic products leads to stimulation of the respiratory muscles. The body suffers from a lack of oxygen, as the circulatory system cannot meet its needs.

    The clinical manifestations of starvation are shortness of breath and bluish coloration of the skin. Cyanosis can occur both due to stagnation in the lungs, and with increased oxygen uptake in the tissues.

    Water retention and swelling

    The reasons for the development of edematous syndrome with a decrease in the strength of heart contractions are:

    • slow blood flow and interstitial fluid retention;
    • reduced excretion of sodium;
    • protein metabolism disorder;
    • insufficient destruction of aldosterone in the liver.

    Initially, fluid retention can be identified by an increase in body weight and a decrease in urine output. Then, from hidden edema, they become visible, appear on the legs or sacral area, if the patient is in a supine position. As failure progresses, water accumulates in the abdominal cavity, pleura, and pericardial sac.

    congestion

    In the lung tissue, blood stasis manifests itself in the form of difficulty breathing, coughing, sputum with blood, asthma attacks, weakening of respiratory movements. In the systemic circulation, signs of stagnation are determined by an increase in the liver, which is accompanied by pain and heaviness in the right hypochondrium.

    Violation of intracardiac circulation occurs with relative insufficiency of the valves due to the expansion of the cavities of the heart. This provokes an increase in heart rate, overflow of the cervical veins. Stagnation of blood in the digestive organs causes nausea and loss of appetite, which in severe cases causes malnutrition (cachexia).

    In the kidneys, the density of urine increases, its excretion decreases, the tubules become permeable to protein, erythrocytes. The nervous system reacts to circulatory failure with rapid fatigue, low tolerance for mental stress, insomnia at night and drowsiness during the day, emotional instability and depression.

    Diagnosis of the contractility of the ventricles of the myocardium

    To determine the strength of the myocardium, an indicator of the magnitude of the ejection fraction is used. It is calculated as the ratio between the amount of blood supplied to the aorta and the volume of the contents of the left ventricle in the relaxation phase. It is measured as a percentage, determined automatically during ultrasound, by the data processing program.

    Increased cardiac output can be in athletes, as well as in the development of myocardial hypertrophy at the initial stage. In any case, the ejection fraction does not exceed 80%.

    In addition to ultrasound, patients with suspected decreased contractility of the heart undergo:

    • blood tests - electrolytes, oxygen and carbon dioxide levels, acid-base balance, kidney and liver tests, lipid composition;
    • ECG to determine myocardial hypertrophy and ischemia, standard diagnostics can be supplemented with exercise tests;
    • MRI to detect malformations, cardiomyopathy, myocardial dystrophy, consequences of coronary and hypertension disease;
    • X-ray of the chest organs - an increase in the cardiac shadow, stagnation in the lungs;
    • radioisotope ventriculography shows the capacity of the ventricles and their contractile capabilities.

    If necessary, ultrasound of the liver and kidneys is also prescribed.

    Watch the video about the methods of examining the heart:

    Treatment in case of deviation

    In case of acute circulatory failure or chronic decompensation, treatment is carried out in conditions of complete rest and bed rest. All other cases require limiting loads, reducing salt and fluid intake.

    Drug therapy includes the following groups of drugs:

    • cardiac glycosides (Digoxin, Korglikon), they increase the strength of contractions, urine output, pumping function of the heart;
    • ACE inhibitors (Lisinopril, Kapoten, Prenesa) - lower the resistance of the arteries and dilate the veins (blood deposition), facilitate the work of the heart, increase cardiac output;
    • nitrates (Izoket, Kardiket) - improve coronary blood flow, relax the walls of veins and arteries;
    • diuretics (Veroshpiron, Lasix) - remove excess fluid and sodium;
    • beta-blockers (Carvedilol) - relieve tachycardia, increase the filling of the ventricles with blood;
    • anticoagulants (Aspirin, Varfarex) - increase blood flow;
    • activators of metabolism in the myocardium (Riboxin, Mildronate, Neoton, Panangin, Preductal).

    Learn more about cardiac dilatation here.

