The global systolic function of the left ventricle is preserved. Violation of local contractility of the myocardium of the left ventricle

Myocardial ischemia causes local disorders of LV contractility, disorders of the global diastolic and systolic function of the LV. In chronic ischemic heart disease, two factors have the greatest prognostic value: the severity of coronary artery disease and the global systolic function of the left ventricle. With transthoracic echocardiography, one can judge coronary anatomy, as a rule, only indirectly: only a small number of patients visualize the proximal sections of the coronary arteries (Fig. 2.7, 5.8). Recently, a transesophageal study has been used to visualize the coronary arteries and study coronary blood flow (Fig. 17.5, 17.6, 17.7). However, this method has not yet received wide practical application for the study of coronary anatomy. The methods for assessing global LV contractility were discussed above. Resting echocardiography, strictly speaking, is not a method for diagnosing coronary heart disease. The use of echocardiography in combination with stress tests will be discussed below, in the chapter "Stress echocardiography".

Figure 5.8. Aneurysmal expansion of the trunk of the left coronary artery: parasternal short axis at the level of the aortic valve. Ao - aortic root, LCA - trunk of the left coronary artery, PA - pulmonary artery, RVOT - outflow tract of the right ventricle.

Despite these limitations, resting echocardiography provides valuable information in coronary artery disease. Chest pain can be cardiac or non-cardiac in origin. Recognition of myocardial ischemia as a cause of chest pain is of fundamental importance for the further management of patients both during outpatient examination and when they are admitted to the intensive care unit. The absence of disturbances in local LV contractility during chest pain virtually excludes ischemia or myocardial infarction as a cause of pain (if the heart is well visualized).

Local LV contractility is assessed in a two-dimensional echocardiographic study conducted from various positions: most often these are the parasternal positions of the long axis of the left ventricle and the short axis at the level of the mitral valve and the apical positions of the two- and four-chamber heart (Fig. 4.2). For visualization of the posterior-basal parts of the LV, the apical position of the four-chamber heart is also used with the downward deviation of the scanning plane (Fig. 2.12). When assessing local LV contractility, it is necessary to visualize the endocardium in the area under study as best as possible. To decide whether local LV contractility is impaired or not, both the movement of the myocardium of the area under study and the degree of its thickening should be taken into account. In addition, local contractility of various LV segments should be compared, and the echo structure of myocardial tissue in the area under study should be examined. It is impossible to rely only on the assessment of myocardial movement: violations of intraventricular conduction, ventricular preexcitation syndrome, electrical stimulation of the right ventricle are accompanied by asynchronous contraction of various segments of the left ventricle, so these conditions make it difficult to assess the local contractility of the left ventricle. It is also hampered by the paradoxical movement of the interventricular septum, which is observed, for example, during volume overload of the right ventricle. Violations of local LV contractility are described in the following terms: hypokinesia, akinesia, dyskinesia. Hypokinesia means a decrease in the amplitude of movement and thickening of the myocardium of the studied area, akinesia - the absence of movement and thickening, dyskinesia - the movement of the studied area of ​​the left ventricle in the direction opposite to normal. The term "asynergy" means non-simultaneous reduction of various segments; LV asynergy cannot be identified with violations of its local contractility.
To describe the identified violations of local contractility of the left ventricle and their quantitative expression, the division of the myocardium into segments is used. The American Heart Association recommends dividing the LV myocardium into 16 segments (Fig. 15.2). To calculate the index of violation of local contractility, the contractility of each segment is evaluated in points: normal contractility - 1 point, hypokinesia - 2, akinesia - 3, dyskinesia - 4. Segments that are not clearly visualized are not taken into account. The score is then divided by the total number of segments examined.

The cause of violations of local LV contractility in coronary heart disease can be: acute myocardial infarction, postinfarction cardiosclerosis, transient myocardial ischemia, permanent ischemia of the viable myocardium (“hibernating myocardium”). We will not dwell on local LV contractility disorders of a non-ischemic nature here. We will only say that cardiomyopathies of non-ischemic origin are often accompanied by uneven damage to various parts of the LV myocardium, so it is not necessary to judge with certainty about the ischemic nature of cardiomyopathy only on the basis of the detection of zones of hypo- and akinesia.

The contractility of some segments of the left ventricle suffers more often than others. Violations of local contractility in the basins of the right and left coronary arteries are detected by echocardiography with approximately the same frequency. Occlusion of the right coronary artery, as a rule, leads to impaired local contractility in the region of the posterior diaphragmatic wall of the left ventricle. Violations of local contractility of the anterior-septal-apical localization are typical for infarction (ischemia) in the basin of the left coronary artery.

