Evaluation of violations of regional contractility of the left ventricle. What will tell the contractility of the myocardium

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

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

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

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

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

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

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

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

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

What is myocardial contractility

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

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

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

Myocardial contractility is also supported by its:

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

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

What determines the contractility of the heart muscle

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

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

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

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

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

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

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

How is myocardial contractility regulated?

The impact of the vagus nerves causes a decrease in:

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

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

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

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

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

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

Significant stimulation also affects myocardial contractility:

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

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

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

The role of calcium and potassium ions

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

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

Drugs that affect myocardial contractility

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

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

What is dangerous violation of contractility

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

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

When can SM be violated

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

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

Violation of myocardial contractility - diagnosis

The most informative methods for studying SM are:

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

Also, to identify the cause of the decrease in SM, a general and biochemical blood test, a coagulogram, a lipid profile 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 a risk of thrombosis (due to hemodynamic disorders associated with impaired CM).

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

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

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

Treatment of SM disorders

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

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

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

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

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

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

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

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

Forecast

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

Albina asks:

Hello. I've had heart failure since early childhood. First, I want to describe what happened in December 2014. I’m 44 years old, since childhood, extrasystoles have been bothering me, but I didn’t feel them before, only three years ago I began to worry about seizures that lasted a few seconds: my heart was somehow incomprehensibly beating, as if it is not alone and falls out in the throat. Such attacks were once every six months, or even less often. In 2012, I did Holter monitoring: 27,000 supraventricular and 83 ventricular extrasystoles, ultrasound of the heart without pathologies. The cardiologist prescribed me drugs, but I didn’t have time to drink them, because I got an operation for an ectopic pregnancy. I always carry anaprilin with me just in case and Corvalol. I noticed that I feel interruptions after I get nervous. In July 2014, she again underwent an operation to remove the tube, she was psychotic all summer. For the second week now I have been feeling tremors in the heart and interruptions, I did the Holter again a week ago: 26,000 supraventricular extrasystoles and 14 ventricular extrasystoles, as well as a sinus rhythm and 1007 moments of arrhythmia, my pressure is 120/90 or 120/100 120/80 110/80 . According to the ultrasound of the heart: the walls of the aorta and valvular structures of increased echogenicity. During physical exertion, I do not feel interruptions, and the rhythm is restored, and I also have sinus tachycardia 90-120. Taking antiarrhythmics, I am afraid of the opposite effect and use only anaprilin if necessary. Help me, I'm afraid of sudden cardiac arrest. Save me, what should I do?

I work as a headmaster in a kindergarten, can I lead a normal life, how to get rid of fear? Can I take Propanorm? Three months later, extrasystoles again made themselves felt. I drink 10 mg of anaprilin per day, sometimes enough for a day, sometimes not. I also take 30 drops of hawthorn tincture and Magne B6, but it’s no use, I’m afraid that my heart will stop abruptly and that’s all ... How deadly is this? I just can’t go to the hospital now, but we don’t have one in the village. (I also suffer from cervicothoracic osteochondrosis, my thyroid gland is normal, on the left behind my back it’s like a stake was hammered into the spine, and my whole chest hurts - ECG only systole) I’m very scared! I would not be afraid, but I feel like a cardiac arrest, and this is where it all starts. Immediately 10 mg of anaprilin under the tongue is then better, but fear and panic are always and I am waiting for them-systole-again. And today they gave a transcript of the cardiogram and there: blockade of the left leg of the bundle of His, EOS to the left, the sinus rhythm is not regular, and this blockade scared me very much, I read that they die very often with it, although this is not on the holter.

Doctor's answer:

Hello! Let's not get nervous. I assure you that supraventricular extrasystole has not yet brought anyone to the grave. So your life is definitely not in danger.

At the same time, such a number of extrasystoles, and even against the background of tachycardia, simply "mechanically" prevents you from living a normal life, so it is better to reduce their number. To do this, you can use the same Inderal, but remember that Inderal is a short-acting drug and works for 3-4 hours, therefore, to achieve the effect, it must be taken 3-4 times a day. To avoid this, try the long-acting beta-blocker metoprolol. Choose the dose together with your cardiologist - I can recommend, without knowing you, not an adequate dose. Or we will have to continue the correspondence.

The hyperechogenicity of the aorta and valvular structures, as well as blockade, also attracts attention. This, again, is not life-threatening, but may be a symptom of progressive atherosclerosis. If you deem it necessary, send a full description of the ECHO and make a lipidogram.

Albina asks:

Thank you. With regard to the blockade, they may say that the blockade is in question, because. according to Holter, it is written that no blockades were detected. Also, what is a lipid profile? And how to treat atherosclerosis? I also want to add that as soon as I hear that ES are not fatal, I immediately calm down, and it seems to be easier for me, because you understand interruptions by interruptions, but I don’t always feel heart upheavals, and in November I felt them for three whole weeks, and then 4 months is not present, only sometimes. But now for 2 months I have been feeling and getting scared, again, everything is getting worse, and anaprilin is not a problem for me how many times a day to take the main thing is that I have already checked it. It’s just that I always have a fear of new drugs, even non-cardiac ones. The cause of ES is not clear. Yesterday I passed tests for thyroid hormones - everything is perfect. Why did you feel a drop in the pulse? Can I continue to take anaprilin 10 mg 2 times a day, sometimes it’s true, and it doesn’t help, but I’m generally afraid to take other drugs like betalok and propanorm. How to live with all this?

Here is a description of ECHO-AORTA-2.8 at a rate of 37; left atrium 3.2 at a rate of up to 3.6; cavity of the left ventricle 5.0 at a rate of up to 5.5; the contractility of the myocardium of the left ventricle is satisfactory; the interventricular septum is thickened 1.1 at a rate of 0.7-0.9; the posterior wall is thickened 1.1 at a rate of up to 1.1; the antiphase is reduced by 2.2 at a rate of up to 1.9; the right ventricle is expanded 1.0 at a rate of 2.6; pathological flows in the cavity of the heart were not detected. Conclusion: the heart cavity is not dilated, myocardial contractility is satisfactory. According to the DCG (UN CLEARLY WRITTEN) - no pathologies. The walls of the aorta and valvular structures of increased echogenicity. And there is a note on the Holter that no blockades were detected.

Doctor's answer:

Lipidogram is a blood test for the level of cholesterol and its fractions. Atherosclerosis, until it is diagnosed, does not need to be treated. As a preventive measure - regular moderate physical activity, hypocholesterol diet. Extrasystoles can be the result of autonomic imbalance (vegetative-vascular dystonia) or, not infrequently, problems with the gastrointestinal tract - gastritis, cholecystitis, pancreatitis, diaphragmatic hernia. In this case, the underlying disease needs to be treated. Anaprilin should be taken only if frequent extrasystoles are of concern. As a course treatment, take valerian preparations or adaptol 1 tablet 2 times a day for 2 months.

