October 24, 2017 No comments

Heart failure is a severe pathological process that in some cases leads to death in a matter of hours (acute heart failure), while in others it progresses over many years (chronic heart failure). This syndrome develops as a consequence of many diseases of the cardiovascular system and requires intensive complex treatment. In chronic heart failure, five-year and ten-year survival rates are 50% and 10%, respectively, from the time of diagnosis.

Definition of the concept and classification

Heart failure is a condition characterized by a decrease in the reserve capacity of the heart.

This definition was proposed by professors V.A. Frolov, T.A. Kazanskaya, G.A. Drozdova and other employees of the Department of General Pathology and Pathological Physiology of the Peoples' Friendship University of Russia on the basis of many years of research into this process. We believe that it is applicable to both acute and chronic heart failure and takes into account even those forms that in the initial stages occur only with a decrease in the functional reserves of the myocardium caused by certain types of functional load.

Classification of heart failure

The classification of heart failure can be based on several different criteria.

I. According to the clinical course:

Chronic.

Acute heart failure is characterized by the rapid development and increase in the severity of hemodynamic disorders. It can lead to the death of the patient in a very short time (from a few minutes to several hours).

Chronic heart failure usually develops over many years and is characterized by alternating periods of exacerbation and periods of compensation.

II. By the value of the minute volume of the heart:

With a reduced minute volume of the heart - in most cases, I heart failure is accompanied by a decrease in minutes - in the volume of the heart, due to a violation of the contractile activity of the left or right ventricles;

With increased cardiac output - with individual slaughter (thyrotoxicosis or beriberi disease), chronic heart failure, despite a decrease in myocardial contractile function, is characterized by an increase in cardiac output due to sinus tachycardia. It should be noted that such a variant of insufficiency has a more unfavorable course, since in this case the energy resources of the myocardium are depleted very rapidly.

III. According to the department of the heart, which is involved in the pathological process.

• left ventricular;
• right ventricular;
• total (both ventricles of the heart are in a state of insufficiency).

IV. According to the etiopathogenetic principle:

• myocardial heart failure, which develops as a result of direct damage to the heart muscle (for example, with myocardial infarction, cardiomyopathy, myocarditis, etc.); overload heart failure - in this case, the pathological process is caused by a chronic significant increase in hemodynamic load, exceeding the ability of the corresponding part of the heart to overcome it (with arterial hypertension, heart defects);
• mixed form - develops, as a rule, in the later stages of congestive heart failure, when myocardial damage occurs as a result of prolonged hemodynamic stress. In this case, the overload is also saved.

Heart failure (HF) is a typical form of the pathology of the cardiovascular system, characterized by the fact that the pumping function of the heart does not provide a level of systemic hemodynamics adequate to the metabolic needs of the body [uncompensated form of HF] or maintains it due to the implementation of pre-existing and / or newly formed compensatory mechanisms of the body [ compensated form of CH].

Forms of heart failure

The following are the main forms of heart failure:

A. Downstream:

a) acute (minutes, hours);

b) chronic (weeks, months, years).

B. According to the severity:

a) compensated;

b) uncompensated.

B. By pathogenesis:

a) myocardial;

b) reloading;

c) mixed (combined - a combination of myocardial and overload).

D. According to the primary disturbed phase of the cardiac cycle:

a) systolic;

b) diastolic.

D. By localization:

a) left ventricular, which is characterized by a decrease in the ejection of blood into the aorta, overdistension of the left heart and stagnation of blood in the pulmonary circulation;

b) right ventricular, which is characterized by a decrease in the release of blood into the pulmonary circulation, overdistension of the right heart and stagnation of blood in the systemic circulation;

c) total (a combination of left and right ventricular failure). Differentiation of the forms of heart failure according to the mechanism of its development is most significant for the practitioner, because allows him to navigate the answer to the main question: “who is to blame for the violation of the pumping function of the heart”? Such "culprits" can be pathogenetically significant changes: 1) contractile properties of the myocardium; 2) preload (significant flow of blood into the cavity of the heart); 3) afterload (decrease in the outflow of blood from the cavities of the heart).

Pathogenesis

Acute heart failure

The cause of acute heart failure is excessive hemodynamic overload of the myocardium. This occurs with gross damage to the heart muscle, for example, with a macrofocal infarction of the left ventricle, accompanied by a sharp decrease in its contractile function.

There are serious disorders of hemodynamics. Overcoming the resulting overload of the heart muscle is possible only with a significant increase in the activity of intact myofibrils, which requires a significant increase in their energy supply.

Under these conditions, hyperfunction of mitochondria occurs. At the same time, the energy generated in them is almost completely spent on providing contractile activity, which allows myofibrils to function in an enhanced mode for a certain period of time. However, as a result of mitochondrial hyperfunction, damage and even destruction can occur, which obviously leads to an increase in energy deficit in the myocardium and, as a result, to a weakening of protein synthesis, which is also necessary for the formation of new mitochondria.

Thus, the deepening of the energy deficit is developing according to the principle of a vicious circle. Ultimately, energy depletion occurs, a sharp weakening of myocardial contractility up to fatal decompensation of the heart.

Chronic heart failure

In chronic heart failure, the myocardium is affected by a less pronounced pathogenic factor than in acute heart failure. Under these conditions, part of the energy generated in hyperfunctioning mitochondria can be spent on ensuring the processes of protein synthesis. As a result, a very important sanogenetic mechanism is activated - the development of myocardial hypertrophy, which makes it possible to overcome excessive load for a long time.

At the same time, myocardial hypertrophy also contains a significant pathogenetic potential, which begins to manifest itself especially sharply at the later stages of its development. The fact is that the development of hypertrophy is accompanied mainly by an increase in the mass of myofibrils (contractile elements experiencing hemodynamic overload), while an increase in the number of mitochondria and the mass of microvessels lags behind.

Thus, per unit mass of the myocardium, the number of mitochondria and the number of vessels in the hypertrophied myocardium becomes relatively smaller compared to the heart muscle of a healthy person. All this sooner or later leads to a shortage of energy production, which becomes chronic. In the myocardium, the so-called hypertrophied heart wear complex, characterized by a deficiency (of oxygen, the death of myofibrils, their replacement with connective tissue elements, a lack of mitochondria.

Myocardial form of heart failure

Myocardial form of heart failure occurs when the myocardium is damaged in the conditions of the development of coronary artery disease, myocarditis, myocardial dystrophy, cardiomyopathies. The pathogenetic basis of this form is pathogenetically significant changes in one of the two main properties of the myocardium - contractility (strength and speed of contraction of cardiomyocytes) and relaxation (speed and depth of relaxation of muscle fibers after their contraction).