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Causes of left ventricular hypertrophy

To cause the walls of the ventricle to thicken and stretch, it can be overloaded with pressure and volume, when the heart muscle needs to overcome the obstacle to blood flow when expelling it into the aorta or push out a much larger volume of blood than is normal. The causes of overload can be diseases and conditions such as:

- arterial hypertension (90% of all cases of hypertrophy are associated with high blood pressure for a long time, as a constant vasospasm and increased vascular resistance develop)
- congenital and acquired heart defects - aortic stenosis, insufficiency of the aortic and mitral valves, coarctation (narrowing of the area) of the aorta
- atherosclerosis of the aorta and the deposition of calcium salts in the leaflets of the aortic valve and on the walls of the aorta
- endocrine diseases - diseases of the thyroid gland (hyperthyroidism), adrenal glands (pheochromocytoma), diabetes mellitus
- obesity of food origin or due to hormonal disorders
- frequent (daily) use of alcohol, smoking
- professional sports - athletes develop myocardial hypertrophy as a response to a constant load on the skeletal muscles and the heart muscle. Hypertrophy in this contingent of individuals is not dangerous if the blood flow to the aorta and the systemic circulation is not disturbed.

Risk factors for the development of hypertrophy are:

- burdened heredity for heart disease
– obesity
gender (usually male)
– age (over 50 years old)
- increased intake of salt
- disorders of cholesterol metabolism

Symptoms of left ventricular hypertrophy

The clinical picture of left ventricular myocardial hypertrophy is characterized by the absence of strictly specific symptoms and consists of manifestations of the underlying disease that led to it, and manifestations of heart failure, rhythm disturbances, myocardial ischemia and other consequences of hypertrophy. In most cases, the period of compensation and absence of symptoms can last for years, until the patient undergoes a planned cardiac ultrasound or notices the appearance of complaints from the heart.
Hypertrophy can be suspected if the following signs are observed:

- a long-term increase in blood pressure, for many years, which is especially difficult to correct with medication and with high blood pressure (more than 180/110 mm Hg)
- the appearance of general weakness, increased fatigue, shortness of breath when performing those loads that were previously well tolerated
- there are sensations of interruptions in the work of the heart or obvious rhythm disturbances, most often atrial fibrillation, ventricular tachycardia
- swelling on the legs, hands, face, more often occurring by the end of the day and disappearing in the morning
- episodes of cardiac asthma, choking and dry cough in the supine position, more often at night
- cyanosis (blue) of the fingertips, nose, lips
attacks of pain in the heart or behind the sternum during exercise or at rest (angina pectoris)
- frequent dizziness or loss of consciousness
At the slightest deterioration in well-being and the appearance of heart complaints, you should consult a doctor for further diagnosis and treatment.

Diagnosis of the disease

Myocardial hypertrophy can be assumed during examination and questioning of the patient, especially if there is an indication of heart disease, arterial hypertension, or endocrine pathology in the anamnesis. For a more complete diagnosis, the doctor will prescribe the necessary examination methods. These include:

- laboratory methods - general and biochemical blood tests, blood for the study of hormones, urine tests.
- X-ray of the chest - a significant increase in the shadow of the heart, an increase in the shadow of the aorta with aortic valve insufficiency, aortic configuration of the heart with aortic stenosis - emphasizing the waist of the heart, shifting the left ventricular arch to the left can be determined.
- ECG - in most cases, the electrocardiogram reveals an increase in the amplitude of the R wave in the left, and the S wave in the right chest leads, deepening of the Q wave in the left leads, displacement of the electrical axis of the heart (EOS) to the left, displacement of the ST segment below the isoline, signs of blockade may be observed left bundle of His bundle.
- Echo - KG (echocardiography, ultrasound of the heart) allows you to accurately visualize the heart and see its internal structures on the screen. With hypertrophy, thickening of the apical, septal zones of the myocardium, its anterior or posterior walls is determined; zones of reduced myocardial contractility (hypokinesia) may be observed. The pressure in the chambers of the heart and large vessels is measured, the pressure gradient between the ventricle and the aorta, the cardiac output fraction (normally 55-60%), the stroke volume and the dimensions of the ventricular cavity (EDV, ESV) are calculated. In addition, heart defects are visualized, if any, were the cause of hypertrophy.
- stress tests and stress - Echo - CG - ECG and ultrasound of the heart are recorded after exercise (treadmill test, bicycle ergometry). Needed to obtain information about the endurance of the heart muscle and exercise tolerance.
- 24-hour ECG monitoring is prescribed to register possible rhythm disturbances, if they were not previously registered on standard cardiograms, and the patient complains of interruptions in the work of the heart.
- according to indications, invasive research methods can be prescribed, for example, coronary angiography to assess the patency of the coronary arteries if the patient has coronary heart disease.
- MRI of the heart for the most accurate visualization of intracardiac formations.

Treatment of left ventricular hypertrophy

Treatment of hypertrophy is primarily aimed at treating the underlying disease that led to its development. This includes the correction of blood pressure, medical and surgical treatment of heart defects, therapy of endocrine diseases, the fight against obesity, alcoholism.

The main groups of drugs aimed directly at preventing further violations of the geometry of the heart are:

- ACE inhibitors (hartil (ramipril), fozicard (fosinopril), prestarium (perindopril), etc.) have oranoprotective properties, that is, not only protect the target organs affected by hypertension (brain, kidneys, blood vessels), but also prevent further remodeling (rearrangement) of the myocardium.
- beta-blockers (nebilet (nebivalol), anaprilin (propranolol), recardium (carvedilol), etc.) reduce the heart rate, reducing the muscle's need for oxygen and reducing cell hypoxia, as a result of which further sclerosis and replacement of sclerosis zones by hypertrophied muscle slow down. They also prevent the progression of angina pectoris, reducing the frequency of attacks of pain in the heart and shortness of breath.
- calcium channel blockers (norvasc (amlodipine), verapamil, diltiazem) reduce the calcium content inside the muscle cells of the heart, preventing the build-up of intracellular structures, leading to hypertrophy. They also reduce heart rate, reducing myocardial oxygen demand.
- combined drugs - prestans (amlodipine + perindopril), noliprel (indapamide + perindopril) and others.