Albina asks:

I was prescribed Betaloc ZOK at 1.25, 2 times a day. Here's what I wanted to ask: in the Holter monitor itself, there are such words: rhythm variability is normal. Turbulence of the heart rate, and in conclusion, in addition to the fact that there are many supraventricular systoles, there is also a sentence: “Violation of the repolarization processes in the myocardium according to the recorded leads.” What does all of this mean?

Doctor's answer:

Do not pay attention to the terms you have indicated - they mean nothing for the evaluation of the ECG and for your condition. These options are designed as additional information for specialists to help assess the nature of cardiac activity.

1. 27.04.2015 at 14:20
2. 27.04.2015 at 14:26
3. 04/27/2015 at 17:26
4. 04/27/2015 at 17:27
5. 05/07/2015 at 11:44

By leaving a comment, you accept the User Agreement

• Arrhythmia
• Atherosclerosis
• Varicose veins
• Varicocele
• Haemorrhoids
• Hypertension
• Hypotension
• Diagnostics
• Dystonia
• Stroke
• heart attack
• Ischemia
• Blood
• Operations
• Heart
• Vessels
• angina pectoris
• Tachycardia
• Thrombosis and thrombophlebitis

• heart tea
• Hypertension
• Pressure bracelet
• Normallife
• Allapinin
• Asparkam
• Detralex

1. General characteristics of calcium channel blockers
2. Why Block Calcium?
3. How are drugs classified?
4. BKK Generations
5. BPC properties
6. Indications for use
7. Side effects
8. Contraindications for use
9. CCB preparations
10. Potassium or calcium blockers?

Arterial hypertension is a disease that requires mandatory drug therapy. Pharmaceutical companies year after year are working on the creation of new, more effective drugs to combat this disease. And today there are a huge number of drugs that can regulate blood pressure. Slow calcium channel blockers (CCBs) or calcium antagonists are one of the groups of drugs that are widely used for this purpose.

General characteristics of calcium channel blockers

Calcium antagonists have a diverse chemical structure, but do not differ in their mechanism of action. It consists in blocking the entry of calcium ions into the cells of the myocardium and the walls of blood vessels through special slow calcium channels. Representatives of the group not only reduce the number of ions of this element that enter the cells, but also affect their movement inside the cells. As a result, the peripheral and coronary blood vessels expand. Due to this pronounced vasodilating effect, a decrease in pressure occurs.

Calcium antagonists are one of the most effective drugs for the treatment of hypertension, belonging to the "first line". They are preferred for the treatment of elderly people with stable angina pectoris, systolic hypertension, dyslipidemia, peripheral circulatory disorders, lesions of the kidney parenchyma.

Why Block Calcium?

Calcium ions play a significant role in regulating the functioning of all organs of the cardiovascular system. They control the heart rate, regulate cardiac activity and the contractile function of myocytes. If there is an excess of ions of this microelement or the processes of its removal from cells are disturbed, then the specific functions of the cell are disrupted, which causes disturbances in the pumping activity of the heart, resulting in increased pressure.

How are drugs classified?

CCBs are classified according to various criteria - chemical structure, duration of action, tissue specificity. Yet the most commonly used classification of calcium channel blockers is based on their chemical structure. According to it, they distinguish:

• phenylalkylamines;
• dihydropyridines;
• benzothiazepines.

Dihydropyridine calcium channel blockers have a predominant effect on the vessels and almost do not reveal it on the myocardium. Due to their vasodilating action, they increase the rate of heart contractions, which makes it impossible for them to be taken by hypertensive patients with heart problems. This negative effect is practically not expressed in drugs of the 2nd and 3rd generation, which have a longer half-life. The ability of drugs of the dihydropyridine series to have an antioxidant, antiplatelet, angioprotective effect, reduce the manifestations of atherosclerotic lesions and increase the effect of statins has been proven. Long-acting dihydropyridines effectively lower blood pressure and practically do not show side effects.

This group includes: nifedipine, isradipine, amlodipine, felodipine, lercanidipine, nitrendipine, lacidipine.

Benzothiazepines and phenylalkylamines, on the contrary, lower the heart rate due to the same effect on the myocardium and blood vessels. This has made them the means of choice for the treatment of patients with hypertension in association with stable angina pectoris.

The drugs of these non-dihydropyridine groups suppress the automatism of the sinus node, lower the contractility of the heart, prevent spasm of the coronary arteries, and reduce peripheral resistance in the vessels. This group includes verapamil and diltiazem.

BKK Generations

There is another classification of calcium antagonists. It is based on the characteristics of the effect on the body, the duration of their action and tissue selectivity. There are calcium channel blockers:

• 1st generation (diltiazem, nifedipine, verapamil);
• 2nd generation (nifedipine SR, felodipine, diltiazem SR, nisoldipine, verapamil SR, manidipine, benidipine, nilvadipine, nimodipine);
• 3rd generation (lacidipine, lecarnidipine, amlodipine).

The first generation is used to a limited extent due to low bioavailability, high risk of side effects, and short-term effect.

The second generation is more perfect in these indicators, however, some representatives also have a short action. When creating the 3rd generation, all the shortcomings of the previous ones were taken into account. As a result, preparations with long-term action, high bioavailability and high tissue selectivity were obtained.

BPC properties

Calcium antagonists are very diverse in their chemical structure, and therefore can have different effects:

• lowering blood pressure;
• regulation of the heart rate;
• reduction of mechanical stress in the myocardium;
• improve cerebral circulation in atherosclerosis of the head vessels;
• prevent thrombosis;
• suppress excessive insulin production;
• lower pressure in the pulmonary artery.

Indications for use

BKK can be used:

• in mono- or combination therapy of hypertension;
• to eliminate systolic hypertension, especially in elderly patients;
• with arterial hypertension and coronary heart disease against the background of diabetes mellitus, gout, kidney disease, bronchial asthma;
• with vasospastic angina;
• for the treatment of stable angina pectoris;
• as an alternative for intolerance to beta-blockers.

Side effects

Medicines in this group have both common and specific side effects for individual subgroups. So, absolutely all BKKs can cause:

• allergic reactions;
• dizziness;
• excessive pressure drop;
• headache;
• peripheral edema (shins and ankles are especially often swollen in elderly patients);
• feeling of "hot flashes" and redness of the face.

Dihydropyridine calcium antagonists can also provoke tachycardia. Most of all, this negative effect is characteristic of nifedipine.