Overload form of heart failure

Overload form of heart failure develops in conditions of overload of the heart:

a) volume (for heart defects with valve insufficiency, congenital non-closure of the interventricular septum, hypervolemia)

b) resistance (for heart defects with stenosis of the openings, coarctation of the aorta, arterial hypertension, polycythemia).

diastolic heart failure

It has been established that diastolic heart failure always includes diastolic dysfunction, but its presence does not yet indicate heart failure. Diastolic heart failure is diagnosed much less frequently than diastolic dysfunction, and is observed in no more than 1/3 of CHF patients.

There are 3 stages of transition from diastolic dysfunction to diastolic heart failure. At the 1st stage, under the influence of various damaging agents (overload, ischemia, infarction, left ventricular hypertrophy, etc.), the process of active relaxation of the myocardium and early filling of the left ventricle is disrupted, which at this stage is completely compensated by the activity of the left atrium, therefore it does not manifest even under load. The progression of the disease and an increase in the rigidity of the LV chamber is accompanied by a forced increase in LV filling pressure (the atrium can no longer cope!), which is especially noticeable during exercise. An even greater difficulty in blood flow to the left ventricle and a pathological increase in pressure in the pulmonary artery are observed, which reduces exercise tolerance (stage 2). A further increase in LV filling pressure (3rd stage) completely “disables” the left atrium; blood flow to the ventricle (blood outflow from the lungs) is critically reduced, which is accompanied by a drop in cardiac output, a sharp decrease in tolerance and congestion in the lungs, i.e., the formation of a detailed picture of CHF.

Thus, the transition from diastolic dysfunction of the left ventricle to diastolic heart failure is due to the classic variant of the development of stagnation caused by a decrease in blood outflow from the lungs, deterioration in active relaxation of the myocardium, and an increase in the rigidity of the LV chamber. Improving active relaxation and increasing compliance of the left ventricular chamber is believed to be the key to solving the problem.

Another feature of diastolic heart failure in comparison with the traditional (classical) variant of its development is a relatively better prognosis - the annual mortality rate in the diastolic variant is approximately two times less than in the "classic" systolic chronic heart failure. However, experts believe that such “well-being” is deceptive, since mortality from systolic CHF is constantly decreasing, and from diastolic heart failure it remains at the same level from year to year, which can be explained by the lack of sufficiently effective treatments for patients with diastolic form of chronic heart failure.

When the pumping function of the ventricles of the heart deteriorates, an increase in preload is able to maintain cardiac output. As a result, the left ventricle undergoes remodeling for a long time: it becomes more elliptical, expands and hypertrophies.

Initially compensatory, these changes eventually increase diastolic stiffness and wall tension (myocardial stress), disrupting the heart, especially during exercise. Increased cardiac wall tension increases oxygen demand and accelerates apoptosis (programmed cell death) of myocardial cells.

Manifestations of hemodynamic disorders

Developed acute heart failure (or exacerbation of chronic) is characterized by a number of disorders, first intraserious, and then systemic hemodynamics.

Tachycardia. This manifestation of heart failure occurs reflexively due to excessive stretching of the vena cava and plays a compensatory role: it provides increased blood flow to organs and tissues by increasing the cardiac output.

Increase in residual systolic volume of the heart. The residual systolic volume is the amount of blood that normally remains in the ventricles of the heart after the end of systole. Against the background of a decrease in myocardial contractility, the residual systolic volume increases in the cavity of the left (or right) ventricle.

Increase in end diastolic pressure. This indicator depends on the residual systolic volume. Obviously, an increase in this volume will be accompanied by an increase in end-diastolic pressure.

Ejection fraction is an important clinical criterion for assessing the state of the contractile function of the left ventricle. The ejection fraction is a ratio that reflects the proportion of left ventricular blood volume expelled into the aorta with each contraction (the ratio of stroke volume to end-diastolic volume). Normally, the ejection fraction in an adult should be 55-75%.

Dilatation of the ventricles of the heart. The expansion of the chambers of the heart develops as a result of an increase in systolic blood volume and an increase in end-diastolic pressure. There are two forms of dilatation of the ventricles of the heart: tonogenic and myogenic.

At tonogenic dilatation the contractile and elastic properties of the myocardium are sufficiently preserved, which in this case obeys the Frank-Starling law, according to which the corresponding chamber of the heart contracts the more efficiently in systole, the more it stretches in diastole.

Myogenic dilatation characterized by a sharp violation of this pattern due to a deep decrease in the elastic properties of the heart muscle. In this case, the myocardium begins to obey the Frank-Starling law to a much lesser extent.

An increase in pressure in the veins, through which blood is delivered directly to the decompensated heart. Against the background of dilatation, when the corresponding ventricle of the heart does not provide the necessary volume of cardiac output, there is a sharp increase in atrial pressure. With decompensation of the contractile activity of the left ventricle, the pressure in the left atrium increases and, as a result, the pressure in the veins of the pulmonary circulation increases. With decompensation of the right ventricle, accordingly, the pressure in the veins of the large circle increases.

Edema. Severe insufficiency of the left ventricle of the heart can lead to pulmonary edema due to stagnation of blood in the pulmonary circulation. In addition, the development of general edema is also possible, since a decrease in the release of blood into the aorta serves as a factor initiating the retention of sodium, and then water in the body. Right ventricular failure is accompanied by stagnation of blood in the systemic circulation, resulting in the development of peripheral edema. They begin to spread from the bottom (from the feet) upwards at a constant speed. Edema of the subcutaneous tissue is more pronounced in the evening.

Hepatomegaly and liver failure. These manifestations are explained by venous congestion in the liver. Hepatomegaly is one of the early symptoms of right ventricular failure and precedes the development of edema. Prolonged venous hyperemia of the liver leads to irreversible morphological changes, in which its functional activity begins to be disturbed. The syndrome of hepatic insufficiency develops.

Cyanosis. This symptom occurs due to insufficient oxygenation of the blood and more intensive utilization of oxygen by the tissues with a weakened blood circulation.