In addition to these drugs, depending on the underlying and concomitant cardiac pathology, the following can be prescribed:

- antiarrhythmic drugs - cordarone, amiodarone
- diuretics - furosemide, lasix, indapamide
- nitrates - nitromint, nitrospray, isoket, cardiket, monocinque
- anticoagulants and antiplatelet agents - aspirin, clopidogrel, plavix, chimes
- cardiac glycosides - strophanthin, digoxin
– antioxidants – mexidol, actovegin, coenzyme Q10
- vitamins and drugs that improve heart nutrition - thiamine, riboflavin, nicotinic acid, magnerot, panangin

Surgical treatment is used to correct heart defects, implantation of an artificial pacemaker (artificial pacemaker or cardioverter - defibrillator) with frequent paroxysms of ventricular tachycardia. Surgical correction of hypertrophy directly is used in case of severe obstruction of the outflow tract and consists in performing the Morrow operation - excision of a part of the hypertrophied cardiac muscle in the area of ​​the septum. In this case, an operation can be performed on the affected heart valves at the same time.

Lifestyle with left ventricular hypertrophy

Lifestyle for hypertrophy is not much different from the main recommendations for other heart diseases. You need to follow the basics of a healthy lifestyle, including eliminating or at least limiting the number of cigarettes you smoke.
The following lifestyle components can be distinguished:

- mode. You should walk more in the fresh air and develop an adequate regime of work and rest with sufficient sleep for the duration necessary to restore the body.

- diet. It is advisable to cook dishes in boiled, steamed or baked form, limiting the preparation of fried foods. Of the products, lean meats, poultry and fish, dairy products, fresh vegetables and fruits, juices, kissels, fruit drinks, compotes, cereals, vegetable fats are allowed. Abundant intake of liquids, table salt, confectionery, fresh bread, animal fats is limited. Alcohol, spicy, fatty, fried, spicy foods, smoked meats are excluded. Eat at least four times a day in small portions.

- physical activity. Significant physical activity is limited, especially with severe obstruction of the outflow tract, with a high functional class of coronary artery disease or in the late stages of heart failure.

Compliance (adherence to treatment). It is recommended to regularly take the prescribed drugs and visit the attending physician in a timely manner in order to prevent the development of possible complications.

Working capacity for hypertrophy (for the working population of persons) is determined by the underlying disease and the presence/absence of complications and concomitant diseases. For example, in case of a severe heart attack, stroke, severe heart failure, an expert commission can decide on the presence of a permanent disability (disability), with a deterioration in the course of hypertension, temporary incapacity for work is observed, recorded on a sick leave, and with a stable course of hypertension and the absence of complications, the ability to work is fully preserved .

Complications of left ventricular hypertrophy

With severe hypertrophy, complications such as acute heart failure, sudden cardiac death, fatal arrhythmias (ventricular fibrillation) may develop. With the progression of hypertrophy, chronic heart failure and myocardial ischemia gradually develop, which can cause acute myocardial infarction. Rhythm disturbances, such as atrial fibrillation, can lead to thromboembolic complications - stroke, pulmonary embolism.

Forecast

The presence of myocardial hypertrophy in malformations or hypertension significantly increases the risk of developing chronic circulatory failure, coronary artery disease and myocardial infarction. According to some studies, the five-year survival of patients with hypertension without hypertrophy is more than 90%, while with hypertrophy it decreases and is less than 81%. However, if drugs are taken regularly to regress hypertrophy, the risk of complications is reduced and the prognosis remains favorable. At the same time, with heart defects, for example, the prognosis is determined by the degree of circulatory disorders caused by the defect and depends on the stage of heart failure, since the prognosis is unfavorable in its later stages.

Therapist Sazykina O.Yu.