    The contractility of the heart ensures the flow of blood to the internal organs and the removal of metabolic products from them. With the development of myocardial diseases, stress, inflammatory processes in the body, intoxication, the strength of contractions decreases. This leads to deviations in the work of internal organs, disruption of gas exchange, edema and stagnant processes.

    To determine the degree of decrease in inotropic function, the ejection fraction index is used. It can be installed with an ultrasound of the heart. To improve the functioning of the myocardium, complex drug therapy is required.

    The onset of the disease is due to a decrease in myocardial contractility.

    May precede myocardial hypertrophy. The tone of the heart muscle and contractility are preserved.

    This pathology directly depends on a decrease in myocardial contractility. With the development of such a disease, the heart ceases to cope with.

    The more extensive the areas of scar tissue, the worse the contractility, conductivity and excitability of the myocardium.

    Myocardial contractility is reduced. Anemia can occur with a lack of iron in the diet, acute or chronic bleeding.

    We will publish information shortly.

    Global contractility of the left ventricular myocardium is preserved

    Tricuspid valve: leaflets thin, regurgitation min, pressure gradient 2.5 mm Hg.

    Prolapse of the anterior leaflet of the MK I degree (0.42 cm)

    Additional trabecula in the cavity l.zh.

    Prolapse of the anterior leaflet of the MK I degree (0.42 cm) - i.e. The mitral valve during systole (contraction) of the left ventricle slightly moves away from the norm into the cavity of the left atrium. Normally, this happens, especially during adolescence.

    Additional trabecula in the cavity l.zh. In other words, there is an additional retaining ligament (ligament type) of the mitral valve.

    Myocardial contractility

    The heart muscle has the ability, if necessary, to increase the volume of blood circulation by 3-6 times. This can be achieved by increasing the number of heartbeats. If, with an increase in the load, the volume of blood circulation does not increase, they speak of a decrease in myocardial contractility.

    Causes of reduced contractility

    The contractility of the myocardium decreases when metabolic processes in the heart are disturbed. The reason for the decrease in contractility is the physical overstrain of a person for a long period of time. If the oxygen supply is disturbed during physical activity, not only the supply of oxygen to cardiomyocytes decreases, but also the substances from which energy is synthesized, so the heart works for some time due to the internal energy reserves of the cells. When they are exhausted, irreversible damage to cardiomyocytes occurs, and the ability of the myocardium to contract is significantly reduced.

    Also, a decrease in myocardial contractility can occur:

    • with severe brain injury;
    • with acute myocardial infarction;
    • during heart surgery
    • with myocardial ischemia;
    • due to severe toxic effects on the myocardium.

    Reduced contractility of the myocardium can be with beriberi, due to degenerative changes in the myocardium with myocarditis, with cardiosclerosis. Also, a violation of contractility can develop with increased metabolism in the body with hyperthyroidism.

    Low myocardial contractility underlies a number of disorders that lead to the development of heart failure. Heart failure leads to a gradual decline in a person's quality of life and can cause death. The first alarming symptoms of heart failure are weakness and fatigue. The patient is constantly worried about swelling, the person begins to quickly gain weight (especially in the abdomen and thighs). Breathing becomes more frequent, attacks of suffocation may occur in the middle of the night.

    Violation of contractility is characterized by a not so strong increase in the force of myocardial contraction in response to an increase in venous blood flow. As a result, the left ventricle does not empty completely. The degree of decrease in myocardial contractility can only be assessed indirectly.

    Diagnostics

    A decrease in myocardial contractility is detected using ECG, daily ECG monitoring, echocardiography, fractal analysis of heart rate and functional tests. EchoCG in the study of myocardial contractility allows you to measure the volume of the left ventricle in systole and diastole, so you can calculate the minute volume of blood. A biochemical blood test and physiological testing, as well as blood pressure measurement, are also carried out.

    To assess the contractility of the myocardium, the effective cardiac output is calculated. An important indicator of the state of the heart is the minute volume of blood.