Non-dihydropyridine representatives of CCB can disrupt atrioventricular conduction, cause bradycardia, and reduce the automatism of the sinus node. Verapamil also often causes constipation and toxic effects on the liver.

Contraindications for use

Reception of BCC is prohibited when:

• severe hypotension;
• systolic dysfunction of the left ventricle;
• acute myocardial infarction;
• severe aortic stenosis;
• hemorrhagic stroke;
• atrioventricular blockade of 2-3 degrees;
• in the 1st trimester of pregnancy;
• while breastfeeding.

With caution and taking into account all the risks, CCB can be applied:

• in the 3rd trimester of pregnancy;
• with cirrhosis of the liver;
• with angina pectoris.

It should be borne in mind that drugs of the non-dihydropyridine group cannot be taken simultaneously with beta-blockers, and dihydropyridine blockers must not be combined with the intake of nitrates, prazosin, magnesium sulfate.

CCB preparations

A joint list of calcium channel blockers used in the treatment of hypertension:

• Verapamil (Isoptin, Lekoptin, Finoptin);
• Diltiazem (Dilren, Cardil, Dilzem);
• Nifedipine (Corinfar, Adalat, Cordaflex, Cordipin-retard);
• Amlodipine (Amlo, Stamlo, Amlovas, Normodipin, Norvasc);
• Felodipine (Felodip, Plendil);
• Nitrendipine (Unipress, Bypress);
• Lacidipine (Lacidip);
• Lercanidipine (Lerkamen).

In no case should you prescribe any drugs yourself. Be sure to undergo an examination and receive appointments from a doctor, taking into account all the characteristics of the body, the severity of the course of the disease and the presence of concomitant diseases.

Potassium or calcium blockers?

It is not uncommon for patients to confuse calcium channel blockers with potassium channel blockers. But they are completely different substances. Potassium channel blockers are class 3 antiarrhythmic drugs. They exert their effect by slowing down the current of potassium through the membranes of cardiomyocytes. This lowers the automatism of the sinus node and inhibits atrioventricular conduction. This group of drugs on the shelves of pharmacies is represented by amiodarone (Cordarone, Amiocordin, Cardiodarone), sotal (Sotalex, SotaGeksal).

Yu.A. Vasyuk, M.V. Kopeleva, A.B. Khadzegov.

Moscow State Medical Dental University.
Department of Clinical Functional Diagnostics RPDO.
Moscow, Russia.

For non-invasive assessment of local contractility of the left ventricular (LV) myocardium, echocardiography is most often used. This accessible and informative technique has a serious drawback associated with the bias of the study. Standard echocardiography allows assessing the local contractility of the studied segment of the left ventricle only visually in comparison with the contractility of neighboring zones; at the same time, the experience and qualifications of the researcher largely influence the result of the assessment. When interpreting stress echocardiography, it is required to evaluate local myocardial contractility in dynamics against the background of exercise, which makes the test results even more subjective. The lack of quantitative diagnostic criteria is the main reason for the low inter- and intra-operator reproducibility of stress echocardiography results.

Tissue (TDG) is an ultrasound technique that makes it possible to quantify local myocardial contractility. The high information content of the tissue in the detection of myocardial dyssynergy was confirmed in an experiment with an acute violation of the coronary blood supply. The results of clinical studies have also shown that tissue dopplerography allows to identify areas of impaired local contractility in patients with acute myocardial infarction - MI and postinfarction cardiosclerosis - PICS. There is evidence of successful use of tissue Doppler ultrasound with dobutamine stress echocardiography.

Currently, tissue dopplerography is extremely rarely used in routine diagnostic practice, since this technique has not yet been sufficiently studied. The literature provides more than a dozen speed, linear and temporal parameters calculated using tissue Doppler sonography, but there are no clear quantitative criteria for hypoakinesia. Changes in tissue Doppler sonography during exercise in healthy individuals and patients with insufficiency of coronary blood supply are described in insufficient detail. A special problem is the phenomenon of post-systolic shortening (PSS), which is recorded during tissue Doppler ultrasound in the areas of ischemia and focal cardiosclerosis. Most authors acknowledge that the appearance of PSU accompanies pathological processes occurring in the myocardium, however, the literature data on how to interpret it are currently contradictory and ambiguous.

The purpose of our study was to study the practical possibilities of tissue Doppler sonography in detecting local contractility disorders in patients with various forms of coronary artery disease. The task was to identify changes in tissue Doppler ultrasound parameters that characterize left ventricular myocardial dyssynergia, both permanent (with postinfarction cardiosclerosis) and transient (with ischemia against the background of pharmacological stress). In doing so, we aimed to develop as specific and easy-to-apply diagnostic criteria as possible based on tissue Doppler findings, which could increase the objectivity and reproducibility of echocardiography and stress echocardiography in the future.

Material and methods

The study included 71 patients, including 51 patients with coronary heart disease and 20 people without cardiovascular pathology, who were examined and treated at the Glavmosstroy hospital (MSCH N47) from 2001 to 2004. Patients with coronary artery disease were divided into 2 groups: the 1st group included 31 patients with postinfarction cardiosclerosis, the 2nd group included 20 patients with stable exertional angina without previous myocardial infarction. Patients with stable angina underwent diagnostic stress echocardiography with dobutamine and atropine according to the standard protocol to identify areas with impaired coronary blood supply. All persons in the control group also underwent stress echocardiography with dobutamine and atropine up to the achievement of submaximal heart rate.

Echocardiography (standard and tissue Doppler) was performed on the Vivid Five ultrasound diagnostic system from General Electric (USA) with a sector probe with a frequency of 3.75 MHz. The movement of longitudinal myocardial fibers was studied in projections along the long axis of the left ventricle from the apical approach. Tissue Dopplerography was performed in 4-, 3-, and 2-chamber projections in each of the 16 segments of the left ventricle and at 4 points of the mitral annulus: at the base of the posterior septal, lateral, inferior, and anterior walls of the left ventricle. The following parameters were evaluated.

1. Peak myocardial velocities: Sm (cm/s) - peak systolic velocity; Em (cm/s) - peak speed of early diastolic relaxation; Am (cm/s) - peak velocity in the phase of atrial systole.
2. Time intervals: systolic (TRS; from the top of the ECG R wave to the top of the Sm peak) and diastolic (TRE; from the top of the R wave on the ECG to the top of the Em peak).
3. Amplitude of systolic displacement of the myocardium (INT) 1 .
4. Peak velocity and amplitude of systolic strain: SR (strain rate) and ST (strain).

1 Displacement (distance traveled) during a cardiac cycle was calculated as the integral of velocity over time. The amplitude of systolic displacement was measured at the time of aortic valve closure.