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A 51-year-old man, from school to this day he plays volleyball, football, basketball (amateur)
He often suffered from lacunar tonsillitis, in 1999 he again had lacunar tonsillitis (purulent) 2 times in a row. They did an ECG: RR interval 0.8; transition zone V3-V4; PQ intervals 0.16; QRS 0.08; QRST 0.36; the QRS complex is not changed AVF is serrated. Conclusion: sinus rhythm with a heart rate of 75 per 1 min, the normal position of the email. axis of the heart, violation of the / stomach. conduction .. In 2001, he was worried about pressing pains in the chest (mostly at rest, in the mornings). He was on outpatient treatment (10 days). cl, there were no examinations, except for the ECG. ECG 2001: signs of LV hypertrophy with subepinardial ischemia of the anterior wall. Violation of intraventricular conduction. The attacks were not long up to 2 minutes and not frequent, mostly without nitroglycerin, he refused at the end of treatment, because. had severe headaches. He didn’t go to the hospital anymore, but he participated in football, volleyball competitions, went fishing for 20 km. At the same time, he was given a duodenal ulcer, he treated the ulcer with folk remedies, but he did not take any drugs from the heart. Until 2007, single seizures that took place in a sitting position, after that nothing bothers at all, seizures have not been repeated even once to this day. He also leads an active lifestyle, there is no shortness of breath, swelling, he always walks, headaches do not bother. In 2008, again, purulent tonsillitis., from t to 41, somehow brought down by that. at home, they brought down sharply to 36.8, but the next day at the doctor's appointment it was already 38.5.
In 2008, he was hospitalized on a planned basis to clarify the diagnosis.
Diagnosis: hypertension 11st. HNS o-1, ischemic heart disease, angina pectoris 1 fc, PICS? Infective endocarditis, remission?, duodenal ulcer, remission
Examination data: Ultrasound of the heart
MK: pressure gradient - norm, regurgitation - subvalve, thickening of PSMK. AK: aortic diameter (not clear further) - 36 mm, aortic diameter at the level of the ascending section - 33 mm, aortic walls are sealed, systolic divergence of the valves - 24, pressure gradient max - 3.6 mm Hg, regurgitation - no, education d = 9.6 mm in the field of RCC-vegetation?. TK-regurgitation subclap, LA-regurgitation subclap. LV: KDR-50 mm, KSR-36mm, PZh-23mm, LP-37mm, MZHP-10.5mm, ZSLZh-10.5mm, FV-49. The pericardium is not changed.
ECG test with doses. physical load (VEM) - negative tolerance test in / sterd
holter.monitoring of ECG: daily dynamics of heart rate - during the day - 63-151, at night - 51-78, sinus rhythm. Ideal arrhythmia: single PVCs - total 586, single PE - total 31, SA blockade with pauses up to 1719 msec - total 16. ECG signs of myocardial ischemia were not registered. They checked the esophagus, put the gastro-duodenitis. Ultrasound of the kidneys - no pathology of the kidneys was detected. An examination at the Institute of the Heart (PE_EchoCG, CVG) was recommended. Didn't take prescribed medicines. In 2009, he wasn't examined anywhere.
2010 — examination at the Regional Cardiology Department Diagnosis: coronary artery disease. Angina pectoris 11fc, PICS (undated), hypertension stage 11, graded, correction to normotension, risk 3. Transient W-P-W syndrome, right coronary leaflet formation, CHF 1 (NYHAI FC)
Examination:
PE Echo-KG: on the right coronary leaflet, a rounded, suspended formation (d 9-10mm) on a pedicle (pedicle 1-6-7mm, thickness 1mm) is located, emanating from the edge of the leaflet
Treadmill: At the 3rd step of the load, the proper heart rate was not reached. The maximum increase in blood pressure! :) / 85 mm Hg. Under load, transient WPW syndrome, type B, single ventricular extrasystole. Changes in ST, ST were not revealed. Tolerance to the load is very high, the recovery period is not slowed down.
24-hour blood pressure monitoring: Daytime hours: max SBP-123, max DBP-88, min SBP-101, min DBP 62. Night hours: max SBP-107, max DBP57, min SBP-107, min DBP-57
Daily ECG monitoring: Con: Sinus rhythm heart rate 46-127 per minute (average-67 per minute). Episodes of elevation and depression of the ST segment were not registered, ventricular ectopic activity: single PVCs-231, Bigeminia (number of PVCs)-0, paired PVCs (couplets)-0, jogging VT (3 or more PVCs)-0. Supraventricular ectopic activity: single NZhES-450, Paired NZhES 9 couplets) -15, runs SVT (3 or more NZhES) -0. Pauses: registered-6. Max. duration-1,547s.
Recommendations: consultation at the Heart Institute to resolve the issue of surgical treatment. Doesn't take medicine. At the next inspection, they wrote that 1 year is given for the work of a gas compressor station driver, then for professional suitability
2011 Heart Institute (from 24.05 to 25.05)
Diagnosis: ischemic heart disease, vasospatic angina pectoris, postinfarction cardiosclerosis (with Q wave posterior undated)
Echo KG: AO-40 ascend + 40 arc 29, S1 22, S2 17, LP-38 * 49 * 59, Vlp 53.9, PZH26, thick. 41, UI35,
SI 2.4, MZHP14, ZSLZH13, PP43-53, NPV17, VTLZH22, Vel / TVI / Pg 0.6 / 1.4, AK is not changed, AK (opened) 20, FK25, Vel / TVI / Pg 0, 9/3.2; \u003d 1.96 m2, slight dilatation of the RA, slight LVH, hypokinesis of the posterolateral, lower walls at the basal level, lower septal segment. LV function is reduced, type 1 LVDD
Coronography (irradiation dose 3.7 mSv): no pathologies, type of blood circulation is right, LVHA is normal Conservative treatment is recommended
07/18/2011 underwent Echo-KG without presenting a diagnosis, just to be checked
Results: Dimensions: KSR-35mm., KDR-54mm., KSO-52ml., KDO 141ml, Ao-31mm, LP-34*38*53mm., PP-35*49mm., PS-4mm., MZHP-13mm ., ZS-12mm., PZh-28mm., La-26mm, NPV-17mm. Function: EF-62%., UO-89 ml., FU-32%. Valves: Mitral valve: Ve-57cm/sec, Va-79cm/sec, VE/Va 41;
-Ch-K position-51-38; aorta: diameter-035; opening of AO cl-21; left ventricle: KDR-59; KSR-42; KDO-171; KSO-79; UO-92; FV-54%; MZHP-15; ZSLZh-14/15
right atrium: long axis-48; short axis-40; right ventricle: parasternal-25; NEP, diameter-23; NEP,% collapse-No.; pulmonary artery: diameter-23; SDLA-No.; aortic class: area-No.; mitral class: area-No.
Conclusion: the aorta is not dilated, moderate dilatation of the left chambers of the heart, symmetric LV hypertrophy, type 1 diastolic dysfunction, LVMI 240g/m (m squared) is above normal, the valves are not changed, there are no local myocardial contractility disorders, global contractility slightly reduced. Ultrasound was done by a doctor of the highest category.
Results of the 2nd study.
AO-37v-35; S1-17; S2-16; LP-34x42x51;
V lp-45ml; PZH-22; KSRLV-44; KDRLV-62; KSO-89; KDO-197; UO-108; FV-55; FU-29; MZHP-12; ZSLZH-12; PP-31x43; pericardium-No; AK-not changed; AK 9 open) -27; FK-23; VeI/TVI/Pg-1.0/4.0; regurgitation-not detected; MK-not changed; FC-32; VeI/Pg-0.5/1.0; regurgitation-not detected; TK-not changed; regurgitation-not detected; LA-25; VeI/Pg-0 .77/2.3; R cf.LA-19.0
Conclusion: BCA-1.93 m2, pronounced LV dilatation (LV end-of-life index-102ml/m2; pronounced eccentric LVH (OTS-0.39; myocardial MI-204g/m2), no significant zones of LV asynergy were identified, LV systolic function is satisfactory , LVDD type 1, valves are not changed, normal pressure in the LA. Ultrasound was done by a doctor of the highest category, head of the cardiology department. We undergo so many ultrasounds to prove that my husband did not have a heart attack, because the results of the examination do not confirm this, and he is fired from work due to the diagnosis.His blood pressure is 123/80, recently it was 130/80, pulse is 72, at the doctor's appointment his blood pressure was 140/82, heart rate was 75. We filed with the expert commission to reconsider the diagnosis. Questions: 1) how are the last ultrasounds of the heart interpreted (given that everything is in order with other examinations? 2) If he had PICS since 2001 or 2004, could he feel so great without any medications? 3) can there be a myocardial infarction with clean coronary vessels? 4) can frequent tonsillitis affect the thickening of the walls (according to the latest ultrasound, we were told that he had a thickening of the walls, which may have been mistaken for a post-infarction scar, and even before that, when he underwent a m / commission, some doctors allegedly saw a scar, others do not, and were very surprised that he had coronary artery disease and a heart attack, because again, nothing was confirmed, but he was stubbornly rewritten from year to year) His parents do not have coronary artery disease, his mother is 78 years old, she has low blood pressure I would like to know What is your opinion on this man? (MRI of the heart is not done in our region, because myocardial scintigraphy is also performed). Thanks in advance for the replies!