    Treatment

    To improve the contractility of the myocardium, drugs are prescribed that improve blood microcirculation and medicinal substances that regulate the metabolism in the heart. To correct impaired myocardial contractility, patients are prescribed dobutamine (in children under 3 years old, this drug can cause tachycardia, which disappears when the administration of this drug is stopped). With the development of impaired contractility due to burns, dobutamine is used in combination with catecholamines (dopamine, epinephrine). In the event of a metabolic disorder due to excessive physical exertion, athletes use the following drugs:

    • phosphocreatine;
    • asparkam, panangin, potassium orotate;
    • riboxin;
    • Essentiale, essential phospholipids;
    • bee pollen and royal jelly;
    • antioxidants;
    • sedatives (for insomnia or nervous overexcitation);
    • iron preparations (with a reduced level of hemoglobin).

    It is possible to improve the contractility of the myocardium by limiting the physical and mental activity of the patient. In most cases, it is sufficient to prohibit heavy physical exertion and prescribe a 2-3 hour rest in bed for the patient. In order for the function of the heart to recover, it is necessary to identify and treat the underlying disease. In severe cases, bed rest for 2-3 days may help.

    Detection of a decrease in myocardial contractility in the early stages and its timely correction in most cases allows you to restore the intensity of contractility and the patient's ability to work.

    Echocardiography: left ventricular systolic function

    For an error-free interpretation of changes in the analysis of the ECG, it is necessary to adhere to the scheme of its decoding given below.

    In routine practice and in the absence of special equipment for assessing exercise tolerance and objectifying the functional status of patients with moderate and severe heart and lung diseases, a 6-minute walk test can be used, corresponding to submaximal.

    Electrocardiography is a method of graphic recording of changes in the potential difference of the heart that occur during the processes of myocardial excitation.

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    Myocardial contractility is the ability of the heart muscle to provide rhythmic contractions of the heart in an automatic mode in order to move blood through the cardiovascular system. The heart muscle itself has a specific structure that differs from other muscles in the body.

    The elementary contractile unit of the myocardium is the sarcomere, which make up muscle cells - cardiomyocytes. Changing the length of the sarcomere under the influence of electrical impulses of the conduction system and provides contractility of the heart.

    Violation of myocardial contractility can lead to unpleasant consequences in the form, for example, and not only. Therefore, if you experience symptoms of impaired contractility, you should consult a doctor.

    The myocardium has a number of physical and physiological properties that allow it to ensure the full functioning of the cardiovascular system. These features of the heart muscle allow not only to maintain blood circulation, ensuring a continuous flow of blood from the ventricles into the lumen of the aorta and pulmonary trunk, but also to carry out compensatory-adaptive reactions, ensuring the adaptation of the body to increased loads.

    The physiological properties of the myocardium are determined by its extensibility and elasticity. The extensibility of the heart muscle ensures its ability to significantly increase its own length without damage and disruption of its structure.

    For reference. The degree of myocardial extensibility during diastole (relaxation of the heart muscle) determines the strength of further myocardial contractions during systole (contraction of the heart muscle, ending with the expulsion of blood from the ventricular cavities).

    The elastic properties of the myocardium ensure its ability to return to its original shape and position after the impact of deforming forces (contraction, relaxation) ends.

    Also, an important role in maintaining adequate cardiac activity is played by the ability of the heart muscle to develop strength in the process of myocardial contraction and perform work during systole.

    For reference. Physiological features are manifested by excitability, myocardial contractility, its conductivity and automatism (automation).

    What is myocardial contractility

    Cardiac contractility is one of the physiological properties of the heart muscle, which implements the pumping function of the heart due to the ability of the myocardium to contract during systole (leading to the expulsion of blood from the ventricles into the aorta and pulmonary trunk (PL)) and relax during diastole.

    Important. Myocardial contractility is distinguished by a clear sequence that maintains the rhythm and continuity of heart contractions.

    First, the contraction of the atrial muscles is carried out, and then the papillary muscles and the subendocardial layer of the ventricular muscles. Further, the contraction extends to the entire inner layer of the ventricular muscles. This ensures a full systole and allows you to maintain a continuous ejection of blood from the ventricles into the aorta and LA.

    Myocardial contractility is also supported by its:

    • excitability, the ability to generate an action potential (to be excited) in response to the action of stimuli;
    • conductivity, that is, the ability to conduct the generated action potential.