We also assessed the parameters of tissue Doppler sonography, which characterize the PSU phenomenon.

1. Amplitude of the post-systolic velocity peak recorded in the isovolumic relaxation phase (Sps). The velocity ratio Sps/Sm was calculated.
2. The shape of the myocardial movement curve during the cardiac cycle. The forms of myocardial motion curves were subdivided into 3 types depending on the presence of PSU: "norm", "step" and "saddle".
3. Post-systolic deformation (STps).

Statistical data processing was carried out using the STATISTICA 5.0 software package (StatSoft Inc., USA, 1999). When analyzing the material for all tissue Doppler parameters, the mean, standard deviation (SD), median (med), 25th and 75th percentiles, minimum and maximum values ​​were calculated.

The absolute and percentage increase in tissue Doppler parameters during exercise is presented as confidence intervals for the mean. The significance of differences in tissue Doppler parameters in the groups was assessed by Student's t-test and non-parametric criteria.

The use of tissue dopplerography in the assessment of local contractility disorders at rest

In order to evaluate the possibilities of tissue Dopplerography in detecting local contractility disorders at rest, we compared the parameters of tissue Dopplerography in patients with postinfarction cardiosclerosis and healthy individuals. Segments of patients with postinfarction cardiosclerosis were divided into 3 subgroups according to the results of two-dimensional echocardiography: normokinetic (n=184), hypokinetic (n=121) and akinetic (n=104). Dyskinetic segments were excluded from the analysis due to their small number (n=4).

In subgroups of segments with impaired local contractility, when compared with the control group, a significant decrease in myocardial velocities was revealed both in systole (Sm) and in early and late diastole (Em and Am). Along with a decrease in velocities in these zones, there was a decrease in the amplitude of systolic displacement (INT), as well as the speed and amplitude of systolic deformation (SR and ST). In the subgroup of segments where there was no systolic increase (akinesia), the values ​​of velocity and linear parameters of tissue Doppler sonography were significantly lower than in the subgroup with a moderate decrease in contractility (hypokinesia). It should be noted that in the subgroup of visually intact segments in patients with postinfarction cardiosclerosis, a slight but significant decrease in the indicated parameters of tissue Doppler ultrasonography was also revealed compared to the control group (Fig. 1).

Rice. one.

The time intervals of TRS and TRE in the hypo- and akinetic segments were significantly increased compared to the segments of the control group (172±59 and 154±53 ms compared to 144±50 ms, p

It should be taken into account that myocardial velocities in intact segments of the left ventricle in patients with postinfarction cardiosclerosis may decrease with a decrease in the overall contractility of the left ventricle. In order to take this factor into account, patients with extensive cicatricial changes and a pronounced decrease in global contractility of the left ventricle (ejection fraction - EF - less than 50%) were excluded from the analysis and then the subgroups were re-compared. In the subgroup of patients with postinfarction cardiosclerosis and preserved EF (at least 50%), compared with the control group, the values ​​of peak velocities, INT, SR, and S were still significantly reduced, and the time intervals were increased. The described changes in tissue dopplerography parameters were revealed not only in hypoakinetic, but also in visually normokinetic segments of patients with postinfarction cardiosclerosis.

Differences between segments with moderate (hypokinesia) and severe (akinesia) degree of contractility disorders according to the results of tissue Dopplerography were small. These subgroups differed only in Sm, Em, and INT values. When patients with left ventricular EF less than 50% were excluded from the analysis, the differences between hypo- and akinetic segments became unreliable (p>0.05). This can be explained by the "pull-up" effect, which leads to a false increase in speed and linear parameters in hypoakinesia zones bordering on the intact myocardium. In patients with high EF and a small volume of the affected myocardium, "pulling up" to a greater extent affects the movement of the postinfarction zones of the left ventricle.

Tissue dopplerography of the mitral annulus (MC) at points located at the base of the walls of the left ventricle, containing two or more segments with reduced contractility, revealed all the signs of myocardial contractile dysfunction described above: a decrease in myocardial velocities and systolic displacement, an increase in TRS and TRE time intervals . At the base of the normokinetic walls of the left ventricle, the Sm, Em, Am, and INT values ​​were higher than in hypoakinesia, but significantly lower than in the control group. SR and S at the level of the mitral ring in patients with postinfarction cardiosclerosis and in the control group did not differ significantly (Fig. 2).

Rice. 2.

PSU was more common in segments with impaired contractility than in the control group. The post-systolic peak of Sps velocity in hypo- and akinesia occurred 3 times or more often (58 and 69%, respectively, versus 18% of the segments; p<0,05), а его амплитуда превышала Sm почти в 10 раз чаще, чем в норме (22 и 23% соответственно против 3% сегментов; p<0,05). В подгруппах гипо- и акинетичных сегментов преобладали "ступенчатая" и "седловидная" формы кривой движения миокарда, в то время как "нормальная" форма встречалась почти в 2 раза реже, чем в контрольной группе (45 и 36% соответственно против 82%; p<0,05). Пик постсистолической деформации Sps в подгруппах с нарушенной локальной сократимостью отмечался в 15 раз и более чаще, чем в норме (38 и 39% соответственно против 2% сегментов; p<0,05). В нормокинетичных сегментах "нормальная" кривая движения встречалась в 53% случаев, что достоверно чаще, чем при гипоакинезии, однако в 1,5 раза реже, чем у здоровых лиц.

On fig. 3-5 shows various variants of PSU in patients with postinfarction cardiosclerosis.

Rice. 3. Tissue dopplerography.

a) Fine.

b) A patient with a high-amplitude peak of postsystolic velocity (Sps) is recorded.

Rice. four. Forms of myocardial movement curves in normal conditions and in patients with postinfarction cardiosclerosis.

a) Fine.

b) With postinfarction cardiosclerosis.

in) With postinfarction cardiosclerosis.

"Saddle" and "stepped" forms of movement are due to the presence of postsystolic displacement of the myocardium, which exceeds the maximum systolic displacement in amplitude.

Rice. 5. Curves of myocardial deformation in normal conditions and in postinfarction cardiosclerosis.

a) Fine.

b) With postinfarction cardiosclerosis. The patient has a high-amplitude peak of post-systolic strain (STps).

The vertical line (AV) in fig. 3-5 corresponds to the closing time of the aortic valve. The presented graphs also show the presence of a basal-apical gradient (decrease in peak myocardial velocities, longitudinal systolic displacement and deformation from the base to the apex of the left ventricle).