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The human heart has great potential - it is able to increase the volume of pumped blood by 5-6 times. This is facilitated by an increase in heart rate, which is observed under the condition of an increased need for organs in nutrients and oxygen. This is the contractility of the myocardium, which allows the heart to adapt to the state of the body in which it is located at the moment.

It happens that when the load increases, the heart continues to work in its usual state, without increasing the frequency of contractions. This contributes to the disruption of metabolic processes in all organs, oxygen starvation. That is why reduced myocardial contractility should be a cause for concern. If it is left unattended, there is a risk of developing complications that manifest themselves in various diseases, more often cardiovascular.

Reasons for the decrease in SS

When, during the examination, the doctor notes reduced contractility of the left ventricular myocardium, it is important to identify the cause of this condition. With its removal, treatment will begin. Sometimes the causative factor is an unhealthy lifestyle, for example, an unbalanced diet, excessive physical activity. The heart has to work in an enhanced mode, but at the same time it does not receive the proper amount of oxygen and nutrients, the myocardium is not able to produce the necessary amount of energy. And if for the first time the internal energy potential is used, which allows maintaining a satisfactory contractility of the myocardium, after its exhaustion, malfunctions in the work of the heart will begin to appear, requiring attention. To restore a normal state of health in this case, it is enough to undergo a course of treatment with drugs that normalize the functional abilities of the organ and metabolic processes in it.

Often the cause of a decrease in the contractile function of the heart muscle is a person's diseases, such as:

• myocardial infarction;
• brain injury;
• surgical intervention;
• ingestion of toxic substances;
• atherosclerotic vascular lesions;
• avitaminosis;
• myocarditis.

Important! It is necessary to think not only about the causes of the violation of local contractility of the heart muscle, but also about its consequences. If this condition persists for a long time, it may result in heart failure, which poses a threat to human life.