Ascites. In the later stages of the development of chronic heart failure, fluid containing protein may accumulate in the abdominal cavity. Ascites is one of the components of the general edematous syndrome, and the appearance of transudate in the abdominal cavity is explained by increased pressure in the peritoneal veins.

hydrothorax. This symptom, which, like ascites, is one of the manifestations of the general edematous syndrome, can occur with both left ventricular and right ventricular heart failure. This is due to the fact that the veins of the visceral pleura belong to the pulmonary circulation, and the parietal - to the large.

Cardiac cachexia. A sharp decrease in body weight and even wasting can be observed in the later stages of the development of heart failure.

Firstly, with decompensation of the activity of the heart, much more energy is required to overcome any load.

Secondly, with right ventricular failure, stagnation of blood in a large circle is accompanied by venous hyperemia of the intestine, leading to edema of its wall. Under these conditions, the process of absorption of nutrients is sharply disrupted.

Changes in the functions of the respiratory system

In addition to hemodynamic disorders, changes in the functions of the respiratory system also appear in heart failure.

Dyspnea. This symptom is due to stagnation of blood in the pulmonary circulation, as well as a violation of blood oxygenation.

Orthopnea. In heart failure, the patient takes a forced position of the body - sitting or lying with a raised headboard. This contributes to a decrease in blood flow to the right side of the heart, due to which there is a decrease in pressure in the pulmonary capillaries.

cardiac asthma. Patients suffering from heart failure often have attacks of shortness of breath and suffocation, mainly at night, accompanied by cough with sputum and bubbling breath.

Pulmonary heart

Cor pulmonale is a clinical syndrome in which there is an increase and expansion of the right side of the heart as a result of an increase in blood pressure in the pulmonary circulation due to chronic diseases of the lungs or bronchi.

According to the clinical course, cor pulmonale can be acute and chronic.

Acute cor pulmonale can be caused by two reasons. Firstly, it is an embolism of the small circle of blood circulation, in which emboli clog more than half of the pulmonary arteries (for example, with thromboembolism or embolism of the small circle). Secondly, massive thrombosis of small circle capillaries in DIC can lead to the occurrence of this syndrome.

Chronic cor pulmonale develops as a result of a prolonged increase in resistance in the pulmonary circulation that accompanies various chronic lung diseases, including emphysema and broncho-obstructive diseases (chronic obstructive bronchitis, bronchial asthma, bronchopulmonary dysplasia, etc.).

These diseases are characterized, among other things, by the appearance of pneumosclerosis of varying severity. In chronic cor pulmonale, a combination of syndromes of right ventricular and respiratory failure is observed. Against this background, there is a combined (circulatory and respiratory) hypoxia. Cor pulmonale is not amenable to effective therapy. Nevertheless, treatment should, if possible, be aimed at correcting the disorders caused by the underlying disease. Otherwise, it is symptomatic.

Chronic heart failure (CHF) is a pathogenic condition predetermined by the inability of the circulatory apparatus to meet the metabolic needs of the body.

Acute HF (syndrome of low cardiac output) is said to occur when its signs appear within a few hours or days from the moment of exposure to the etiological factor.

Pathogenesis

Chronic heart failure (CHF) is the most common cause of disability and mortality in people with vascular anomalies. According to the materials of the national registries of European countries, the general prevalence of CHF among the adult population is within four percent and increases in proportion to age, including more than ten percent among people over sixty-six years of age. In addition to a significant prevalence, CHF is also characterized by a high level of hospitalization and an unfavorable prognosis: more than 50% of patients die within 5 years after the onset of the first signs of chronic heart failure. In most countries of the world, including Russia, the proportion of the population of older age groups is growing, the issue of studying chronic heart failure is becoming increasingly important. The most popular etiological factors of CHF are arterial hypertension, coronary heart disease and their combination.

It is known that lipid peroxidation products (LPO) change the processes of cell division and growth, form swelling and even decay of mitochondria, deactivate thiol enzymes that are involved in respiration and glycolysis, oxidizing the SH-groups of proteins, tocopherols, and phospholipids. In recent years, the role of the systemic inflammatory response in the progression of CHF has been proven. According to the results of one of the studies, changes in the functional state of the liver were found in 61% of patients with stage II A and in all patients with stage II B of chronic heart failure. In patients with II B stage of CHF, cholestatic, cytolytic and mesenchymal-inflammatory syndromes were pronounced, as well as the development of hepatocellular insufficiency. In patients with PA at the stage of CHF, cholestatic syndrome prevailed in 42.6% of cases. Patients with chronic heart failure were characterized by disturbances in the lipid peroxidation system - antioxidant protection, the formation of a systemic inflammatory response, which was accompanied by the development of metabolic intoxication and was more pronounced in patients with II B stage of CHF. The relationship between the pathogenetic links of CHF progression and the violation of the functional state of the liver was revealed. Thus, the obtained results indicate the need for differentiated use of hepatoprotective therapy already at the first stages of the pathological process in order to prevent the progression of the disease, increase the effectiveness of treatment and reduce the refractoriness to therapy in patients with CHF.

Diagnostics chronic heart failure

Cardiac MRI is a versatile and highly accurate non-invasive study that makes it possible to visualize ventricular volumes, evaluate overall function, wall contractility, myocardial viability, myocardial thickness, thickening, myocardial mass and tumors, heart valves, detect congenital malformations and pericardial changes.

• CT scan.
• CT angiography is used in patients with coronary artery disease with exercise or a stress test.
• Radionuclide ventriculography.Radionuclide ventriculography is recognized as a relatively accurate method for establishing LVEF and is more often performed to determine myocardial blood supply, which in turn provides information about myocardial viability and the presence of ischemia.
• Determination of lung function.It is used to identify or exclude pulmonary causes of dyspnea and to assess the role of respiratory diseases in the patient's dyspnea.
• Cardiac catheterization.Cardiac catheterization is not needed for the routine diagnosis and treatment of patients with heart failure (HF), but may indicate the etiology and prognosis after revascularization.
• Angiography of the heart.Coronary angiography is considered in patients with heart failure and exertional angina or with suspected LV ischemic dysfunction. Coronary angiography is also indicated in patients with refractory HF of unknown etiology and in patients with confirmed severe mitral regurgitation or aortic valve disease that can be corrected surgically.
• Right heart catheterization (RHC).KPOS provides valuable hemodynamic information on filling pressure, vascular resistance, and cardiac output. Observation of hemodynamic changes makes it possible to assess the effectiveness of treatment in patients with severe HF, refractory to treatment.
• Ambulatory ECG monitoring (according to Holter).Ambulatory ECG monitoring is valuable in the presence of arrhythmia symptoms (eg, palpitations or syncope) and for monitoring ventricular rate in patients with atrial fibrillation.