Significant differences between hypo- and akinetic segments in terms of PSU characteristics were not found, although in the subgroup of akinetic segments PSP was recorded somewhat more often. In normokinetic segments in patients with postinfarction cardiosclerosis, Sps and STps peaks were determined much more often than in the control group (53 and 30% compared to 18 and 2% of cases, respectively; p<0,05). ПСУ также было выявлено в 68% точек митрального кольца, расположенных у основания стенок левого желудочка с нарушенной сократимостью.

According to our data, a high-amplitude peak of post-systolic velocity, displacement, or deformation recorded by tissue Doppler sonography is a highly specific criterion for impaired local contractility, since this sign was detected in most dyssynergic segments and only in 9% of segments in the control group (see table). According to this criterion, signs of contractile dysfunction were also detected in 52% of visually normokinetic segments of patients with myocardial infarction.

Table. The effectiveness of the diagnostic criterion using the characteristics of the PSU.

Note. n is the number of segments that satisfy the condition.

In screening examinations, tissue at the level of the mitral annulus can be used to assess the movement of the left ventricular wall as a whole. Since the parameters of tissue dopplerography of the mitral annulus depend on the state of global contractility, this method should be used in patients with left ventricular EF of at least 50%. Decreased Sm (less than 5 cm/s) in combination with a reduced amplitude of systolic displacement (less than 0.9 cm) indicates dyssynergy of the wall under study. This feature was found in 96% of dyssynergic and 70% of normokinetic left ventricular walls in patients with postinfarction cardiosclerosis and preserved global contractility and only in 26% of left ventricular walls in the control group.

The use of tissue dopplerography in identifying areas with impaired coronary blood supply against the background of pharmacological stress

To study the possibilities of tissue Dopplerography in detecting myocardial ischemia, we compared the indicators of tissue Dopplerography in the group of patients with stable angina and in the control group during stress echocardiography with dobutamine and atropine. None of the patients with angina pectoris had areas of initially impaired contractility. The stress test in all patients with angina pectoris was positive; in 50% of cases, the reason for stopping the test was the ischemic dynamics of the ECG, in 50% - the identification of zones of myocardial dyssynergy. Cardiac arrhythmias were registered in 4 patients with stable angina pectoris. In the control group, no cardiac arrhythmias were detected.

Dynamics of parameters of segmental tissue Doppler ultrasound against the background of stress echocardiography in the control group

The number of left ventricular segments in the control group with satisfactory visualization quality was 313 at rest, 291 at low doses, and 280 at peak stress echocardiography.

As the dose of dobutamine was increased in the control group, two main types of changes in tissue Doppler parameters were observed. The first type is a constant reliable increase in the absolute values ​​of the parameter at all stages of the load. Such dynamics was characteristic of the Sm, Am, and SR indices. The second type of dynamics is a significant increase in the values ​​of the parameter at low doses, followed by its decrease at the peak of the load. Such dynamics was observed in Em, INT and ST values. The decrease in Em, INT and ST at the peak of the load was significant, but small in amplitude; while the values ​​of these parameters remained increased compared to their initial value.

Against the background of an increase in heart rate in healthy individuals, a significant (p

Against the background of dobutamine infusion, on segmental tissue Doppler sonography in the control group, the PSU phenomenon in the form of postsystolic velocity and displacement peaks was significantly more frequently recorded. At the peak of the load, the frequency of detection of the "saddle" form of systolic movement increased by 4 times or more compared with the initial value and 2.5 times compared with the data obtained using low doses. Nevertheless, in healthy individuals, the Sps amplitude, as a rule, did not exceed Sm.

The described features of the normal dynamics of tissue Doppler ultrasound parameters against the background of a stress test can be useful in the development and use of quantitative criteria for contractile dysfunction of the left ventricular myocardium.

Dynamics of indicators of segmental tissue Doppler ultrasound during stress echocardiography in patients with stable angina pectoris

Before the start of exercise in the group of patients with stable angina, compared with the control group, there was a slight lengthening of the TRE interval (517±53 ms versus 503±45 ms, respectively; p=0.004), as well as a decrease in the Em/Am index (med 0.76; 0 .48-1.2 vs. med 0.95; 0.64-1.33, respectively; p=0.001) and an increase in the Sm/Em index (med 0.93; 0.64-1.25 vs. med 0.75; 0.52-1.02, respectively, p=0.002). At the same time, the amplitudes of peak velocities, systolic displacement, as well as the strain rate and strain did not differ significantly.

Against the background of infusion of small doses of dobutamine, the values ​​of Sm and Em in patients with stable angina pectoris decreased compared with those in the control group (5.52±4.13 cm/s compared with 6.49±2.90 cm/s and 4.86 ±2.68 cm/s compared to 5.83±2.68 cm/s respectively p

The amplitude and dynamics of indicators of segmental tissue Dopplerography at the time of dobutamine infusion cessation in patients with stable angina and healthy individuals differed significantly. Significant signs of systolic-diastolic dysfunction were registered at the peak of the load in the group of patients with angina pectoris: reduced values ​​of myocardial velocities Sm (6.31±4.87 cm/s compared with 8.19±3.58 cm/s; p The signs described above contractile dysfunction were also reliably detected in patients with angina pectoris on tissue dopplerography of the mitral annulus at the peak of stress echocardiography.

Based on the results obtained, criteria for ischemia were proposed, using the indicators of tissue Dopplerography of the studied segment and tissue Dopplerography of the mitral annulus at the base of the studied wall of the left ventricle. We propose to consider an increase in peak systolic velocity Sm of less than 50% in combination with a negative increase in systolic displacement INT at the peak of stress echocardiography as a specific sign of ischemia. According to this criterion, 31% of the segments of the left ventricle in the group of patients with stable angina showed signs of contractile dysfunction at the peak of stress echocardiography. A highly specific sign of ischemia is also a reduced Sm velocity (less than 8 cm/s) at the peak of stress echocardiography at the point of the mitral annulus at the base of the left ventricular wall under study. This sign was present in 33% of the walls of the left ventricle in patients with angina pectoris and only in 12% of the walls in the control group.

As an additional sign of myocardial ischemia, which has low sensitivity, but high specificity, the appearance of post-systolic shortening in the form of a high-amplitude post-systolic peak of velocity, displacement or deformation was noted on tissue Dopplerography.