How to detect reduced myocardial CV

Symptoms such as:

• increased fatigue;
• weakness;
• shortness of breath, difficulty breathing;
• dizziness, especially after physical exertion.

Such signs indicate the presence of various disorders and diseases, but should not be ignored. A cardiologist will send him for examination in order to obtain complete information regarding the patient's state of health. Usually, the following studies are sufficient to make an accurate diagnosis:

1. ECG is the most informative method of examination. It allows differentiating satisfactory contractility of the left ventricular myocardium from reduced contractility, providing full information about the patient's health status. To have more detailed data, an ECG is performed with a load using a special exercise bike. If after physical exertion the contractility of the myocardium is preserved, then there are no pathologies. Doctors also recommend Holter monitoring, which allows you to monitor heart rate in different human conditions.
2. Ultrasound of the heart. No less informative method. With its help, it is possible to determine the presence of changes in the structure and size of the organ, myocardial excitability, as well as other processes occurring in the heart during its work.
3. Laboratory blood tests. They make it possible to diagnose inflammatory diseases or metabolic disorders, which can also cause a violation of the contractility of the heart muscle.

After completion of the examination, the patient will be prescribed treatment, which is carried out in most cases by a conservative method.

Features of treatment

When it is noted that the contractility of the heart muscle is reduced due to improper work and rest or nutrition, a person will be given general recommendations that involve restoring the normal balance of states of activity and rest, they can prescribe vitamin preparations that replenish the energy reserves of the middle layer of the heart.

If global contractility is diagnosed, longer treatment will be needed here. It usually involves the patient taking the following drugs:

• phosphocreatine;
• panangin;
• riboxin;
• iron preparations;
• mother's milk.

Additionally, treatment will be carried out aimed at eliminating the root cause of the pathological condition. His tactics depend on the disease that provoked the development of a decrease in the contractility of the heart muscle. If there are cardiac diseases, drugs aimed at normalizing blood circulation, stabilizing excitability processes in the myocardium, as well as antiarrhythmic drugs will be used.

Normokinesis and its definition

If you are interested in the question regarding what normokinesis is, then under this term often used in medical practice, doctors understand the ratio of a person’s state (physical or emotional) and indicators of the contractility of the heart muscle. Based on this, a conclusion is made about the patient's state of health, the need for treatment.

To draw up a specific therapy program, doctors will need to conduct a complete examination of the patient in order to accurately determine the cause of such a condition. Next, therapy will begin, aimed at normalizing the work of the heart and restoring the necessary indicators of its contractility.

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

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

Bioelectric bases of myocardial contractility

heart beat cycle

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

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

Video: more about the biochemistry of myocardial contractility

Why do you need to know about myocardial contractility?

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

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

Myocardial contractility according to ECG

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

Myocardial contractility by echocardiography

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

photo: assessment of myocardial contractility on echocardiography with exercise

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

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

sections of the heart muscle on echocardiography

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

Normal contractility of the heart and violations of myocardial contractility

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

Based on this, the following concepts can be distinguished:

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

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

What diseases are associated with violations of myocardial contractility?

graphs of changes in myocardial contractility in various situations

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

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 causes of a 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 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 increased physical activity decreases, so there is an insufficiency of the pumping function. Over time, against the background of complete decompensation, symptoms of reduced contractility appear even at rest.

Learn more about the complications of myocardial infarction here.

The function is preserved - an indicator of the norm?

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

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

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

Reasons for changing state

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

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

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

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

Manifestations of reduced myocardial contractility

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

Classification of acute disorders of cerebral circulation

Changes in gas exchange

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

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

Water retention and swelling

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

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

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

congestion

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

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

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

Diagnosis of the contractility of the ventricles of the myocardium

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

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

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

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

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

Watch the video about the methods of examining the heart:

Treatment in case of deviation

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

Drug therapy includes the following groups of drugs:

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

Learn more about cardiac dilatation here.

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

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

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

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

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

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

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

We will publish information shortly.

Global contractility of the left ventricular myocardium is preserved

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

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

Additional trabecula in the cavity l.zh.

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

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

Myocardial contractility

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

Causes of reduced contractility

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

Also, a decrease in myocardial contractility can occur:

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

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

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

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

Diagnostics

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

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

Treatment

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

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

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

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

Echocardiography: left ventricular systolic function

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

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

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

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Even with proper medical treatment, mortality from heart failure remains high. Most clinical trials did not include patients with severe or end-stage heart failure (stage D). These patients are often indicated for heart transplantation.

However, in 2001, there were 40,000 patients on the waiting list for heart transplants in the United States, while only 2,102 were performed. To close this gap, some alternative to heart transplantation is needed. Many surgical interventions are being developed to at least improve the condition of patients and allow them to survive until heart transplantation. Improvements in cardiac surgery and a better understanding of the changes that occur in heart failure have led to the proliferation of some new surgical treatments. However, data on the safety and effectiveness of many methods is still insufficient. This article discusses elective operations for heart failure (myocardial revascularization, mitral valve surgery, cardiomyoplasty, geometric reconstruction of the left ventricle - Dora operation) and emergency measures of circulatory support (up to a completely artificial heart). Surgical interventions should be accompanied by active medical treatment.