Treatment chronic heart failure

Pharmacotherapy.

Treatment with ACE inhibitors for HF has been shown to improve ventricular function and patient well-being, reduce hospital visits for worsening HF, and increase survival. ACE inhibitors are prescribed to patients if the LVEF is less than 40%, regardless of symptoms.

Initiation of beta-blockers.

1) Beta-blockers may be cautiously initiated for hospital discharge in recent decompensation.
2) Visits every four weeks to increase the dose of beta-blockers (in some patients, titration may be slower). Do not increase the dose if there are signs of worsening heart failure, symptomatic hypotension (including dizziness), or excessive bradycardia (pulse less than 50 per minute).

In the presence of atrial fibrillation, digoxin is the main means of controlling the ventricular rate, due to its ability to suppress AV conduction. With preserved sinus rhythm, the appointment of digoxin is also justified in severe systolic dysfunction - frequent paroxysms of suffocation and left ventricular failure. Digoxin is especially indicated for patients with enlarged heart, ischemic origin of CHF.

Aldosterone antagonists (spironolactone) control only part of the sodium, are excreted by the kidneys, but this is enough for spironolactone (veroshpiron) to provide an increase in diuresis in the range of 20-25%.

Neuroendocrine model and neuroendocrine antagonists in the treatment of CHF. Views on how to properly treat CHF have changed over the decades and it seemed that this is not such a big problem, just that pharmacologists have not yet found the “ideal” means of auxiliary inotropic support for damaged myocardium, but this is a matter of time. Unfortunately, it turned out that everything is much more complicated. Strategic approaches to the treatment of myocardial dysfunction were being improved in accordance with the possibilities of pharmacotherapy at that time.

The heart is a "pump" that does not work well, so this pump must be constantly stimulated with digoxin. With the advent of diuretics, new treatment options have opened up. Not only the heart, but also the kidneys are to blame for severe symptoms.
Unfortunately, modern medications (valsartan, losartan) in the treatment of CHF have not demonstrated an effectiveness that exceeds ACE inhibitors. Therefore, their use is advisable only in cases of intolerance to ACE inhibitors.

If there is a pharmacological group of cardioprotective action, then beta-blockers (BAB) should be the first representative. It is obvious that the key point in the cardioprotection of beta-blockade is to counteract the cardiotoxic effect of unprofitable portions of norepinephrine. Under its influence, cardiomyocytes are overfilled with calcium and quickly die. One of the four BBs - metoprolol succinate, bisoprolol, carvedilol and nebivalol, in the absence of contraindications, should be used in all patients with chronic heart failure, and what is important - only after the patient's stable condition has been achieved.

In the presence of decompensation, the use of calcium channel blockers (CCBs) only exacerbates the clinical course of CHF due to their pronounced cardiodepressive effect. The use of BCC may be justified in predominantly diastolic CHF. The appointment of short-acting dihydropyridines (nifedipine) is accompanied by significant sympathetic activation, so patients with chronic heart failure, with rare exceptions (bradycardia), they are contraindicated.

Although chronic heart failure is a rather severe clinical syndrome, and the symptoms significantly worsen the quality of life, modern pharmacotherapy allows maintaining a relatively satisfactory functional state of the patient for a long time. Therefore, the constant regular intake of basic treatment means includes certain responsibilities.

Heart transplant

Heart transplantation is the accepted treatment for end-stage HF. Transplantation, given the right selection criteria, significantly improves survival rates, exercise tolerance, faster return to work, and improved quality of life compared to conventional treatment.

Significant breakthroughs have been made in the technology of left ventricular support (LVAD) and artificial heart devices. Current indications for the use of PPL and an artificial heart include transplantation and management of patients with acute severe myocarditis. Although experience is still limited, devices may be considered for long-term use while the final procedure is being planned.

Ultrafiltration

Ultrafiltration is considered to reduce fluid overload of the lungs (pulmonary and/or peripheral edema) in selected patients and to correct hyponatremia in symptomatic patients refractory to diuretics.

Remote monitoring

Remote monitoring can be defined as the long-term collection of information about the patient and the ability to view this information without his presence.

Continuous analysis of these data and effective use of the device can activate notification mechanisms when clinically significant changes are detected and therefore facilitate patient management. Remote monitoring may reduce the use of health care resources by reducing hospitalization rates for chronic HF and readmissions.

Thromboembolism warnings

• Antithrombotic therapy to prevent thromboembolism is recommended for all patients with AF, unless there are contraindications.

• In patients with AF at high risk of stroke/thromboembolism, long-term oral anticoagulant therapy with vitamin K antagonists is recommended unless contraindicated.

CHF is a pathophysiological syndrome that develops as a result of various diseases of the cardiovascular system, leading to a decrease in the pumping function of the heart and insufficient blood supply to organs and tissues.

Ethology:

1. Myocardial damage:
2. Hemodynamic myocardial overload:
3. Violation of diastolic filling of the ventricles: stenosis of the left or right atrioventricular orifice, exudative and constrictive pericarditis, restrictive cardiomyopathy)
4. Increased metabolic needs of tissues (HF with high minute volume): anemia, thyrotoxicosis.

Pathogenesis : 1. The main trigger of CHF is a decrease in myocardial contractility and a drop in cardiac output, which causes a decrease in perfusion of a number of organs and activation of compensatory mechanisms (sympathetic-adrenal system, renin-angiotensin-aldosterone system, etc.).
2. Catecholamines (norepinephrine) cause peripheral vasoconstriction of arterioles and venules, increase venous return to the heart, and equalize reduced cardiac output to normal (compensatory response). However, in the future, activation of the sympathetic-adrenal system leads to the progression of CHF (catecholamines activate the RAAS, tachycardia worsens the filling of the heart in diastole, and other decompensation reactions).
3. Spasm of renal arterioles + hypoperfusion of the kidneys against the background of CHF Þ activation of the RAAS Þ hyperproduction of angiotensin II (a powerful vasopressor; potentiates myocardial hypertrophy and remodeling) and aldosterone (increases sodium reabsorption and plasma osmolality, activates the production of ADH, which retains water). An increase in BCC, on the one hand, normalizes cardiac output (compensation), on the other hand, it potentiates dilation and damage to the heart (decompensation).
4. An important role in the development of CHF also belongs to endothelial vascular dysfunction (decrease in the production of endothelial vasorelaxant factor), hyperproduction of a number of cytokines: IL, TNF-a (impairs the transport of calcium ions into cells, inhibits PVK dehydrogenase, leading to ATP deficiency, triggers apoptosis of cardiomyocytes ).