Discussion

Changes in the parameters of tissue Dopplerography, which were noted in subgroups of hypokinetic segments of the left ventricle, fully correspond to the changes in tissue Dopplerography described in the literature in areas with impaired coronary blood supply. In addition to the known signs of impaired local contractility, we analyzed changes in the myocardial motion curve. Presumably, the “deformation” of the myocardial movement curve is a consequence of both systolic and diastolic dysfunction. The decrease in peak systolic velocity Sm caused by ischemia, the appearance of zero and negative mean systolic velocities, the “delay” of early diastole, and the appearance of high-amplitude PSU together lead to the fact that the path traveled by the myocardial region acquires a “stepped” or “saddle” shape. This means that with dyssynergy in the second half of systole, the myocardium stops contracting or its short-term relaxation is noted; in this case, after the closure of the aortic valve, an additional pseudocontraction (PSC) occurs. According to our data, "stepped" and "saddle" forms of systolic movement are sensitive signs of impaired contractility.

The results obtained allowed us to conclude that for a simplified diagnosis of violations of local contractility of the left ventricle, it is possible to use the assessment of tissue Doppler ultrasound parameters at the level of the mitral annulus (at the base of the studied wall of the left ventricle). Many authors believe that tissue dopplerography of the mitral annulus reflects the state of not so much local as global contractility of the left ventricle, since tissue dopplerography of the mitral annulus depends on left ventricular EF. This study showed that tissue Doppler parameters of the mitral annulus at the base of intact and dyssynergic walls of the left ventricle differ significantly even if only patients with normal left ventricular EF are compared. Therefore, the indicators of tissue Dopplerography of the mitral annulus can be used if necessary to quickly assess the contractility of the left ventricular wall as a whole, provided that the patient does not have a reduced EF.

In our opinion, attempts to clearly delineate the segments and walls of the left ventricle with varying degrees of impaired local contractility using tissue Doppler sonography are unpromising. Tissue Dopplerography allows to detect myocardial dyssynergy with high sensitivity, but we failed to distinguish hypokinesia from akinesia on the basis of tissue Dopplerography data. The question of whether tissue Dopplerography is informative in assessing the degree of local contractility disorders requires further study with the obligatory comparison of the results with the data of an objective verifying technique, such as sonomicrometry or PET.

The results obtained did not have fundamental inconsistencies with the previously described changes in tissue Doppler sonography, which occur in normal conditions and in coronary artery disease against the background of dobutamine infusion. At the same time, we identified two types of tissue Doppler dynamics: a stepwise increase proportional to the dose of dobutamine, and a "two-phase" dynamics, which is an increase with low doses and a slight decrease at the peak of the load. The "biphasic" type of dynamics of the Em, INT and ST indicators is presumably associated with an increase and subsequent decrease in the stroke and minute volumes of the left ventricle, which occurs during exercise. We regard the decrease in INT and ST as an early sign of the depletion of the contractile reserve, preceding the decrease in stroke and minute volume. Decreased early diastolic filling rate Em is most likely due to high heart rate; a similar relationship has been previously described in the literature.

Most authors consider the peak systolic velocity Sm to be one of the most informative indicators of tissue Doppler ultrasound in diagnostic stress echocardiography, however, they recognize its use as limited, since this indicator depends on the location of the segment under study. In this regard, it was proposed to use different quantitative criteria for ischemia for segments of the basal, middle and apical localization or to calculate the normal value of Sm for each level of the left ventricle using regression analysis. According to our results, the optimal parameters for diagnosing IHD were the percentage increase in Sm and the percentage increase in INT, since these indicators differed the most in the segments of patients with IHD and healthy individuals. The data obtained are consistent with the results of the work of S. Dagdelen et al. , which revealed a significant correlation between the percentage increase in Sm during dobutamine infusion and the level of coronary fractional blood flow measured during catheterization. It was also noted that the percentage increase in Sm and INT does not decrease, but significantly increases from the base to the top of the left ventricle; this allowed us to propose diagnostic criteria for coronary artery disease that are uniform for all segments of the left ventricle. According to the results of the MYDISE study, Sm and INT measurements have high inter- and intra-operator reproducibility. The sensitivity and specificity of the algorithmic criteria proposed by us were similar to those obtained by J. Voigt et al. , but turned out to be somewhat lower than in most published works. However, the criteria presented by us were formed without the use of a verifying technique, so they only demonstrate the possibilities of using tissue Doppler ultrasound during stress echocardiography for the diagnosis of coronary artery disease.

Conclusion

Tissue dopplerography is highly sensitive in detecting local contractility disorders, including those not diagnosed by conventional echocardiography. Tissue Doppler criteria are applicable to quantify myocardial motion both at rest and during stress echocardiography. For simplified detection of myocardial dyssynergy in patients with preserved left ventricular EF, criteria based on tissue dopplerography of the mitral annulus can be used. One of the specific signs of impaired contractile function is PSU, recorded with tissue Doppler at rest.

