Myocardial contractility is satisfactory. Aging of the cardiovascular system

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;
at acute infarction myocardium;
during heart surgery
with myocardial ischemia;
due to heavy toxic effects to 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 gradual decline quality of human life and can lead to his 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 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. Also held biochemical analysis blood and physiological testing, blood pressure measurement.

To assess the contractility of the myocardium, the effective cardiac output. 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 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. Can help in severe cases bed rest within 2-3 days.

Identification of a decrease in myocardial contractility by 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 fatty acids etc.), mimicking the “behavior” of the main metabolic substrates (glucose, fatty acids, etc.).

In patients IHD method PET allows non-invasive study of regional myocardial blood flow, glucose and fatty acid metabolism, and oxygen uptake. PET has proven to be an indispensable method in the diagnosis 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.

Echocardiographic study in patients with coronary artery disease allows to obtain 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 congestion in the veins great circle blood circulation and (indirectly) - the value 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 complex use 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. At the same time, one should keep in mind the strong dependence of EF on the magnitude of pre- and afterload: EF may decrease with hypovolemia (shock, acute blood loss etc.), a decrease in blood flow to the right heart, as well as 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) attitude maximum speeds(or rate 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 patients with CAD 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.

As recommended American Association 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 access along the short axis (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 abnormalities are given in Chapter 6. Patients with stable exertional angina who have had a previous MI may have echocardiographic evidence of a large-focal or (less commonly) 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 total number examined LV segments (n):

High values of this indicator in patients with MI or postinfarction cardiosclerosis are often associated with increased risk lethal outcome.

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(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 (TEPS). 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 PEES and dipyridamole or dobutamine tests are more convenient, since all studies are carried out in the horizontal position of the patient.

Sensitivity and specificity of stress echocardiography in 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, is widely used in Lately 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. However, it should be borne in mind that with more high doses dobutamine aggravated signs of myocardial ischemia and contractility falls 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 coronary vessels contrast agent. Being the “gold standard” in the diagnosis of coronary artery disease, coronary angiography makes it possible to determine the nature, localization 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 IHD (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 defects hearts requiring surgical correction;
patients with obliterating atherosclerosis arteries lower extremities directed to surgery;
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;
at severe violations ventricular rhythm.

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). At the mouth of the right and left CA, 5–10 ml of a radiopaque substance are injected, and X-ray film or video recording 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%;

V. III degree - more than 75%;

d. IV degree - occlusion of the CA.

Left anatomical type 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, rear wall PP, 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 common (about 80-85% of cases) 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 coronary angiography contrast agent is sequentially introduced 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 ischemic damage 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, to pump more blood with increasing loads, respectively, 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 long time exposes himself to excessive physical exertion that exhausts the body, over time, a decrease in the contractile function of the myocardium can 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, 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 is 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 appoint 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 disorder is a heart or vascular disease, treat in the first place will be his. Only then, after re-diagnosis, electrocardiography, will they make a conclusion about the success of therapy.

What is myocardial contractility normokinesis

When the doctor examines the 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 on this moment.

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

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, to pump more blood with increasing loads, respectively, to supply all organs with the right amount of nutrients, ensuring their correct uninterrupted operation.

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 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

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:

phosphocreatine;
riboxin;
panangin or asparkam;
iron preparations;
mother's milk.

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

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.

In contact with

Myocardial contractility

Progressive myocardial sclerosis, focal atrophy of muscle fibers with symptoms of protein-lipoid dystrophy, nested hypertrophy of muscle fibers, dilatation of the heart are the main morphological features old heart.

One of the main reasons for the development of dystrophic and atrophic changes in the myocardium during aging is a violation of energy processes, the development of hypoxia.

With aging, the intensity of tissue respiration of the myocardium decreases, the conjugation of oxidation and phosphorylation changes, the number of mitochondria decreases, their degradation occurs, the activity of individual links of the respiratory chain changes unevenly, the glycogen content decreases, the concentration of lactic acid increases, the intensity of glycolysis is activated, the amount of ATP and CP decreases, falls activity creatine phosphokinase (CPK).

It is known that myocardial contractility is controlled by a variety of mechanisms, the most important of which are the Frank-Starling mechanism and direct inotropism, which is closely related to the adrenergic effect on the heart. At the same time, it has been shown that the Frank-Starling mechanism suffers significantly with age.

This is associated with a decrease in the elasticity of muscle fibrils as such, with an increase in low-elastic connective tissue, with the appearance of atrophic changes and hypertrophy of individual muscle fibers, as well as with changes within the actomyosin complex itself.

It should also be noted that there is a violation of the properties of myocardial contractile proteins, a change in the actomyosin complex. Bing (Bing, 1965) believes that the aging heart gradually loses the ability to translate into mechanical work the energy received in the process of its formation.

The author found a decrease in the contractile capacity of actomyosin filaments in old people. In addition, it was noted that the amount of myofibrillar proteins decreases with age. Undoubtedly, all these changes can cause functional insufficiency myocardium.