Classification

1. By origin: due to volume overload, due to pressure overload, primary myocardial
2. According to the cardiac cycle: systolic form, diastolic form, mixed form
3. According to the clinical variant: left ventricular, right ventricular, biventricular (total)
4. According to the value of cardiac output: with low cardiac output, with high cardiac output
The severity of CHF.
1. According to Vasilenko-Strazhesko:
Stage I (initial) - latent HF, manifested only during physical exertion (shortness of breath, tachycardia, fatigue).
II stage (expressed) - expressed violations of hemodynamics, organ function and metabolism
IIA - moderately pronounced signs of heart failure with hemodynamic disturbances in only one circle
IIB - strongly pronounced signs of heart failure with hemodynamic disturbances in a large and small circle
Stage III (final, dystrophic) - severe hemodynamic disorders, persistent changes in metabolism and functions of all organs, irreversible changes in the structure of tissues and organs, complete disability.
I FC. The patient does not experience restrictions in physical activity. Ordinary exercise does not cause weakness (lightheadedness), palpitations, shortness of breath, or anginal pain.

II FC. Moderate limitation of physical activity. The patient feels comfortable at rest, but the performance of ordinary physical activity causes weakness (lightheadedness), palpitations, shortness of breath, or anginal pain.

Cardiologist

Higher education:

Cardiologist

Kuban State Medical University (KubGMU, KubGMA, KubGMI)

Level of education - Specialist

Additional education:

"Cardiology", "Course on magnetic resonance imaging of the cardiovascular system"

Research Institute of Cardiology. A.L. Myasnikov

"Course on functional diagnostics"

NTSSSH them. A. N. Bakuleva

"Clinical Pharmacology Course"

Russian Medical Academy of Postgraduate Education

"Emergency Cardiology"

Cantonal Hospital of Geneva, Geneva (Switzerland)

"Course in Therapy"

Russian State Medical Institute of Roszdrav

Chronic heart failure (CHF) is a consequence of pathologies of the heart and blood vessels, depriving the heart muscle of the ability to provide the blood supply necessary for the body. Pathologies are characterized by impaired blood flow inside the heart and on the periphery, changes in the structure of the heart muscle, negative changes in the nervous and fluid regulation of blood flow, congestive manifestations in the circulatory system.

Systematics of CHF

In cardiology and therapy, two main classifications of heart failure are used:

• N. Strazhesko and V. Vasilenko, approved in 1935;
• NYHA (New York Heart Association) since 1964.

N. Strazhesko and V. Vasilenko systematized the pathological condition according to the severity of its manifestations:

• Stage 1 - a latent form of insufficiency of blood circulation (rapid heartbeat, shortness of breath), physical activity causes overwork. This is heart failure, the definition of which is very difficult;
• Stage 2A - stagnation of blood in the pulmonary circle, amenable to supportive treatment (more pronounced manifestations of shortness of breath with the most minor physical exertion);
• 2B stage - stagnation in the systemic circulation of blood, pathology of the "right heart"; violations are not amenable to therapeutic effects (dyspnea persists at rest);
• Stage 3 - insufficiency of blood circulation is chronic (serious changes in blood flow, irreversible manifestations of blood stagnation in the blood supply system; irreversible disorders in the structure and morphology of organs, general exhaustion of the body, absolute disability).

The NYHA systematics is based on the functional dependence of the state on physical activity:

• Class I - there are no restrictions, the usual physical activity does not provoke fatigue, manifestations of shortness of breath and rapid heartbeat;
• Class II - moderate restraint of physical activity, the load causes fatigue, rapid heartbeat, shortness of breath, and sometimes heart pain. At rest, the comfortable state of the body is restored;
• Class III - significant restraint of physical activity. Unpleasant symptoms appear even with low physical exertion, the condition returns to normal at rest;
• Class IV - any physical activity leads to discomfort, signs of heart failure persist even at rest.

The pathogenesis of chronic heart failure

The pathogenesis of CHF is due to the occurrence of many reactions leading to systemic disorders (immune, hemodynamic, neurohumoral). Each reaction has a certain effect on the mechanisms of development of heart failure, the interaction of many of them provokes the rapid progression of the pathology. The process is usually started:

1. Volume overload (anomalies of the heart with reverse blood flow - valvular insufficiency, consequences of coronary artery bypass grafting);
2. Pressure overload (narrowing of valve openings, hypertension);
3. Hypertrophy of the heart muscle due to lesions of the coronary arteries (endocrine pathologies - diabetes, hyperthyroidism), inflammatory diseases (dystrophy, myocarditis, cardiomyopathy) and other cardiac pathologies (neoplasm, impaired protein metabolism);
4. Dysfunction of the ventricles of the heart (violation of the extensibility of the walls of the heart, pericarditis).

Accelerate the progression of heart failure:

• psycho-emotional and physical overload;
• arrhythmias (including medicinal ones);
• infectious pathologies;
• anemia;
• renal hypertension.

When starting the development of CHF, neurohumoral mechanisms are activated, enhancing the complex effect. The predominance of the role of one or another mechanism determines the clinical picture of the pathology.

For more than a hundred years of studying heart failure, several variants of pathogenesis have come to the fore, but they all considered separate aspects of this complex problem. Among the priority models of pathogenesis were noted:

• cardiac (heart) - weakening of the reserve of the heart muscle (1908) and a decrease in myocardial contractility (1964);
• cardiorenal (heart, kidneys) - violations of hemodynamic functions, hormonal failures, functional pathologies of nervous structures, kidneys (1978);
• circulatory (peripheral blood supply) - disturbances in the activity of the heart, peripheral blood vessels, sympathetic nervous system, kidneys, renin-angiotensin system (1982);
• neurohumoral (sympathoadrenal and renin-angiotensin-aldosterone systems) - the effect of hemodynamics and neurohumoral reactions on functional disorders of the heart muscle (1989).

According to the neurohumoral model, chronic heart failure develops according to the uniform laws of pathophysiology and does not depend on the etiology of the occurrence of disorders. The main role in this is assigned to the chronic activity of the neurohumoral system - it "solo" from the moment of primary myocardial damage to the death of the patient. One of the mandatory stages of the process is the remodeling of the heart muscle (structural and geometric changes).

