Heart failure

Heart failure is a consequence of a violation of filling or contraction of the ventricles of the heart, which determines a decrease in pumping function of the heart, accompanied by typical symptoms: shortness of breath and rapid fatigue. Cardiomyopathy is a general term for primary cardiac muscle diseases. There are four main types of cardiomyopathies: dilated, hypertrophic, infiltrative and restrictive. From the terms of secondary cardiomyopathies: hypertensive, ischemic, valvular, etc. - now the decision to refuse is accepted. Any of these options can lead to heart failure.

[1], [2], [3], [4], [5], [6], [7]

Epidemiology

Heart failure (CH) affects about 5 million people in the United States. More than 500,000 new cases are registered annually.

[8], [9], [10], [11], [12], [13], [14], [15], [16],

Causes of the heart failure

Both cardiac and systemic factors can worsen heart function and lead to the development of heart failure. Cardiac factors include myocardial damage (eg, acute with myocardial infarction or myocarditis, chronic with fibrosis associated with various disorders), valve pathology, arrhythmia (tachyarrhythmias or bradyarrhythmias) and a decrease in the number of functioning myocardium (i.e., ischemia). Systemic factors include any conditions requiring an increase in cardiac output, for example anemia (lead to heart failure with high ejection), or limiting release (afterload), for example, systemic hypertension.

The traditional distinction between left and right ventricular failure is somewhat erroneous, because the heart is a holistic system similar to a pump, and changes in one chamber ultimately affect the work of the whole heart. However, these terms determine the localization of the greatest lesion, leading to heart failure, and can be useful for initial diagnosis and treatment.

Left ventricular insufficiency usually develops with coronary heart disease (CHD), arterial hypertension, aortic stenosis, most forms of cardiomyopathies, acquired regurgitation of the mitral or aortic valve and congenital heart defects (eg, interventricular septal defect, functioning arterial duct with large discharge).

Right ventricular failure is usually caused by previous left ventricular failure (leading to an increase in pulmonary venous pressure and pulmonary arterial hypertension, ie, to right ventricular overload) or severe lung disease (then this condition is called pulmonary heart disease). Other causes include multiple pulmonary embolism, veno-occlusive lung disease, right ventricular infarction, primary pulmonary hypertension, tricuspid regurgitation or stenosis, mitral stenosis and stenosis of the valve or pulmonary artery. Some conditions mimic right ventricular failure, but the functioning of the heart can be normal; they include volume overload and increased systemic venous pressure in polycythaemia or massive transfusions, acute renal failure with sodium and water retention that lead to hyperhydration. Simulated hollow veins can also imitate the clinic of right ventricular failure.

Insufficiency of both ventricles occurs in diseases that damage the entire myocardium (for example, viral myocarditis, amyloidosis, Chagas disease).

Heart failure with a high ejection occurs when there is a constant need for high CB, which can eventually lead to the inability of the normal heart to maintain the required ejection. Conditions that can lead to an increase in CB include severe anemia, beriberi, thyrotoxicosis, progressive Paget's disease, arteriovenous fistula, and persistent tachycardia. CB is high in various forms of cirrhosis, but most of the fluid retention occurs due to hepatic mechanisms.

Cardiomyopathy - a general term that reflects the disease of the myocardium, was previously used to describe etiology (for example, ischemic or hypertonic cardiomyopathy) leading to secondary myocardial damage. Currently, this term is used to refer to primary ventricular myocardial damage, which is not caused by congenital anatomical defects, valvular, systemic or pulmonary vascular disorders, primary pericardial diseases or components of the conduction system, and IHD. Cardiomyopathy is often idiopathic and is classified as stagnant dilated, hypertrophic or infiltrative-restrictive cardiomyopathy.

[17], [18], [19], [20], [21], [22]

Pathogenesis

Heart contractility, ventricular function and myocardial oxygen demand are determined by preload, afterload, availability of nutrients (eg, oxygen, fatty acids, glucose), heart rate and heart rate, and the mass of a viable myocardium. Cardiac output (CB) is proportional to the heart rate per unit of time and stroke volume; it is also affected by venous return, peripheral vascular resistance and neurohumoral factors.

Preload - the state of the heart at the end of its phase of relaxation (diastole) just before contraction (systole). Preload indicates the degree of terminal diastolic extension of the myocardial fibers and the final diastolic volume, which is affected by the diastolic ventricular pressure and the structure of the myocardial wall. As a rule, the end diastolic pressure of the left ventricle (LV), especially if it is above the norm, serves as an acceptable indicator of preload. Dilation, hypertrophy and changes in left ventricular dilatability change preload.

Postnagruzka - force of resistance to contraction of myocardial fibers at the beginning of systole. It is determined by intraventricular pressure, volume and wall thickness during the opening of the aortic valve. Clinically, systemic blood pressure during or immediately after the opening of the aortic valve represents a peak systolic wall tension and is approaching postload.