Doc (Dock, 1956) as one of the reasons for the violation of myocardial contractility in old age sees a violation of mineral metabolism, in particular excess accumulation Na+ ions. According to Burger (Burger, 1960), with age, the content of water, K+ and Ca2+ ions in the heart muscle decreases. Michel (1964) indicates that a change in the chemical environment (transmineralization, a decrease in energy-rich phosphates) proceeds in parallel with the limitation of myocardial contractility, its compensatory capacity.

It has been shown that with age the content of the intracellular Na+ ion increases, while the content of the K+ ion decreases. The repolarization phase of AP is lengthened in this case. It is known that the depolarization wave, propagating along the outer membrane of the muscle cell, also captures the T-tubular system and penetrates into the elements sarcoplasmic reticulum (SR), which causes the release of calcium from the SPR tanks.

The calcium "volley" leads to an increase in the concentration of the Ca2+ ion in the sarcoplasm, as a result of which the Ca2+ ion enters the myofibrils and binds there to the Ca2+ reactive protein troponin. Due to the elimination of tropomyosin repression, actin and myosin interact, i.e., contraction.

The onset of subsequent relaxation is determined by the rate of reverse transport of the Ca2+ ion in the SPR, which is carried out by the system of transport Ga-Mg-dependent ATP-ase and requires a certain amount of energy consumption. A change in the K+/Na+ ratio can affect the state of the potassium-sodium pump.

It can be assumed that the resulting changes in the K + / Na + ratio and disturbances in the calcium pump can significantly impair myocardial contractility and diastolic relaxation of the heart in old age.

In addition, in old animals, changes were also detected in the SPR - thickening and compaction of the T-karals system, a decrease in their specific gravity in the cell, there is an increase in contacts between the sarcolemma and vesicles of the SPR, which, as is known, provide the optimal rate of exit and entry of the Ca2+ ion into the SPR. Under these conditions, the optimal possibilities for the implementation of systole and diastole are violated, especially with functional stress.

As is known, the synchronization of the activity of individual muscle cells is essential in ensuring the contractility of the heart. It is largely determined by the state of the intercalated discs, i.e., the place of contact of individual myocardial cells. At the same time, in an experiment on old animals (Frolkis et al., 1977b), when applying a load, a distinct broadening of these disks was found - with a 3-4-fold increase in the distance between them.

This causes difficulty in conducting excitation between individual cells, disruption of the synchronization of their contraction, lengthening of systole and a decrease in contractility. At the same time, the synchronization of the processes of contraction of individual myocardial fibers depends on the adrenergic influence. Hence, the observed weakening of adrenergic influences on the heart in old age (Verkhratsky, 1963; Shevchuk, 1979) can aggravate the disturbance of inotropic mechanisms, as well as the synchronization of contractions of myocardial fibers.

In addition, with age, the effect of the direct inotropic effect of the sympathetic nervous system to the myocardium. All this limits the mobilization of energy processes and contributes to the development of heart failure with an increase in the load on the heart.

The decrease in myocardial contractility with age, even at rest, is evidenced by numerous data obtained in the study of cardiac activity using various methods studies (analysis of the phase structure of the cardiac cycle, ballistocardiography, electrocardiography, rheocardiography, echocardiography, etc.).

A decrease in myocardial contractility is especially clearly detected in the elderly and old people in conditions of strenuous activity. Under the influence of functional loads (muscle activity, injection of adrenaline, etc.), elderly and old people often experience energy-dynamic myocardial insufficiency.

The decrease in myocardial contractility with age also reflects the volumetric and linear ejection velocity, the initial growth rate of intraventricular pressure, the values of which naturally decrease with age (Korkushko, 1971; Tokar, 1977).

In the elderly and old people, the work of the heart decreases (Tokar, 1977; Strandell, 1976). Of the presented in table. 27 data shows that in old animals of different species, compared with young animals, the maximum rate of increase in intraventricular pressure, the maximum rate of shortening of myocardial fibers, the contractility index, and the intensity of functioning of myocardial structures decrease.

Phase structure of the cardiac cycle

With age, the phase structure of the activity of the heart also changes. According to Korkuszko (1971) and Turner (1977), in elderly and old people, there is an elongation of the electromechanical systole of the left ventricle of the heart, mainly due to an increase in the period of tension.

This direction of the shift depends on the increase in the phase of isometric contraction (the phase of increase in intraventricular pressure), while the phase of asynchronous contraction (transformation) does not change significantly with age. This is especially clearly seen from the calculation of the intrasystolic index of the isometric contraction phase.

The period of ejection in people at the age of 60 years is most often shortened, which should be related to the decrease in cardiac output usually observed at this age. At the same time, an increase in the phase of rapid expulsion of blood and a shortening of the phase of slow expulsion are revealed.

Such a redistribution in the phase structure - a prolongation of the rapid ejection phase, can be associated with a decrease in myocardial contractility in the presence of increased peripheral vascular resistance. The prolongation of the fast ejection phase and the shortening of the slow ejection are also confirmed when registering a rheogram and an electrokymogram with ascending department aorta and its arches.

The calculation of the ratio of the period of exile to the period of tension (Blumberger coefficient) indicates that the work spent directly on the ejection of blood from the left ventricle during systole requires more myocardial tension and is performed over a longer period of time.