With CHF, changes in the activity of the neurohumoral system are expressed:

• activation of the process of converting nerve impulses into humoral ones (sympathoadrenal system - SAS);
• activation of the regulation of pressure and volume of blood circulating in the body (renin-angiotensin-aldesterone system - RAAS);
• excessive production of antidiuretic hormone - ADH (vasopressin);
• disruption of the peptide hormone system;
• functional change in the cells lining the blood vessels and endocardium (endothelium);
• excessive production of specific proteins that contribute to inflammatory processes (pro-inflammatory cytokines);
• activation of apoptosis - programmed death of cardiomyocytes;
• geometric and structural transformations of the heart.

Activation of the sympathoadrenal system

The sympathetic-adrenal system is the unity of the sympathetic nervous system (controls the functions of peripheral organs) and the adrenal system (a set of neurogenic cells that produce norepinephrine and adrenaline). When it is activated, regulatory reactions are transformed into a mechanism for the development of stress-diseases. The vigorous activity of the sympathoadrenal system for some time ensures the normal functioning of the heart, stable pressure and blood supply to tissues and organs. But over time, her hyperactivity provokes:

• excessive venous and arteriole compression;
• an increase in the volume of blood circulating in the body;
• an increased need for an increased supply of oxygen;
• serious disruptions in the rhythm of the heart (up to ventricular fibrillation);
• cardiotoxic manifestations (pronounced depletion of myocardial energy reserves, sometimes necrotic lesions);
• changes in the structure of cardiomyocytes (muscle cells of the heart);
• the formation of accumulations of platelets and microthrombi in the system of small vessels.

Activation of the renin-angiotensin-aldosterone system

Excessive RAAS activity in the initial phase of progression of heart failure also supports hemodynamics and ensures optimal blood supply to tissues and organs. Prolonged hyperactivity of the renin-angiotensin-aldosterone system leads to serious consequences:

• an increase in the sensitivity of the myocardium to the effects of a hyperactive sympathoadrenal system (pronounced ventricular arrhythmias);
• enlargement of the heart, its structural changes, apoptosis and replacement of cardiomyocytes with connective tissue cells (fibrosis);
• hypertrophy and structural changes in blood vessels;
• activation of vasopressin production.

Excessive secretion of vasopressin

Patients with CHF are characterized by excessive activity of the nuclei of the hypothalamus in the production of antidiuretic hormone. It is called:

• low blood pressure in patients with low cardiac output;
• high levels of angiotensin-II and adrenaline in the blood;
• accumulation in the tissues of sodium and thickening of the blood.

Excessive production of vasopressin contributes to an increase in the reverse absorption of water in the tubules of the kidneys, an increase in blood volume in the vessels, and swelling. In addition, vasopressin activates vascular tone. The increased need of the heart for oxygen becomes one of the reasons for the progression of CHF.

Malfunction of the natriuretic system

The natriuretic system opposes the RAAS, ADH, and the sympathoadrenal system. The polypeptides secreted by the myocardium are similar in molecular structure and mechanism of action. The most important are atrial and cerebral natriuretic peptides. Their concentration is increased by cardiac pathologies, which are characterized by high pressure in the cardiac regions and excessive atrial stretching:

• chronic vascular insufficiency;
• ischemia;
• hypertension;
• activity of neurohormones;
• oxygen deficiency;
• physical overload;
• use of opium alkaloids.

CHF is characterized by an increase in the concentration of atrial natriuretic hormone with a reduced natriuretic response. This situation causes the rapid development of heart failure, a predisposition to edema and serious hemodynamic disturbances. Assessment of the level of natriuretic hormones, especially brain, is a defining prognostic and diagnostic marker of CHF.

Endothelial dysfunction

CHF causes negative changes in the functions of the cell layer lining the inner surface of the vessels and cavities of the heart:

• an increase in the functionality, production and concentration in the blood of a peptide with a pronounced ability to constrict blood vessels, which increases the resistance to blood flow (endothelin-1). This peptide promotes an increase in the size of the heart, activates the production of collagen, the growth of connective tissue and the physiological death of cardiomyocytes;
• hyperactivity of angiotensin-converting enzyme;
• a decrease in the production of nitric oxide, which promotes vasodilation;
• growth of endothelial hemostatics;
• decrease in the secretion of prostacyclin, which has antiplatelet and anticoagulant effects;
• activation of the production of superoxide radicals with a pronounced negative effect on the heart muscle.

Excessive secretion of pro-inflammatory cytokines

Cytokines are small informational molecules. They are regularly produced by individual cells and tissues in response to specific stimulation. Only a few cytokines affect the mechanisms of CHF development, primarily TNF - tumor necrosis factor-α. This cytokine causes the development of heart pathologies and reduces its contractility. The mechanisms of action of TNF are complex and diverse. They affect the processes occurring in the cells of the muscles and endothelium of the microvasculature of the myocardium, in the cells of the smooth muscles of the walls of blood vessels, in calcium channels, cause an increase in the size of the heart, a change in its structure.

Activation of apoptosis of cardiomyocytes

Normally, cell death (apoptosis) is the removal of affected cells and parallel tissue repair. In CHF, the process of apoptosis is activated, losing the adaptive function. As a result, the number of capable cardiomyocytes decreases, which lowers the contractility of the heart and causes the development of its insufficiency. Programmed cell death in CHF is recognized as one of the main mechanisms that negatively affect the contractility of the heart.

Heart remodeling

An increase in the mass of the heart and the accumulation of excess blood (dilatation) in the left ventricle lead to a change in its shape, affecting the contractility of the heart. Research has established the stages of heart remodeling that predetermine the development of CHF. Cardiovascular pathologies trigger the mechanisms of stimulation of various body systems.

For example, with hypertension, prolonged pressure loading contributes to the growth of the walls of the left ventricle. Its parameters are preserved, as well as the systolic function. This is how diastolic HNS is formed during concentric remodeling.

A classic example of the formation of systolic heart failure is structural and geometric changes in dilated cardiomyopathy. The shape of the heart at the same time becomes more rounded, its contractility decreases, the walls of the left ventricle become thinner, mitral regurgitation is noted. This is an eccentric type of remodeling.

After a heart attack, a significant loss of myocardial cells leads to overloads in the tissues bordering the area of ​​necrosis and in distant zones of the myocardial wall. Such a redistribution of loads contributes to the accumulation of blood in the ventricle, it hypertrophies and acquires a spherical shape. The remodeling process continues for several months, negatively affecting the pumping ability of the heart. Often, the situation is complicated by the pathology of the mitral valve and the manifestation of an aneurysm. This is also eccentric remodeling.