    The contractility of the heart also depends on the automatism of the heart muscle, which is manifested by the independent generation of action potentials (excitations). Due to this feature of the myocardium, even a denervated heart is able to contract for some time.

    What determines the contractility of the heart muscle

    Attention. Myocardial contractility (SM) can be influenced by the nervous system, various hormones and drugs.

    The physiological characteristics of the heart muscle are regulated by vagus and sympathetic nerves that can affect the myocardium:

    • chronotropic;
    • inotropic;
    • bathmotropic;
    • dromotropic;
    • tonotropically.

    These effects can be both positive and negative. Increased myocardial contractility is called a positive inotropic effect. A decrease in myocardial contractility is called a negative inotropic effect.

    For reference. The regulation of heart rate is carried out due to the chronotropic action (positive - an increase in heart rate, or negative - a decrease in heart rate).

    Bathmotropic effects are manifested in the effect on the excitability of the myocardium, dromotropic - in a change in the ability of the heart muscle to conduct.

    Regulation of the intensity of metabolic processes in the heart muscle is carried out through a tonotropic effect on the myocardium.

    How is myocardial contractility regulated?

    The impact of the vagus nerves causes a decrease in:

    • myocardial contractility,
    • action potential generation and propagation,
    • metabolic processes in the myocardium.

    That is, it has exclusively negative inotropic, tonotropic, etc. effects.

    The influence of sympathetic nerves is manifested by an increase in myocardial contractility, an increase in heart rate, an acceleration of metabolic processes, as well as an increase in the excitability and conductivity of the heart muscle (positive effects).

    Very important! It should be noted that myocardial contractility also largely depends on blood pressure.

    With reduced blood pressure, stimulation of a sympathetic effect on the heart muscle occurs, an increase in myocardial contractility and an increase in heart rate, due to which compensatory normalization of blood pressure is carried out.

    With an increase in pressure, a reflex decrease in myocardial contractility and heart rate occurs, which makes it possible to lower blood pressure to an adequate level.

    Significant stimulation also affects myocardial contractility:

    • visual,
    • auditory,
    • tactile,
    • temperature, etc. receptors.

    This causes a change in the frequency and strength of heart contractions during physical or emotional stress, being in a hot or cold room, as well as when exposed to any significant stimuli.

    Of the hormones, adrenaline, thyroxine and aldosterone have the greatest influence on myocardial contractility.

    The role of calcium and potassium ions

    Also, potassium and calcium ions can change the contractility of the heart. With hyperkalemia (an excess of potassium ions), there is a decrease in myocardial contractility and heart rate, as well as inhibition of the formation and conduction of the action potential (excitation).

    Calcium ions, on the contrary, contribute to an increase in myocardial contractility, the frequency of its contractions, and also increase the excitability and conductivity of the heart muscle.

    Drugs that affect myocardial contractility

    They have a significant effect on myocardial contractility. This group of drugs is able to have a negative chronotropic and positive inotropic effect (the main drug of the group is digoxin in therapeutic doses increases myocardial contractility). Due to these properties, cardiac glycosides are one of the main groups of drugs used in the treatment of heart failure.

    Also, SM can be affected by beta-blockers (reduce myocardial contractility, have negative chronotropic and dromotropic effects), Ca channel blockers (have a negative inotropic effect), ACE inhibitors (improve diastolic function of the heart, contributing to an increase in cardiac output in systole) and etc.

    What is dangerous violation of contractility

    Reduced myocardial contractility is accompanied by a decrease in cardiac output and impaired blood supply to organs and tissues. As a result, ischemia develops, metabolic disorders occur in tissues, hemodynamics are disturbed and the risk of thrombosis increases, heart failure develops.

    Attention! A sharply reduced global myocardial contractility is accompanied by a pronounced stagnation of blood in the pulmonary circulation, the appearance of severe shortness of breath (even at rest), hemoptysis, edema, and liver enlargement.