The diastolic period of the cardiac cycle also undergoes age-related restructuring - the period of isometric relaxation and the phase of rapid filling are lengthened with a relative shortening general period filling.

Peripheral circulation

In large arterial trunks with aging, sclerotic thickening of the intima, the inner membrane, atrophy of the muscle layer, and a decrease in elasticity develop. According to Garis (Harris, 1978), the elasticity of large arterial vessels in people aged 70 years is halved compared to that in people 20 years of age.

Venous vessels are also subject to significant restructuring. However, changes in the veins are much less pronounced than in the arteries (Davydovsky, 1966). According to Burger (Burger, 1960), the physiological sclerosis of the arteries is weakened towards the periphery.

However, ceteris paribus, changes in the vascular system are more pronounced in the lower extremities than in the upper ones. At the same time, the changes are more significant on the right hand than on the left (Hevelke, 1955). The loss of elasticity of arterial vessels is also evidenced by numerous data related to the study of the velocity of propagation of the pulse wave.

It has been noted that with increasing age there is a regular acceleration of the propagation of the pulse wave through large arterial vessels (Korkushko, 1868b; Tokar, 1977; Savitsky, 1974; Burger, 1960; Harris, 1978). An increase in the speed of propagation of the pulse wave through arterial vessels with age is observed to a greater extent in the vessels of the elastic type - the aorta (Se), and in the sixth decade this indicator already begins to prevail over the velocity of propagation of the pulse wave through the vessels of the muscular type (Sm), which is reflected in a decrease in the SM/SE ratio.

With age, the total elastic resistance (E0) of the arterial system also increases. As is known, due to the elasticity of the aorta, arteries, a significant part of the kinetic energy during systole is converted into potential energy of the stretched vascular walls, which makes it possible to transform an intermittent blood stream into a continuous one.

Thus, sufficient elasticity of the vessels makes it possible to distribute the energy released by the heart for the entire period of its activity, and thus the most favorable conditions for the work of the heart are created. However, these conditions change significantly with age. First of all, and to a greater extent, the large arterial vessels of the systemic circulation, especially the aorta, change, and only at older ages does the elasticity of the pulmonary artery and its large trunks decrease.

As already mentioned above, as a result of the loss of elasticity of large arterial trunks, a large percentage of the energy is expended by the heart to overcome the resistance that prevents the outflow of blood, and to increase pressure in the aorta. In other words, the activity of the heart becomes less economical with age.

It's confirmed the following facts(Korkushko, 1968a, 1968b, 1978). In the elderly and old, in comparison with young people, there is an increased expenditure of energy by the left ventricle of the heart. For a group of people aged 20–40 years, this indicator is 11.7 ± 0.17 W; for the seventh decade, 14.1 ± 0.26; for the tenth, 15.3 ± 0.57 W (p
It is noted that the increase in energy consumption by the left ventricle goes to perform the least productive part of the work of the heart - overcoming the resistance of the vascular system. This position characterizes the ratio of the total elastic resistance of the arterial system (E0) to the total peripheral vascular resistance (W). With age, this E0/W ratio naturally increases, averaging 0.65 ± 0.075 for 20–40 years old, 0.77 ± 0.06 for the seventh decade, 0.86 ± 0.05 for the eighth decade, 0.93 ± 0.04 for the ninth decade, and 1.09 ± 0.075 for the tenth decade. .

Along with the increase in stiffness of the arterial vessels, loss of elasticity, there is an increase in the volume of the arterial elastic reservoir, especially the aorta, which to a certain extent compensates for its function.

However, it should be emphasized that such a mechanism is inherently passive and is associated with a long-term effect of stroke volume on the aortic wall, which has lost its elasticity. However, in more late age an increase in volume does not go hand in hand with a decrease in elasticity, and therefore the function of the elastic reservoir is impaired.

This conclusion is valid not only for the aorta, but also for the pulmonary artery. Moreover, the loss of elasticity of large arterial vessels impairs the adaptive capacity of the pulmonary and systemic circulation to sudden and significant overloads.

With age, the total peripheral vascular resistance increases both in humans and in animals of different species (Table 27). Moreover, these changes are associated not only with functional changes (in response to a decrease in cardiac output), but also with organic ones due to sclerosis, a decrease in the lumen of small peripheral arteries.

Thus, the progressive decrease in the lumen of small peripheral arteries, on the one hand, reduces blood supply and, on the other hand, causes an increase in peripheral vascular resistance. It should be noted that the same type of changes in the total peripheral vascular resistance hides a different topography of shifts in regional tone.

N.I. Arinchin, I.A. Arshavsky, G.D. Berdyshev, N.S. Verkhratsky, V.M. Dilman, A.I. Zotin, N.B. Mankovsky, V.N. Nikitin, B.V. Pugach, V.V. Frolkis, D.F. Chebotarev, N.M. Emanuel

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

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.

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.

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

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).

Identification 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.