Literature

1. Nikitin N.P., Witte K.K., Thackray S.D. Longitudinal Ventricular Function: Normal Values ​​of Atrioventricular Annular and Myocardial Velocities Measured with Quantitative Two-dimensional Color Doppler Tissue Imaging. J Am Soc Echocardiogr 2003; 16:906-921.
2. Varga A., Picano E., Dodi C. Madness and method in stress echo reading. Eur Heart J 1999; 20:1271-1275
3. Pasquet A., Armstrong G., Beachler L. Use of Segmental Tissue Doppler Velocity to Quantitate Exercise Echocardiography. J Am Soc Echocardiogr 1999; 12:901-912.
4. Alekhin M., Sedov V., Sidorenko B. Possibilities of stress echocardiography in the detection of viable myocardium. Cardiology 1999; 2:86-91.
5. Derumeaux G., Ovize M., Loufoua J. et al. Doppler tissue imaging quantitates regional wall motion during myocardial ischemia and reperfusion. Circulation 2000; 101: 1390-1397.
6. Edvardsen T., Aakhus S., Endresen K. Acute regional myocardial ischemia identified by 2-dimensional multiregion Doppler imaging tissue technique. J Am Soc Echocardiogr 2000; 13:986-994.
7. Hoffmann R., Lethen H., Marwick T. et al. Analysis of institutional observer agreement in interpretation of dobutamine stress echocardiograms. J Am Coll Cardiol 1996; 27:330-336.
8. Voigt J.U., Exner B., Schmiedehausen K. et al. Strain-Rate Imaging During Dobutamine Stress Echocardiography Provides Objective Evidence of Inducible Ischemia. Circulation 2003; 29 107:16 2120-2126.
9. Fraser A.G., Payne N., Madler C.F. Feasibility and reproducibility of off-line tissue Doppler measurement of regional myocardial function during dobutamine stress echocardiography. Eur J Echocardiogr 2003; 4:43-53.
10. Skulstad H., Edvardsen T., Urheim S., Rabben S. Postsystolic Shortening in Ischemic Myocardium: Active Contraction or Passive Recoil? Circulation 2002; 106:718.
11. Voigt J.U., Lindenmeier G., Exner B. Incidence and characteristics of segmental postsystolic longitudinal shortening in normal, acutely ischemic, and scarred myocardium. J Am Soc Echocardiogr 2003; 16:415-423.
12. Alam M., Hoglund C., Thorstrand C. Longitudinal systolic shortening of the left ventricle: an echocardiographic study in subjects with and without preserved global function. Clin Physiol 1992; 12:443-452.
13. Leitman M., Sidenko S., Wolfa R. Improved detection of inferobasal ischemia during dobutamine echocardiography with doppler tissue imaging. Am Soc Echocardiogr 2003; 16:403-408.
14. Palka P., Lange A., Fleming A.D. et al. Age-related transmural peak mean velocities and peak velocity gradients be Doppler myocardial imaging in normal subjects. Eur Heart J 1996; 17:940-950.
15. Afridi I., Quinones M., Zoghbi W., Cheirif J. Dobutamine stress echocardiography: sensitivity, specificity and predictive value for future cardiac events. Am Heart J 1994; 127: 1510-1515.
16. Katz W.E., Gulati V.K., Mahler C.M., Gorcsan J. Quantitative evaluation of the segmental left ventricular response to dobutamine stress by tissue Doppler echocardiography. Am J Cardiol 1997; 79:1036-1042.
17. Altinmakas S., Dagdeviren B., Turkmen M. et al. Usefulness of pulse-wave Doppler tissue sampling and dobutamine stress echocardiography for identification of false positive inferior wall defects in SPECT. Jpn Heart J 2000; 41:2:141-152.
18. ain P., Short L., Baglin T. Development of a fully quantitative approach to the interpretation of stress echocardiography using radial and longitudinal myocardial velocities. J Am Soc Echocardiogr 2002; 15:759-767.
19. Dagdelen S., Yuce M., Emiroglu Y., Ergelen M. Correlation between the tissue Doppler, strain rate, strain imaging during the dobutamine infusion. and coronary fractional flow reserve during catheterization: a comparative study. Intern J Cardiology 2005; 102:127-136.
20. Madler C.F., Payne N., Wilkenshoff U. Non-invasive diagnosis of coronary artery disease by quantitative stress echocardiography: optimal diagnostic models using off-line tissue Doppler in the MYDISE study. Eur Heart J 2003; 24:1584-1594.
21. Voigt J.U., Nixdorff U., Bogdan R. et al. Comparison of deformation imaging and velocity imaging for detecting regional inducible ischaemia during Dobutamine stress echocardiography Eur Heart J 2004; 25:1517-1525.
22. Sutherland G., Merli R.E. Can we quantify ischaemia during Dobutamine stress echocardiography in clinical practice? Eur Heart J 2004; 25:1477-1479.

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

Causes of reduced contractility

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

Also, a decrease in myocardial contractility can occur:

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

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

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

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

Diagnostics

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

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

Treatment

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

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

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

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

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 he who performs the greatest work of expelling blood, and this work is estimated by ejection fraction and stroke volume, that is, by the amount of blood that is ejected into the aorta with each cardiac cycle.

Bioelectric bases of myocardial contractility

heart beat cycle

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

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

Video: more about the biochemistry of myocardial contractility

Why do you need to know about myocardial contractility?

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

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

Myocardial contractility according to ECG

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

Myocardial contractility by echocardiography

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

photo: assessment of myocardial contractility on echocardiography with exercise

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

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

sections of the heart muscle on echocardiography

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

Normal contractility of the heart and violations of myocardial contractility

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

Based on this, the following concepts can be distinguished:

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

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

What diseases are associated with violations of myocardial contractility?

graphs of changes in myocardial contractility in various situations

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

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

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

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

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

Are there clinical manifestations of impaired contractility?

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

Should contractility disorders be treated?

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

Are there possible consequences?

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

What 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, which make up muscle cells - cardiomyocytes. Changing the length of the sarcomere under the influence of electrical impulses of the conduction system and provides contractility of the heart.

Violation of myocardial contractility can lead to unpleasant consequences in the form 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 that allow it to ensure the full functioning of the cardiovascular system. These features of the heart muscle allow not only to maintain blood circulation, ensuring a continuous flow of blood from the ventricles into the lumen of the aorta and pulmonary trunk, but also to carry out compensatory-adaptive reactions, ensuring the adaptation of the body to increased loads.

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

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?

The impact of the vagus nerves causes a decrease in:

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

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

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

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.

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

The role of calcium and potassium ions

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

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

Drugs that affect myocardial contractility

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

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

What is dangerous violation of contractility

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

When can SM be violated

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

• myocardial hypoxia;
• ischemic heart disease;
• severe atherosclerosis of the coronary vessels;
• myocardial infarction and postinfarction cardiosclerosis;
• heart aneurysms (there is a sharp decrease in the 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

The most informative methods for studying SM are:

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

Also, to identify the cause of the decrease in SM, a general and biochemical blood test, a coagulogram, a lipid profile 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 a risk of thrombosis (due to hemodynamic disorders associated with impaired CM).

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

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

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, folic acid, vitamin B12 preparations (depending on the type of anemia).

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

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

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

Forecast

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

These articles may be of interest too

Bacterial endocarditis is a severe infectious disease.

What is valvular regurgitation, diagnosis and treatment.

What is the danger of pulmonary edema in myocardial infarction, treatment.

Leave your comment X

Search

Categories

new entries

Copyright ©18 Heart Encyclopedia

What will tell the contractility of the myocardium

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

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

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

Increased heart rate

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

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

Learn more about the complications of myocardial infarction here.

The function is preserved - an indicator of the norm?

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

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

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

Reasons for changing state

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

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

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

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

Manifestations of reduced myocardial contractility

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

Classification of acute disorders of cerebral circulation

Changes in gas exchange

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

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

Water retention and swelling

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

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

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

congestion

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

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

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

Diagnosis of the contractility of the ventricles of the myocardium

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

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

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

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

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

Watch the video about the methods of examining the heart:

Treatment in case of deviation

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

Drug therapy includes the following groups of drugs:

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

Learn more about cardiac dilatation here.

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

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

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

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

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

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

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

We will publish information shortly.

ASSESSMENT OF LEFT VENTRICULAR REGIONAL CONTRACTILITY DISTURBANCES

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

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

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

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

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

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

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

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

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

1. Acute myocardial infarction (MI).

2. Postinfarction cardiosclerosis.

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

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

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

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

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

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

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

1 point - normal contractility;

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

3 points - severe hypokinesia;

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

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

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

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

ACQUIRED HEART DEFECTS

STENOSIS OF THE LEFT ATRIOVENTRICULAR HOLE (MITRAL STENOSIS)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

3) significant turbulence in the movement of blood.