A comprehensive characterization of remodeling indicators served as the basis for distinguishing two stages in the progression of CHF: adaptive remodeling (stage 2A) and maladaptive (stage 2B). The symptoms of CHF during long-term development (stage 2B) are not particularly affected by the sequence of ventricular lesions.

This is due to the common pathogenesis: excessive activity of neurohumoral systems, fluid accumulation, heart remodeling accompany all forms of chronic heart failure. But a few years after the first manifestations of CHF, the patient often shows signs of insufficiency of one or another ventricle.

The syndrome of chronic heart failure is the final stage of the course of a variety of heart pathologies. Factors contributing to the development of heart failure are potentially reversible. Their elimination or suppression can delay the manifestation of this dangerous condition, and sometimes even save the patient's life. Unlike diseases that contribute to the development of CHF, provoking factors do not cause pathology on their own. They can serve as an impetus for its manifestation only against the background of a decrease in the compensatory abilities of the heart muscle.

The monograph presents a new scientific concept of the study of the heart and blood vessels as a system built on the principle of the golden ratio. The structure of the heart is based on affine symmetry, and the basis of its functional activity is the symmetry of transformations. In healthy people, there is a harmony in the functioning of the heart and blood vessels, in patients with chronic heart failure, it is disturbed. Methods for diagnosing acute and chronic heart failure and its severity based on the relationship between temporal and volumetric indicators of the work of the heart are proposed. They allow you to monitor the dynamics of the course of the syndrome and the effectiveness of the treatment. An important place in the monograph is given to the principles and methods of treatment of patients with chronic heart failure and drugs used in this pathology. The publication is intended for cardiologists, internists and general practitioners.

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by the LitRes company.

PATHOGENESIS OF CHRONIC HEART FAILURE

As already discussed in the previous chapter, diseases of the cardiovascular system are considered to be the cause of the development of CHF. It sounds at least strange. According to this formulation, the disease is the cause of the development of its sign (syndrome), and not he - its manifestation. The cause of the development of CHF is a violation of the contractile function of the heart, and it is associated with systolic and diastolic dysfunction (Meyerson F. Z., 1978; Sonnenblick E. H., Downing S. E., 1963). This condition develops in patients with pathology of various structures of the heart. Therefore, the mechanism of violation of the pumping function of the heart in various diseases may be different. In some cases, primary damage to cardiomyocytes (myocardial insufficiency) occurs (A. G. Obrezan, 2007; A. G. Obrezan, I. V. Vologdina, 2002). This is observed in the following diseases:

- acute myocardial infarction;

- cardiac ischemia;

- postinfarction cardiosclerosis;

- myocarditis;

– primary cardiomyopathy;

- secondary cardiomyopathies (myocardial dystrophy).

In other cases, a violation of the contractile function of the myocardium is due to a change in intracardiac hemodynamics or an increase in the total peripheral vascular resistance, which entails an increased load on the myocardium. This picture occurs when:

- congenital and acquired heart defects;

- arterial hypertension;

– primary and secondary pulmonary hypertension;

- an increase in the volume of circulating blood.

Much less often, a violation of the propulsive activity of the heart is associated with mechanical factors, as in the following diseases:

- constrictive pericarditis and cardiac tamponade;

- amyloidosis and myocardial fibroelastosis.

Regardless of what underlies this or that disease - direct damage to the myocardium, pressure and / or volume overload, mechanical factors - this leads to a decrease in the contractile function of the heart, to a violation of CO, resulting in a decrease in blood supply to organs and tissues. The pathogenesis of CHF includes morphological disorders of the heart and blood vessels caused by the underlying disease, prolonged increased load (with arterial hypertension, the total peripheral vascular resistance increases) and a cascade of sequentially activated compensatory mechanisms, i.e. changes in the regulation of the state of the cardiovascular system.

The determining moment in the occurrence of CHF will be those morphological changes in the heart that are characteristic of cardiovascular diseases. No heart damage - no heart failure. This is an axiom.

It is well known that any disease is based on structural damage to the organ. This leads to a violation of its functions, which manifests itself in the signs of the disease. One of the signs of heart damage is heart failure.

However, the onset of symptoms does not always coincide with structural failure; it is usually delayed. This is because genetically determined and adaptive compensation mechanisms are triggered. They provide reconstruction of partially damaged or modification of the remaining intact structures of the affected organ and are aimed at restoring impaired functions. Regardless of the causes of diseases of the cardiovascular system, activation of a number of compensatory mechanisms aimed at maintaining cardiac activity, blood pressure and the necessary perfusion of organs and tissues is observed.

Apparently, one of the first manifestations of compensation is the regeneration of tissues with high mitotic activity or organ hypertrophy due to hyperplasia of the organelles of those cells that do not have mitotic activity (Meyerson F.Z., 1978; Sarkisov D.S., 1987). Cardiomyocytes, according to most researchers, are not able to divide, and therefore can only hypertrophy due to an increase in the number of mitochondria and other organelles. However, some authors admit the possibility of division of these cells and even the presence of stem cells in the myocardium. Myocardial hypertrophy is the main mechanism for compensating the activity of the heart. It helps to maintain the force of contraction of the heart and general hemodynamics.

The launch of such compensatory reactions is due to the activation of the gene apparatus of intact cells of the affected organ. If the tissue has a low mitotic activity, then this is manifested by an increase in the synthesis of RNA (ribonucleic acid) at some loci of DNA (deoxyribonucleic acid) and hypertrophy of cells and the organ as a whole. This fully applies to the muscle tissue of the heart. In organs with high mitotic activity, tissue regeneration is enhanced by cell DNA replication followed by division.

The material basis of the compensatory reactions of the affected heart is hyperplasia (an increase in the number of structures) or an increase in the mass of intracellular components in each cell. The compensatory process involves not only the damaged organ, but also other organs and systems that perform functions similar to it (Sarkisov D.S., 1987).

Regardless of what reasons caused the change in structures, the response (compensatory) reaction to this damage will be of the same type. The exact same reaction will follow with prolonged increased physical exertion, as well as loads associated with an increase in resistance to blood flow in the vessels, which is accompanied by an increase in blood pressure.

In medicine, unfortunately, there is no clear distinction between such concepts as "adaptation" and "compensation". Often one concept is replaced by another, and even more often the term "adaptive-compensatory reactions" or "mechanisms" is used. This can be explained by the fact that the modification of structures that occurs after damage to an organ (in particular, the heart) or is associated with a change in individual environmental factors is carried out in the same way, namely, by activating certain genes, increasing the production of RNA and protein (Khlebovich V V., 1991). However, there is still a difference between adaptation and compensation.