    When can SM be violated

    A decrease in SM can be observed against the background of:

    • severe atherosclerosis of the coronary vessels;
    • myocardial infarction and postinfarction cardiosclerosis;
    • (there is a sharp decrease in the contractility of the myocardium of the left ventricle);
    • acute myocarditis, pericarditis and endocarditis;
    • (the maximum violation of SM is observed when the adaptive capacity of the heart is depleted and cardiomyopathy is decompensated);
    • brain injury;
    • autoimmune diseases;
    • strokes;
    • intoxication and poisoning;
    • shocks (with toxic, infectious, pain, cardiogenic, etc.);
    • beriberi;
    • electrolyte imbalances;
    • blood loss;
    • severe infections;
    • intoxication with the active growth of malignant neoplasms;
    • anemia of various origins;
    • endocrine diseases.

    Violation of myocardial contractility - diagnosis

    The most informative methods for studying SM are:

    • standard electrocardiogram;
    • ECG with stress tests;
    • Holter monitoring;
    • ECHO-K.

    Also, to identify the cause of the decrease in SM, a general and biochemical blood test, a coagulogram, a lipidogram are performed, a hormonal profile is assessed, an ultrasound scan of the kidneys, adrenal glands, thyroid gland, etc. is performed.

    SM on ECHO-KG

    The most important and informative study is an ultrasound examination of the heart (estimation of ventricular volume during systole and diastole, myocardial thickness, calculation of minute blood volume and effective cardiac output, assessment of the amplitude of the interventricular septum, etc.).

    Assessment of the amplitude of the interventricular septum (AMP) is one of the important indicators of volume overload of the ventricles. AMP normokinesis ranges from 0.5 to 0.8 centimeters. The amplitude index of the posterior wall of the left ventricle is from 0.9 to 1.4 cm.

    A significant increase in amplitude is noted against the background of a violation of myocardial contractility, if patients have:

    • insufficiency of the aortic or mitral valve;
    • volume overload of the right ventricle in patients with pulmonary hypertension;
    • ischemic heart disease;
    • non-coronary lesions of the heart muscle;
    • heart aneurysms.

    Do I need to treat violations of myocardial contractility

    Myocardial contractility disorders are subject to mandatory treatment. In the absence of timely identification of the causes of SM disorders and the appointment of appropriate treatment, it is possible to develop severe heart failure, disruption of the internal organs against the background of ischemia, the formation of blood clots in the vessels with a risk of thrombosis (due to hemodynamic disorders associated with impaired CM).

    If the contractility of the myocardium of the left ventricle is reduced, then development is observed:

    • cardiac asthma with the appearance of a patient:
    • expiratory dyspnea (impaired exhalation),
    • obsessive cough (sometimes with pink sputum),
    • bubbling breath,
    • pallor and cyanosis of the face (possible earthy complexion).

    Attention. Violations of the SM of the right ventricle is accompanied by the appearance of shortness of breath, a decrease in working capacity and exercise tolerance, as well as the appearance of edema and an enlarged liver.

    Treatment of SM disorders

    All treatment should be selected by a cardiologist, in accordance with the cause of the SM disorder.

    To improve metabolic processes in the myocardium, drugs can be used:

    • riboxin,
    • mildronata,
    • L-carnitine,
    • phosphocreatine,
    • b vitamins,
    • vitamins A and E.

    Potassium and magnesium preparations (Asparkam, Panangin) can also be used.

    Patients with anemia are shown iron, folic acid, vitamin B12 preparations (depending on the type of anemia).

    If lipid imbalance is detected, lipid-lowering therapy may be prescribed. For the prevention of thrombosis, according to indications, antiplatelet agents and anticoagulants are prescribed.

    Also, drugs that improve the rheological properties of blood (pentoxifylline) can be used.

    Patients with heart failure may be prescribed cardiac glycosides, beta-blockers, ACE inhibitors, diuretics, nitrate preparations, etc.

    Forecast

    With timely detection of SM disorders and further treatment, the prognosis is favorable. In the case of heart failure, the prognosis depends on its severity and the presence of concomitant diseases that aggravate the patient's condition (postinfarction cardiosclerosis, heart aneurysm, severe heart block, diabetes mellitus, etc.).

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