Coronary artery bypass grafting for ischemic cardiomyopathy

With severe damage to the coronary arteries, the blood supply to the myocardium suffers and cardiomyocytes undergo hypoxia, as a result of which their work is disrupted.

With myocardial infarction, necrosis occurs, and then scars are formed that are unable to contract. The areas of the myocardium adjacent to the infarction undergo mechanical stretching, as a result of which, over time, the left ventricle is restructured, its cavity increases, and systolic and diastolic function deteriorates.

Severe ischemia, in addition to myocardial infarction, can cause its stunning and transition to a state of "hibernation" (sleeping myocardium). At the same time, cardiomyocytes can remain viable and, when their blood supply is restored, restore their function. Dormant and stunned myocardium can be detected by special methods.

Myocardial stunning is the loss of contractility due to short-term acute ischemia.

The dormant myocardium occurs in chronic ischemia, the loss of contractility allows it to remain viable. The dormant myocardium continues to capture glucose from the blood, but the mass of contractile proteins in it decreases and glycogen accumulates.

Clinical Significance

Often, especially with initial heart damage, ischemia may manifest itself not as angina pectoris, but as heart failure.

In about two-thirds of cases, the main cause of impaired contractility is damage to the coronary arteries. Coronary angiography is indicated in all cases where an ischemic origin of dilated cardiomyopathy is suspected.

Occasionally, coronary artery disease overlaps with dilated cardiomyopathy of another etiology. In this case, the degree of impaired contractility does not correspond to the severity of coronary artery disease. In these patients, the feasibility of revascularization is questionable.

There are no reliable data on the effectiveness of coronary artery bypass grafting in ischemic cardiomyopathy. However, according to clinical observations and case-control studies, with the right selection of patients, coronary bypass surgery improves the prognosis for ischemic cardiomyopathy. Therefore, when the left ventricular ejection fraction is greater than 15%, the end-diastolic size of the left ventricle is less than 65 mm, the distal bed of the coronary arteries suitable for shunting, and a large amount of ischemic or dormant myocardium, coronary bypass grafting is indicated. These recommendations are conditional, in many clinics coronary bypass surgery is made even more seriously ill. However, for those who require continuous IV infusion of inotropic agents, coronary bypass surgery is usually not performed.

In severe left ventricular systolic dysfunction and dormant myocardium, coronary artery bypass grafting can be as effective as heart transplantation (three-year survival rate is approximately 80%).

It is generally believed that a significant improvement justifying surgery is possible if the proportion of dormant and ischemic, but working myocardium is more than 60%.

Perioperative mortality increases if more than 40% of the left ventricle is scar tissue or non-viable (metabolically inactive) myocardium.

Coronary bypass surgery for severe heart failure is part of a complex treatment that may also include the following: valve repair, geometric reconstruction of the left ventricle (Dora operation), destruction of sources of ventricular tachycardia and labyrinth surgery (Cox operations) or isolation of pulmonary veins for atrial fibrillation. To achieve the maximum effect, it is necessary to continue active drug treatment after the operation.

Operations on the mitral valve

Regardless of the cause of left ventricular dysfunction, left ventricular dilatation and reshaping lead to mitral regurgitation. This, in turn, leads to an overload of the left ventricle with volume, its further dilatation, and further enhances mitral insufficiency.

Damage to the valve itself and its ring, ischemia and infarction of the papillary muscles, changes in the shape of the left ventricle, thinning of the myocardium and dilatation of the left ventricle, divergence of the papillary mice and valve cusps with a violation of their closure contribute to mitral insufficiency.

• Restoration of valve occlusion by annuloplasty reduces mitral regurgitation and improves the shape of the left ventricle; this may increase cardiac output in dilated cardiomyopathy. With ischemic cardiomyopathy, mitral valve repair, however, is less effective than with damage to the valve itself.

• The subvalvular structures are kept as intact as possible.

• In some patients, mitral valve repair improves well-being, but it is not clear whether it affects survival.

• The convergence of the mitral valve leaflets according to Alfieri sometimes gives more reliable results compared to simple annuloplasty.

• Mitral valve replacement is not required in most cases, the prognosis after it is much worse than after plastic surgery.

  Treatment of diastolic heart failure

  Diastolic heart failure is treated differently than systolic: the leading role is played by a decrease in blood pressure, elimination of myocardial ischemia and a decrease in KDD in the left ventricle.

  Reverse development of left ventricular hypertrophy.

  • Antihypertensive drugs.
  • Surgery (eg, valve replacement for aortic stenosis)

  Increased compliance of the left ventricle

  • Reduced afterload.
  • Elimination of myocardial ischemia.
  • Calcium antagonists (?)

  Prevention and treatment of ischemia

  • Beta blockers.
  • Nitrates.
  • Surgical treatment of coronary artery disease

  Preload Reduction

  • Diuretics.
  • Nitrates.
  • ACE inhibitors.
  • low salt diet

  Decreased heart rate

  • Beta blockers.
  • Verapamil.
  • Digoxin (with atrial fibrillation).
  • Cardioversion (for atrial fibrillation)

  In arterial hypertension, lowering blood pressure helps prevent the progression of left ventricular hypertrophy, and sometimes achieve its reverse development. In addition, lowering blood pressure helps to improve left ventricular diastolic filling, reduce left atrial stress, and maintain sinus rhythm.