The meaning of the term "adaptation" used in medicine does not quite correspond to the biological understanding of this process. When individual elements of the environment change in the body, certain organs and their functions are modified to meet the conditions of the changed environment. This process is called adaptive, or phenotypic, modification and is a morphofunctional response of the body to changes in external factors, including prolonged increased physical activity (Grant V., 1991; Shmalgauzen I.I., 1982). In the medical literature, this process is called adaptation in the broad sense of the word. Adaptation (adaptation) is considered as a process of adapting a person to changing environmental conditions. It turns out to be a tautology. Compensation is an adaptive response to damage to body structures, which consists in compensating the functions of a damaged organ by modifying its undamaged tissues or other organs. Compensation is the result of genotypic (phylogenetic) adaptation. Therefore, it is stylistically incorrect to call these reactions compensatory-adaptive. If they had not been developed in the process of genotypic adaptation, then the life expectancy of living organisms would have sharply decreased. Any damage, disease of the body would lead to their rapid death.

When heart structures are damaged, it is precisely compensatory reactions and mechanisms that develop to maintain the pumping function of the heart. Myocardial hypertrophy, which occurs in patients with damage to the structures of the heart and is caused by increased load, is caused by a violation of intracardiac and / or vascular hemodynamics. The term "adaptation", proposed by F. Z. Meyerson (1978) to explain changes in the structures of the heart during its load and diseases, is not entirely successful. It does not accurately reflect the essence of the ongoing processes.

There can be no adaptation of the body to the disease, since the disease is a process of maladaptation. In this case, we can only talk about compensation for impaired functions of the body, and not adaptation to the pathological process that has developed in the human body.

After this remark, we return to the pathogenesis of CHF. The study of CHF should be based not so much on “risk factors”, largely conjectural, but on an accurate understanding of the mechanisms of the formation and development of pathological processes (Sarkisov D.S., 2000). To understand the mechanism of occurrence of CHF, it is necessary to clearly understand the stages of the processes that lead the body to this state.

When the heart structures are damaged or overloaded with resistance to the expulsion of blood from the heart, a cascade of compensatory reactions occurs. The so-called compensatory modification of the heart develops. One of the early manifestations of compensatory reactions in the main diseases of the circulatory system is cardiac hypertrophy. This process occurs immediately after damage to the structures of the heart or exposure to increased stress. In experiments on animals, it was found that already 5-6 days after damage to the structures of the heart or increased physical activity, hyperplasia of cell organelles and hypertrophy of myocardial muscle fibers are clearly detected (Meyerson F.Z., 1978). The mass of the organ increases not due to an increase in the number of cells, but due to their hypertrophy. The experiment shows that if this process is artificially slowed down, then the life expectancy of sick animals will decrease significantly.

This is supported by biochemical data. It has been shown that suppression of RNA synthesis on structural genes by actinomycin D completely prevents the synthesis of nucleic acids and the development of myocardial hypertrophy, which leads to rapid death of animals from HF. Due to hypertrophy, the heart muscle is capable, within certain limits, of performing a greater amount of work for a long time and without signs of obvious insufficiency than a non-hypertrophied damaged muscle.

The meaning of such compensation is to maintain the force of contraction of the ventricles. The main consequence of cardiac hypertrophy is that the increase in organ function is distributed in its increased mass.

With myocardial hypertrophy, the force per unit area of ​​the cross-sectional area of ​​the heart wall remains practically unchanged. Thus, by increasing the mass of the myocardium, the contractile function of the affected heart is maintained. Thanks to this mechanism, the heart can provide the level of functioning necessary for the body for a long time. Unfortunately, myocardial hypertrophy cannot continue indefinitely. This process continues until all structures capable of hypertrophy are involved.

The increase in heart mass even in patients with initially intact myocardium under pressure load (hypertension) has its limits. The thickness of the wall of the ventricle can increase by 1.5 - 2 times, i.e., the process of hypertrophy is not unlimited. As soon as the maximum of hypertrophy is reached, there is an elongation of muscle fibers and a sharp dilatation of the cavities of the heart, the death of cardiomyocytes is accelerated, and connective tissue develops in their place.

To maintain vascular tone and blood pressure with reduced CO, activation of the SAS occurs - the second mechanism for compensating cardiac activity. It is manifested by tachycardia, aimed at replenishing the value of the minute volume of blood circulation. According to G. F. Lang (1958), increased heart rate is an appropriate compensation mechanism. Catecholamines enhance the function of the cardiovascular system by accelerating metabolic processes, maintain vascular tone and blood pressure at the proper level, carry out venous vasoconstriction, which increases venous return of blood to the heart (Anthony G., 1986).

The inotropic effect of catecholamines is manifested by an increase in the force of contraction and the rate of relaxation of the ventricles. At this time, the heart works like a healthy person during exercise. There is a decrease in ESV and EDV, due to the influence of the sympathetic nervous system. As a result, myocardial contractility increases regardless of the initial stretching of the heart muscle. Such a restructuring allows, with the same BWW, to eject blood against a higher pressure, to maintain or increase the stroke volume due to the CSR. We noted similar changes in patients with CHF I FC.

In this category of patients, a clear decrease in ESV and, to a lesser extent, EDV were revealed with normal indicators of VR, i.e., their heart works as if in a mode of increased load. Activation of the CAS has not only a positive inotropic, but also a positive chronotropic effect on the heart and thus supports CO and peripheral hemodynamics. With an increase in heart rate and a decrease in the duration of the cardiac cycle, diastole is shortened first of all. However, the filling of the ventricles suffers little, since the bulk of the blood enters at the beginning of diastole. Under the influence of the sympathetic nervous system, the rate of their relaxation clearly increases due to the positive chronotropic effect.

In the middle of the twentieth century. it was found that an increase in contraction force can be caused by the influence of the amplifying nerve of the heart, discovered by I. P. Pavlov, by influencing myocardial metabolism (Raiskina M. E., 1955). With the help of radioactive research methods, an increase in the intensity of the exchange of high-energy phosphorus compounds in the heart was revealed.

End of introductory segment.

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The following excerpt from the book Chronic heart failure (pathogenesis, clinic, diagnosis, treatment) (Yu. S. Malov, 2013) provided by our book partner -