Myocardial contractility

Our body is designed in such a way that if one organ is damaged, the whole system suffers, as a result, this entails a general exhaustion of the body. The main organ in human life is the heart, which consists of three main layers. One of the most important and susceptible to damage is the myocardium. This layer is a muscle tissue, which consists of transverse fibers. It is this feature that allows the heart to work many times faster and more efficiently. One of the main functions is the contractility of the myocardium, which may decrease over time. It is the causes and consequences of this physiology that should be carefully considered.

The contractility of the heart muscle decreases with ischemia of the heart or myocardial infarction

It must be said that our cardiac organ has a fairly high potential in the sense that it can increase blood circulation if necessary. Thus, this can occur during normal sports, or during heavy physical labor. By the way, if we talk about the potential of the heart, then the volume of blood circulation can increase up to 6 times. But, it happens that myocardial contractility falls by various reasons, this already speaks of its reduced capabilities, which should be diagnosed in time and the necessary measures taken.

Reasons for the decline

For those who do not know, it should be said that the functions of the myocardium of the heart represent a whole algorithm of work that is not violated in any way. Due to the excitability of cells, the contractility of the heart walls and the conductivity of the blood flow, our blood vessels receive a portion of useful substances, which is necessary for full performance. Myocardial contractility is considered satisfactory when its activity increases with increasing physical activity. It is then that we can talk about full health, but if this does not happen, you should first understand the reasons for this process.

It is important to know that decreased contractility of muscle tissue may be due to the following health problems:

avitaminosis;
myocarditis;
cardiosclerosis;
hyperthyroidism;
increased metabolism;
atherosclerosis, etc.

So, there can be a lot of reasons for reducing the contractility of muscle tissue, but the main one is one. With prolonged physical exertion, our body may not get enough of not only the necessary portion of oxygen, but also the amount of nutrients that is necessary for the life of the body, and from which energy is produced. In such cases, first of all, internal reserves are used, which are always available in the body. It is worth saying that these reserves are not enough for a long time, and when they are exhausted, an irreversible process occurs in the body, as a result of which cardiomyocytes (these are the cells that make up the myocardium) are damaged, and the muscle tissue itself loses its contractility.

In addition to the fact of increased physical exertion, reduced contractility of the left ventricular myocardium may occur as a result of the following complications:

severe brain damage;
a consequence of an unsuccessful surgical intervention;
diseases associated with the heart, for example, ischemia;
after myocardial infarction;
a consequence of toxic effects on muscle tissue.

It must be said that this complication can greatly spoil the quality of human life. In addition to a general deterioration in human health, it can provoke heart failure, which is not a good sign. It should be clarified that myocardial contractility must be maintained under all circumstances. To do this, you should limit yourself to overwork during prolonged physical exertion.

Some of the most noticeable are the following signs of reduced contractility:

fast fatiguability;
general weakness of the body;
fast weight gain;
rapid breathing;
swelling;
attacks of nocturnal suffocation.

Diagnosis of reduced contractility

At the first of the above signs, you should consult a specialist, in no case should you self-medicate, or ignore this problem, since the consequences can be disastrous. Often, to determine the contractility of the myocardium of the left ventricle, which can be satisfactory or reduced, a conventional ECG is performed, plus echocardiography.

Echocardiography of the myocardium allows you to measure the volume of the left ventricle of the heart in systole and diastole

It happens that after an ECG it is not possible to make an accurate diagnosis, then the patient is prescribed Holter monitoring. This method allows a more precise conclusion to be drawn. constant surveillance electrocardiograph.

In addition to the above methods, the following apply:

ultrasound examination (ultrasound);
blood chemistry;
blood pressure control.

Methods of treatment

In order to understand how to conduct treatment, you first need to conduct qualified diagnostics which will determine the degree and form of the disease. For example, global contractility of the left ventricular myocardium should be eliminated using classical methods of treatment. In such cases, experts recommend drinking medications that help improve blood microcirculation. In addition to this course, drugs are prescribed, with the help of which it is possible to improve the metabolism in the heart organ.

Medicinal substances are prescribed that regulate the metabolism in the heart and improve blood microcirculation

Of course, in order for the therapy to have the proper result, it is necessary to get rid of the underlying disease that caused the disease. In addition, when it comes to athletes, or people with increased physical workload, here, for starters, you can get by with a special regimen that limits physical activity and recommendations for daytime rest. In more severe forms, bed rest is prescribed for 2-3 days. It is worth saying that this violation can be easily corrected if diagnostic measures are taken in time.

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What is myocardial contractility and what is the danger of reducing its contractility

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, of which 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 of, for example, heart failure and not only. Therefore, if you experience symptoms of impaired contractility, you should consult a doctor.

Features of the myocardium

The myocardium has a number of physical and physiological properties allowing 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.

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.

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 (LS)) and relax during diastole.

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

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

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.

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?

Impact vagus nerves causes a decrease:

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).

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:

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.

from hormones, greatest influence myocardial contractility is affected by adrenaline, thyroxine and aldosterone.

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

Preparations of cardiac glycosides have a significant effect on myocardial contractility. This group drugs can have a negative chronotropic and positive inotropic effect (the main drug of the group - 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), 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.