  Calcium antagonists not only have a hypotensive effect, but also improve the relaxation of the left ventricle. It is assumed that ACE inhibitors and angiotensin receptor blockers give the same effect; in addition, they are able to prevent cardiosclerosis and even lead to its reverse development. So far, however, calcium antagonists and ACE inhibitors have not been proven to reduce mortality in diastolic heart failure.

  Left ventricular hypertrophy predisposes to subendocardial myocardial ischemia even in the absence of CAD. Ischemia makes the left ventricle even less compliant, which exacerbates diastolic dysfunction. Since coronary blood flow occurs primarily in diastole, tachycardia impairs the perfusion of subendocardial myocardium, so it is very important to reduce heart rate in such cases. For this purpose, b-blockers and calcium antagonists (verapamil or diltiazem) are prescribed.

  In coronary atherosclerosis, coronary bypass surgery or balloon angioplasty is indicated.

  With pulmonary congestion, a quick effect is usually obtained by reducing preload with diuretics and nitrates. However, even a small decrease in the volume of the stubborn left ventricle can cause a sharp drop in diastolic pressure in it, stroke volume, cardiac output and blood pressure. It is therefore important to avoid excessive preload reduction.

  Due to the inflexibility of the left ventricle, its filling is disturbed at the beginning and in the middle of diastole, and atrial systole (atrial pumping) makes an increasing contribution. Therefore, to maintain cardiac output, it is important to maintain sinus rhythm. With atrial fibrillation, electrical or medical cardioversion is indicated. Prior to it, anticoagulants are prescribed and heart rate is reduced with b-blockers, calcium antagonists, or digoxin.

  Prof. D.Nobel

  "Treatment of diastolic heart failure" article from the section Cardiology

  Additional Information:

  Treatment of heart failure. heart failure drugs

  

  

  

  

  Treatment of heart failure is aimed at reducing the increased excitability of the respiratory center; reduction of blood stagnation in the pulmonary circulation; increase in the contractile function of the myocardium of the left ventricle.

  The patient is provided with rest in a sitting position, with legs down or half-sitting (in the absence of a collaptoid state). The patient is freed from restrictive clothing, and fresh air is supplied to the room.

  To reduce the excitability of the respiratory center, narcotic analgesics are administered subcutaneously (morphine, promedol in combination with atropine to reduce the vagotropic effect of narcotic drugs). Quite often, only the use of these drugs stops an attack of cardiac asthma. With a decrease in blood pressure after the administration of drugs, vascular agents (mezaton, cordiamin) are injected subcutaneously.

  

  Reducing blood stasis in the vessels of the small circle (with elevated or normal blood pressure) is achieved by applying tourniquets to the limbs and bleeding up to 200-300 ml of blood. A hot foot bath with mustard also helps. If blood pressure is elevated, then intravenous administration of aminophylline, as well as subcutaneous ganglion blockers, is effective.

  An increase in the contractile function (of the left ventricle) is achieved by intravenous administration of fast-acting cardiac glycosides (strophanthin or corglicon).

  If an attack of cardiac asthma develops in a patient with mitral stenosis, then it is impossible to use cardiac glycosides, as this will further enhance the work of the heart and cause an even greater blood flow to the heart, leading to a further increase in congestion in the vessels of the small circle. In such cases, a fast-acting diuretic (furosemide) should be administered intravenously. It should be noted that ganglion blockers and diuretics are contraindicated in patients with reduced blood pressure. After the relief of an asthma attack, such patients should be constantly monitored, since a recurrence of an attack is possible.

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 left ventricular myocardium, 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.

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

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

The elementary contractile unit of the myocardium is the sarcomere, 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 volume overload of the ventricles. AMP normokinesis ranges from 0.5 to 0.8 centimeters. The amplitude index of the posterior wall of the left ventricle is from 0.9 to 1.4 cm.

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

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

Do I need to treat violations of myocardial contractility

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

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

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

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.).

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

The heart muscle is the most enduring in the human body. The high performance of the myocardium is due to a number of properties of myocardial cells - cardiomyocytes. These properties include automatism (the ability to independently generate electricity), conductivity (the ability to transmit electrical impulses to nearby muscle fibers in the heart) and contractility - the ability to contract synchronously in response to electrical stimulation.

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

Bioelectric bases of myocardial contractility

heart beat cycle

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

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

Video: more about the biochemistry of myocardial contractility

Why do you need to know about myocardial contractility?

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

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

Myocardial contractility according to ECG

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

Myocardial contractility by echocardiography

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

photo: assessment of myocardial contractility on echocardiography with exercise

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

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

sections of the heart muscle on echocardiography

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

Normal contractility of the heart and violations of myocardial contractility

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

Based on this, the following concepts can be distinguished:

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

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

What diseases are associated with violations of myocardial contractility?

graphs of changes in myocardial contractility in various situations

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

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 causes of a 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

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Indicators of myocardial contractility

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

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

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

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

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

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

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

Formula (130) is the most convenient, and the resulting value is close to 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.