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

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

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

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

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

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

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

MITRAL VALVE INSUFFICIENCY

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

There are 2 main forms of mitral regurgitation:

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

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

The causes of relative mitral insufficiency are:

1) mitral valve prolapse;

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

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

4) rupture of tendon threads;

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

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

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

1) an increase in the size of the LP;

2) hyperkinesia of the posterior wall of the LA;

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

4) myocardial hypertrophy and dilatation of the LV cavity.

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

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

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

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

The method of color Doppler scanning differs in the greatest information content and clarity in the detection of mitral regurgitation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Doppler echocardiographic signs of aortic insufficiency.

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

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

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

THREE-LEAVEL VALVE INSUFFICIENCY

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

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

DIAGNOSIS OF PERICARDIAL LESIONS

Echocardiographic examination allows diagnosing various types of pericardial lesions:

1) dry pericarditis,

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

3) constrictive pericarditis.

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

Effusion in the pericardial cavity. In the presence of a pathological effusion in the pericardial cavity that exceeds the normal volume of serous fluid (about 10 ml), an echocardiogram reveals separation of the pericardial sheets with the formation of an echo-negative space behind the posterior wall of the left ventricle, and diastolic separation of the pericardial sheets is of diagnostic value. The movement of the parietal sheet of the pericardium decreases or disappears altogether, while the excursion of the epicardial surface of the heart increases (hyperkinesia of the epicardium), which serves as an indirect sign of the presence of fluid in the pericardial cavity.

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

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

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

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

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

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

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

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

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

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

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

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

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

There are 3 forms of CMP:

1) hypertrophic cardiomyopathy,

2) dilated CMP,

3) restrictive ILC.

Hypertrophic cardiomyopathy (HCM) is characterized by

1) severe LV myocardial hypertrophy,

2) a decrease in the volume of its cavity

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

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

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

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

2. Anterior systolic movement of the mitral valve leaflets.

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

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

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

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

7. Mitral regurgitation and dilatation of the left atrium.

Echocardiographic features of hypertrophic cardiomyopathy

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

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

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

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

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

2) mild myocardial hypertrophy,

3) a sharp decrease in systolic and diastolic function,

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

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

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

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

1) significant thickening of the endocardium,

2) myocardial hypertrophy of both ventricles,

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

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

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

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

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

3. Prolapse of the mitral and tricuspid valves.

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

5. Relative insufficiency of the mitral and tricuspid valves.

6. The presence of intracardiac parietal thrombi.

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

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

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

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

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

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

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

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

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

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

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

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

Causes of reduced contractility

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

Also, a decrease in myocardial contractility can occur:

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

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

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

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

Diagnostics

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

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

Treatment

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

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

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

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

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 for various reasons, this already indicates 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:

1. severe brain damage;
2. a consequence of an unsuccessful surgical intervention;
3. diseases associated with the heart, for example, ischemia;
4. after myocardial infarction;
5. 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 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:

1. ultrasound examination (ultrasound);
2. blood chemistry;
3. 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

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.

Paroxysmal ventricular tachycardia can start suddenly and also end abruptly. AT.

Vegetovascular dystonia in children today is quite common, and its symptoms are not the same.

Thickening of the walls of the aorta - what is it? This is a fairly complex anomaly that can become.

In order to be able to cure such an ailment as hypertension of the 3rd degree, you need to carefully.

Many women are interested in the safety of the combination of "hypertension and pregnancy." Compulsory.

Few people know exactly what vegetovascular dystonia is: the reasons for its appearance,.

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

Violation of myocardial contractility can lead to unpleasant consequences in the form 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 that allow it to ensure the full functioning of the cardiovascular system. These features of the heart muscle allow not only to maintain blood circulation, ensuring a continuous flow of blood from the ventricles into the lumen of the aorta and pulmonary trunk, but also to carry out compensatory-adaptive reactions, ensuring the adaptation of the body to increased loads.

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

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?

The impact of the vagus nerves causes a decrease in:

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

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

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

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.

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

The role of calcium and potassium ions

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

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

Drugs that affect myocardial contractility

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

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

What is dangerous violation of contractility

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

When can SM be violated

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

• myocardial hypoxia;
• ischemic heart disease;
• severe atherosclerosis of the coronary vessels;
• myocardial infarction and postinfarction cardiosclerosis;
• heart aneurysms (there is a sharp decrease in the 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

The most informative methods for studying SM are:

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

Also, to identify the cause of the decrease in SM, a general and biochemical blood test, a coagulogram, a lipid profile 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 a risk of thrombosis (due to hemodynamic disorders associated with impaired CM).

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

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

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, folic acid, vitamin B12 preparations (depending on the type of anemia).

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

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

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

Forecast

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

These articles may be of interest too

What is Ebstein anomaly, diagnosis and treatment

Bacterial endocarditis is a severe infectious disease.

What is pacemaker migration, symptoms and treatment

What is valvular regurgitation, diagnosis and treatment.

Leave your comment X

Search

Categories

new entries

Copyright ©18 Heart Encyclopedia

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 he who performs the greatest work of expelling blood, and this work is estimated by ejection fraction and stroke volume, that is, by the amount of blood that is ejected into the aorta with each cardiac cycle.

Bioelectric bases of myocardial contractility

heart beat cycle

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

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

Video: more about the biochemistry of myocardial contractility

Why do you need to know about myocardial contractility?

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

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

Myocardial contractility according to ECG

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

Myocardial contractility by echocardiography

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

photo: assessment of myocardial contractility on echocardiography with exercise

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

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

sections of the heart muscle on echocardiography

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

Normal contractility of the heart and violations of myocardial contractility

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

Based on this, the following concepts can be distinguished:

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

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

What diseases are associated with violations of myocardial contractility?

graphs of changes in myocardial contractility in various situations

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

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

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

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

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

Are there clinical manifestations of impaired contractility?

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

Should contractility disorders be treated?

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

Are there possible consequences?

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

Myocardial contractility is normal

and adolescent gynecology

and evidence-based medicine

and health worker

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 cf.) according to the intraventricular pressure curve (Fig. 7.):

The S 1 line is drawn, based on the FCG recording, along the first high-frequency oscillation of the first tone, and the X line is drawn from the point where the blood pressure begins to rise. 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. In this way:

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:

Given the closeness of the values ​​of diastolic pressure in the aorta and the brachial artery, in (129), one can use the value of DD, 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 the true value of the 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 of 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 question 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).

1. ISM according to Veragut and Kraienbühl:

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

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

1. According to F. Z. Meyerson (1975):

where CPIP is the developed pressure in the ventricle.