When can SM be violated

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

myocardial hypoxia;
coronary disease hearts;
severe atherosclerosis of the coronary vessels;
myocardial infarction and postinfarction cardiosclerosis;
aneurysms of the heart (observed a sharp decline contractility of the myocardium of the left ventricle);
acute myocarditis, pericarditis and endocarditis;
cardiomyopathies (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

Most informative methods SM studies 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 volumetric 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 the risk of thrombosis (due to hemodynamic disorders associated with impaired SM).

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).

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:

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

Patients with anemia are shown iron supplements, folic acid, vitamin B12 (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 violations of the CM 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 aggravating the patient's condition (postinfarction cardiosclerosis, heart aneurysm, severe heart block, diabetes mellitus, etc.).

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Myocardial contractility: concept, norm and violation, treatment of low

The heart muscle is the most enduring in the human body. The high performance of the myocardium is due to a number of properties of myocardial cells - cardiomyocytes. 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 it that carries out the most great job ejection of blood, and this work is evaluated 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 the 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 serious illness myocardium. 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 contraction of the atria and ventricles (PQRST) have right kind, without changing 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 the 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 on ultrasound of the heart is assessed based on the quality of the reflection 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 myocardial contractility is within the normal range according to the ultrasound of the heart, but the patient has a number of complaints from the heart (pain, shortness of breath, swelling, etc.), the patient is shown to undergo 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:

Myocardial hypoxia in ischemic heart disease,
Necrosis (death) of cardiomyocytes in acute myocardial infarction,
Scar formation in postinfarction cardiosclerosis and LV aneurysm,
Acute myocarditis is an inflammation of the heart muscle caused by infectious agents (bacteria, viruses, fungi) or autoimmune processes (systemic lupus erythematosus, rheumatoid arthritis and etc),
Postmyocardial cardiosclerosis,
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 more harmless reasons a decrease in myocardial contractility can be noted beriberi, myocardial dystrophy (with general exhaustion of the body, with dystrophy, anemia), as well as acute infectious diseases.

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 clinical symptoms the patient has those that are characteristic of a particular pathology. 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. Heart rhythm disturbances are common atrial fibrillation and ventricular extrasystole), as well as syncope (fainting) conditions due to low cardiac output, and, as a result, a small 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?

Speaking of what are the consequences given state, 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 myocardial infarction, 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 causative disease significantly improves prognosis, and patient survival increases.

Myocardial contractility is normal

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Indicators of myocardial contractility

Along with changes in the performance of the heart, due to circumstances external to the myocardium (the value of venous blood return and end-diastolic pressure, i.e. preload; pressure in the aorta, i.e. afterload), from a practical point of view, it is essential to identify those shifts in pumping functions that are determined by their own myocardial circumstances (metabolic features, elastic-viscous properties of the muscle, etc.). These "internal" properties for the myocardium are called the inotropic state, or contractility. Thus, myocardial contractility should be understood as the ability to develop a certain force and speed of contractions without changing the initial length of the fiber. This ability is determined by the properties of myocardial cells, which depend mainly on the amount of energy consumed. We emphasize that when implementing the “length-tension” dependence or the Starling mechanism, the use of the concept of contractility is not well justified, since the initial length of the muscle fiber changes in this case.

Own myocardial energy-dynamic circumstances determine not only the strength and speed of myocyte contraction, but also the speed and depth of muscle fiber relaxation after contraction.

By analogy with the concept of contractility, this ability should be called the “relaxation” of the myocardium. Taking into account a certain conditionality of such a division of concepts (contraction and relaxation are two phases of a single process), along with the absence of ideas about “relaxation” in physiological terminology, we considered it possible to describe the formulas for calculating relaxation characteristics in the same chapter.

It is generally accepted that the relationship between pressure in the ventricular cavity and the rate of its change during isovolumic (isometric) contraction is in good agreement with the force-velocity relationship. Thus, one of the criteria for myocardial contractility is the maximum rate of increase in intraventricular pressure in the phase of isometric contraction (dp / dt max), since this indicator does not depend much on changes in blood flow (i.e., load "at the entrance") and on pressure in aorta (i.e. loads "at the exit"). Usually dp / dt max is recorded when measuring intraventricular pressure under conditions of catheterization of its cavity (Fig. 6). Since dp / dt max is the first derivative of pressure, this indicator is recorded using a differentiating RC chain.

In the absence of the latter, it is possible to calculate the average rate of pressure increase in the ventricle in the phase of isometric contraction (dp / dt av.) according to the intraventricular pressure curve (Fig. 7.):

Line S 1 is drawn, based on the FCG recording, along the first high-frequency oscillation of the first tone, and line X is drawn from the point where the blood pressure rises. From Fig. 7 it becomes clear that the point of intersection of the line X with the intraventricular pressure curve reflects the value of the end-isometric pressure, and the interval S 1 - X is the duration of the isometric contraction phase. Thus:

However, taking into account the fact that the end-isometric intraventricular pressure is almost equal to the diastolic pressure in the aorta (see Fig. 7), it is possible to do without catheterization of the heart cavities, calculating the indicator using the formula:

Taking into account the closeness of the values of diastolic pressure in the aorta and the brachial artery, in (129), one can use the DD value determined by the Korotkov method. Finally, often in clinical practice, not the value of diastolic pressure is used, but the approximate value of the "developed" pressure in the isometric phase, for which the conditional value of the left ventricular end-diastolic pressure, which is taken as 5 mm Hg, is subtracted from the diastolic pressure. Then the formula becomes:

Formula (130) is the most convenient, and the resulting value is close to true value average rate of pressure increase.

For the right ventricle, the average rate of pressure increase in the isometric contraction phase is calculated by the formula:

where DD l.a. - diastolic pressure in the pulmonary artery; KDD p.pr. - end-diastotic pressure in the right atrium; FIS pr.zhel. - phase of isometric contraction of the right ventricle.

Taking into account the small value of QDD a.p., it can be neglected, then the formula is simplified (Dastan, 1980):

Myocardial contractility also reflects the magnitude of intraventricular pressure in systole. Taking into account the fact that the end-systolic pressure in the right ventricle corresponds approximately to the systolic pressure in the pulmonary artery, and the increase in pressure occurs in the phase of isometric contraction and partially in the phase of rapid expulsion, L.V. ventricle (SSPD) according to the formula:

The state of myocardial contractility can also be judged by two simple indicators contractility (PS). Their calculation also requires only data on diastolic pressure and systole phase structure:

Both of these figures are closely correlated with dp/dt max.

Finally, the contractility of the myocardium to some extent can be represented by the ratio of the temporal characteristics of systole. The calculated value is called the temporary indicator of contractility (TTS).

FBI - the duration of the phase of rapid expulsion of blood.

In view of the fact that a number of researchers consider the influence of the volume load “at the input” and the load with the resistance “at the output” on the value of dp / dt max to be significant, and thus cast doubt on the height of the information content of this parameter as an indicator of contractility, a significant number of different indices have been proposed contractility (ISM).

ISM according to Veragut and Kraienbühl:

where VZhD - intraventricular pressure at the time of the peak of the first derivative.

ISM according to Singel and Sonnenblick:

where II T is the integral isometric stress, calculated as the area of a triangle bounded by the pressure rise curve, perpendicular from the point maximum pressure in the isometric phase and a horizontal straight line at the level of end-diastolic pressure.

where CPIP is the pressure developed in the isometric phase, i.e. difference between end-isometric and end-diastolic pressures in the ventricle.

what is the time from ECG R wave to peak dp/dt max.

The “internal contractility index” described by Tully et al. is similar. as time from ECG Q wave to peak dp/dt max. According to these authors, there is a close correlation of this parameter with the value of the index dp/dt max / VZhD, and the decrease in time T - dp/dt max reflects an increase in contractility.

However, changes in indices 4 and 5 are usually considered together with changes in the value of dp/dt max. Indexes, apparently, are intended to be used only for dynamic observation in the same patient.

Frank-Levinson contractility index:

where r is the end-diastolic radius of the left ventricle, calculated from the end-diastolic volume. The use of the concept of "radius" is based on the conditional assumption that at the end of the isometric phase the left ventricle is spherical and its circumference is 2 Pg.

The rate of shortening of the contractile element (Use) can be calculated with a certain degree of error by the formula proposed by Levin et al.:

However, all the above indices to some extent characterize only one of the aspects of the concept of contractility, namely, related to the magnitude of stress, i.e. strength. According to similar data (M.P. Sakharov et al., 1980), the contractility of the myocardium layout can be assessed based on the analysis of its two main components of its sides or characteristics (strength and speed). The strength characteristic of contractility reflects the maximum possible value of isometric (isovolumic) pressure in the ventricle (Pm), and the velocity characteristic - the maximum possible blood flow velocity in the exile phase in the absence of counterpressure in the aorta (IM). With a certain degree of error, both of these characteristics can be calculated without catheterization of the heart and aorta in a non-invasive examination:

where K - regression coefficient = 0.12; DD - diastolic blood pressure; T ex. - duration of the period of exile; FIS - duration of the isometric contraction phase; Rho - regression coefficient = 400 mm Hg.

where a is the shape factor of the blood flow curve = 1.8; MCV - minute volume of blood; MS - mechanical systole; SD - systolic blood pressure; Rm - force characteristic of contractility, calculated according to (143).

In conclusion, it should be pointed out that recently serious doubts have appeared that it is theoretically possible in principle to express myocardial contractility in the form of a calculated index that does not depend on changes in the initial length of the muscle fiber. In practice, the characteristic of the contractility of the heart muscle, determined by internal, myocardial causes proper, is of great importance, little dependent on the external conditions of pre- and afterload. For a practitioner, it is important to establish the cause of a decrease in the performance of the heart, i.e. statement of the role of changes in pressure in the aorta, end-diastolic pressure, or violation of the intrinsic contractile properties of the myocardium. In solving such practical task calculation of contractility indices provides invaluable assistance.

The ability of the ventricular myocardium to relax can first of all be judged by the maximum rate of intraventricular pressure drop in the isometric relaxation fzz (-dp/dt max), a directly recorded chain in the form of negative peaks of the curve (see Fig. 6). It is also possible to calculate the average rate of pressure drop (-dp/dt cf.) by analogy with the formula for calculating contractility (130).

where FIR is the duration of the isometric relaxation phase.

The rate of relaxation is also indicated by the temporal index of myocardial relaxation (VLR) and the volumetric relaxation index (VR).

where PND is the duration of the filling period, FBN is the fast filling phase.

where EDV is the end-diastolic volume and ESV is the end-systolic volume of the ventricle.

Similar to contractility indices, myocardial relaxation indices (IR) can be calculated.

According to F. Z. Meyerson (1975):

where CPIP is the developed pressure in the ventricle.

Simplified relaxation indices:

Based on the principles described above, a significant number of other formulas for calculating relaxation indices can be derived, however, like contractility indices, all IRs without exception give only an approximate idea of the myocardial ability to relax, and therefore it is advisable to use not one, but several IRs.

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

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.

Diagnostics

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

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).

Myocardial contractility

The contractility of the heart muscle decreases with ischemia of the heart or myocardial infarction

It must be said that our cardiac organ has a fairly high potential in the sense that it can increase blood circulation if necessary. Thus, this can occur during normal sports, or during heavy physical labor. By the way, if we talk about the potential of the heart, then the volume of blood circulation can increase up to 6 times. But, it happens that myocardial contractility falls for various reasons, this already indicates its reduced capabilities, which should be diagnosed in time and the necessary measures taken.

Reasons for the decline

It is important to know that decreased contractility of muscle tissue may be due to the following health problems:

avitaminosis;
myocarditis;
cardiosclerosis;
hyperthyroidism;
increased metabolism;
atherosclerosis, etc.

In addition to the fact of increased physical exertion, reduced contractility of the left ventricular myocardium may occur as a result of the following complications:

severe brain damage;
a consequence of an unsuccessful surgical intervention;
diseases associated with the heart, for example, ischemia;
after myocardial infarction;
a consequence of toxic effects on muscle tissue.

Some of the most noticeable are the following signs of reduced contractility:

Diagnosis of reduced contractility

Echocardiography of the myocardium allows you to measure the volume of the left ventricle of the heart in systole and diastole

It happens that after an ECG it is not possible to make an accurate diagnosis, then the patient is prescribed Holter monitoring. This method allows you to make a more accurate conclusion, with the help of constant monitoring of the electrocardiograph.

In addition to the above methods, the following apply:

ultrasound examination (ultrasound);
blood chemistry;
blood pressure control.

Methods of treatment

In order to understand how to carry out treatment, first you need to conduct a qualified diagnosis, which will determine the degree and form of the disease. For example, global contractility of the left ventricular myocardium should be eliminated using classical methods of treatment. In such cases, experts recommend drinking medications that help improve blood microcirculation. In addition to this course, drugs are prescribed, with the help of which it is possible to improve the metabolism in the heart organ.

Medicinal substances are prescribed that regulate the metabolism in the heart and improve blood microcirculation

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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 method in the diagnosis 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

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.

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.

Assessment of violations of regional contractility of the left ventricle

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 (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).

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).

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.

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, localization 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

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.

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.

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%;

V. 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.

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 pools. 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).

The degree of CA narrowing also has an important prognostic value. Narrowing of the lumen of the coronary arteries by 70% or more is considered hemodynamically significant. Stenosis of the coronary artery up to 50% is regarded as hemodynamically insignificant. However, it should be borne in mind that the specific clinical manifestations of coronary artery disease depend not only on the degree of narrowing of the coronary artery, but also on many other factors, for example, on the degree of development of collateral blood flow, the state of the hemostasis system, autonomic regulation of vascular tone, propensity to spasm of the coronary arteries, etc. In other words, even with a relatively small narrowing of the CA or in its absence (according to CAG), under certain circumstances, extensive acute MI can develop. On the other hand, it is not uncommon for a well-developed network collateral vessels even complete occlusion of one CA for a long time may not be accompanied by the onset of MI.

Character score collateral circulation has, therefore, an important diagnostic value. Usually, with a significant and widespread lesion of the coronary artery and a long course of coronary artery disease, a well-developed network of collaterals is detected in CAH (see Fig. 5.39), while in patients with a “short” ischemic history and stenosis of one coronary artery, collateral circulation is less pronounced. The latter circumstance is of particular importance in cases of sudden thrombosis, accompanied, as a rule, by the occurrence of widespread and transmural necrosis of the heart muscle (for example, in relatively young patients with coronary artery disease).

Selective angiocardiography of the left ventricle (left ventriculography) is part of the protocol for an invasive study of patients with coronary artery disease referred for surgery myocardial revascularization. It complements the results of CAG and allows for a quantitative assessment of organic and functional disorders LV. Left ventriculography can:

detect regional disorders of LV function in the form of local limited areas of akinesia, hypokinesia and dyskinesia;
diagnose LV aneurysm and assess its location and size;
identify intracavitary formations (parietal thrombi and tumors);
objectively assess the LV systolic function based on the invasive determination of the most important hemodynamic parameters (EF, ESV, EDV, SV, MO, SI, SI, average speed circular shortening of fibers, etc.);
evaluate the state of the valvular apparatus of the heart, including congenital and acquired pathological changes in the aortic and mitral valves, which may affect the results of surgical myocardial revascularization.

Local disorders of LV contractility are an important sign of focal myocardial damage, the most characteristic of IHD. To identify LV asynergy ventriculograms are recorded during systole and diastole, quantitatively assessing the amplitude and nature of the movement of the wall of various LV segments. On fig. 5.42 shows an example local disturbance ventricular contractility in a patient with coronary artery disease. The most common causes of LV "asynergy" in patients with stable exertional angina are cicatricial changes heart muscle after myocardial infarction, as well as severe myocardial ischemia, including “hibernating” and “stunned” myocardium.

To calculate hemodynamic parameters, quantitative processing of images of the left ventricular cavity recorded in one of the projections at the end of systole and diastole is carried out. The calculation methodology is described in detail in Chapter 6.

Treatment of patients with stable exertional angina should be directed to:

1. Elimination or reduction of symptoms of the disease, primarily angina attacks.

2. Increasing tolerance to physical activity.

3. Improving the prognosis of the disease and preventing the occurrence unstable angina, MI and sudden death.

To achieve these goals, a complex of therapeutic and preventive measures is used, including non-drug, drug and, if necessary, surgical treatment and providing for an active impact on the main links in the pathogenesis of coronary artery disease:

antiplatelet therapy (prevention of platelet aggregation and parietal thrombosis);
antianginal (antiischemic) drugs (nitrates and molsidomine, b-blockers, slow calcium channel blockers, etc.);
the use of cytoprotectors;
treatment and prevention of progression of LV dysfunction;
drug and non-drug correction of the main risk factors for coronary artery disease (HLP, hypertension, smoking, obesity, carbohydrate metabolism disorders, etc.);
if necessary - treatment and prevention of rhythm and conduction disorders;
radical surgical elimination of CA obstruction (myocardial revascularization).

Currently, the positive impact of most of the listed directions and methods of treatment on the prognosis of coronary artery disease and the incidence of unstable angina, myocardial infarction and sudden death has been proven.

Antiplatelet therapy is carried out to prevent "exacerbations" of coronary artery disease, as well as the occurrence of unstable angina and myocardial infarction. It is aimed at preventing parietal thrombosis and, to a certain extent, at maintaining the integrity fibrous membrane atherosclerotic plaque.

It has been repeatedly mentioned above that the basis of the “exacerbations” of IHD and the occurrence of unstable angina pectoris (UA) or MI is the rupture of an atherosclerotic plaque in the coronary artery with the formation on its surface, first of a platelet (“white”), and then a fibrin (“red”) parietal thrombus. The initial stage of this process, associated with platelet adhesion and aggregation, is described in detail in section 5.2. A simplified diagram of this process occurring on the surface of an atherosclerotic plaque is shown in Fig. 5.43.

Recall that as a result of atherosclerotic plaque rupture, subendothelial tissue structures and the lipid core of plaques, the contents of which fall on the surface of the gap and into the lumen of the vessel. The exposed components of the connective tissue matrix (collagen, von Willebrand factor, fibronectin, liminin, vitronectin, etc.), as well as lipid core detritus containing tissue thromboplastin, activate platelets. The latter, with the help of glycoprotein receptors (Ia, Ib) located on the surface of platelets, and von Willebrand factor, adhere (adhere) to the surface of the damaged plaque, forming here a monolayer of platelets loosely associated with the damaged endothelium.

Activated and reshaped platelets release inducers of subsequent explosive self-accelerating aggregation: ADP, serotonin, platelet factor 3 and factor 4, thromboxane, adrenaline, etc. (“release reaction”). At the same time, the metabolism of arachidonic acid is activated and, with the participation of the enzymes cyclooxygenase and thromboxane synthetase, thromboxane A 2, which also has a powerful aggregating and vasoconstrictor action.

As a result, a second wave of platelet aggregation occurs and a platelet aggregate (“white” thrombus) is formed. It should be remembered that during this stage of aggregation, platelets tightly bind to each other with the help of fibrinogen molecules, which, interacting with platelet IIb / IIIa receptors, tightly “stitch” platelets together. At the same time, with the help of von Willebrand factor, platelets attach to the underlying subendothelium.

Subsequently, the coagulation system of hemostasis is activated and a fibrin thrombus is formed (see Chapter 6).

Thus, adhesion and aggregation of platelets is the first initial stage of thrombosis, the most important links of which are:

the functioning of specific platelet receptors (Ia, Ib, IIb / IIIa, etc.), which provide adhesion and final aggregation of platelets, and
activation of arachidonic acid metabolism.

It is well known that arachidonic acid is cell membranes platelets and vascular endothelium. Under the action of an enzyme cyclooxygenases it turns into endoperoxides. Later in platelets under the action of thromboxane synthetase endoperoxides are converted to thromboxane A 2, which is a powerful inducer of further platelet aggregation and at the same time has a vasoconstrictor effect (Fig. 5.44).

In the vascular endothelium, peroxides are converted to prostacyclin, which has opposite effects: it inhibits platelet aggregation and has dilating properties.

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