The Frank-Starling law describes the relationship between preload and heart function. According to the law, usually systolic contractility (represented by stroke volume or CB) is proportional to preload within the normal physiological range. Contractility is difficult to measure without cardiac catheterization, but it is well reflected by the ejection fraction (EF) - the percentage expression of the final diastolic volume ejected with each contraction (left ventricular stroke volume / terminal diastolic volume).

Cardiac reserve is the ability of the heart to increase its work in comparison with the resting state in response to emotional or physical stress. During maximum stress, the body's intake of oxygen can increase from 250 to 1500 ml / min or more. Mechanisms include increased heart rate, systolic and diastolic volumes, stroke volume and oxygen consumption by tissues (the difference between O ₂ content in arterial blood and mixed venous or blood in the pulmonary artery). In well-trained adult young people, during maximum exercise, the heart rate may increase from 55-70 per minute (at rest) to 180 per minute, and CB may increase from 6 to 25 l / min or more. At rest, arterial blood contains approximately 18 ml of oxygen per 1 blood, and mixed venous blood or pulmonary artery blood is about 14 ml / dl.

Thus, oxygen consumption is approximately 4.0 ml / dL, but with increasing demand, it can increase to 12-14 ml / dl. These mechanisms also participate in compensation for heart failure.

With heart failure, the heart may not deliver the tissues needed for the metabolism of blood, and the associated increase in pulmonary or systemic venous pressure can lead to the fullness of the peripheral organs. A similar condition can occur with violations of the systolic or diastolic function of the heart (more often - both).

With systolic dysfunction, the ventricle shrinks slightly and is not fully emptied, leading initially to an increase in diastolic volume and pressure. Later PV decreases. There are violations in the expenditure of energy, energy supply, electrophysiological functions, there is a violation of contractility with intracellular calcium metabolism disorders and the synthesis of cyclic adenosine monophosphate (cAMP). The prevalence of systolic dysfunction is a common occurrence in heart failure due to myocardial infarction. Systolic dysfunction can develop mainly in the left ventricle or right ventricle; The failure of the left ventricle often leads to the development of a lack of the right ventricle.

With diastolic dysfunction, the filling of the ventricle fails, leading to a decrease in the final diastolic volume of the ventricle, an increase in the end diastolic pressure, or both. Contractility and, consequently, PV remain normal, and PV may even increase, as a poorly filled LV decreases more fully to maintain cardiac output. A marked decrease in the filling of the left ventricle can lead to a small SV and the presence of systemic manifestations. Increased pressure in the atrium leads to stagnant phenomena in the lungs. Diastolic dysfunction usually develops if the ventricle relaxes (an active process), increases the rigidity of the ventricle, constrictive pericarditis, or stenosis of the atrioventricular valve. Resistance to filling increases with age, probably reflecting a decrease in the number of myocytes and interstitial collagen deposition. Thus, diastolic dysfunction is quite typical for the elderly. Diastolic dysfunction is thought to be predominant in hypertrophic cardiomyopathy, diseases that lead to the development of ventricular hypertrophy (eg, arterial hypertension, severe aortic stenosis), and amyloid infiltration of the myocardium. Filling and functions of the left ventricle can also worsen in those cases where, due to a pronounced increase in pressure in the right ventricle, the interventricular septum swells to the left.

With left ventricular failure, CB decreases and pulmonary venous pressure increases. Because the pulmonary capillary pressure exceeds the oncotic pressure of blood plasma proteins (approximately 24 mm Hg), the liquid part of the blood penetrates from the capillaries into the intercellular space and the alveoli, forming swelling at the periphery and / or reducing pulmonary function and increasing the frequency of respiratory movements. There is an increase in lymphatic drainage, but it can not compensate for the increase in the amount of fluid in the lungs. The noted accumulation of fluid in the alveoli (pulmonary edema) significantly changes the ventilation-perfusion ratio (W / P): neoxygenated pulmonary arterial blood passes through poorly ventilated alveoli, which leads to a decrease in the partial pressure of oxygen in the arterial blood (pO2) and causes dyspnea. However, dyspnea may occur before an I / P disorder, probably due to an increase in pulmonary venous pressure and an increase in respiratory work; The exact mechanism of this phenomenon is unclear. With severe or chronic left ventricular failure, the appearance of pleural effusion in the right side of the thorax and later on both sides is characteristic, which further aggravates dyspnea. The minute ventilation increases, and thus pCO2 decreases and the pH of the blood increases (respiratory alkalosis). Interstitial edema in the area of small airways can interfere with ventilation, increasing pCO2 - a sign of threatening respiratory failure.

With insufficient right ventricle, there is an increase in systemic venous pressure, which is accompanied by transudation of fluid into the intercellular space, and gradual appearance of edema, primarily peripheral tissues (foot and ankle) and abdominal organs. First and foremost, liver function suffers, although there is a worsening of the function of the stomach and intestines, possibly accumulation of fluid in the abdominal cavity (ascites). Right ventricular failure usually causes a mild impairment of liver function, usually with a slight increase in the amount of bound and free bilirubin, prothrombin time and activity of hepatic enzymes (eg, alkaline phosphatase, ACT, ALT). A damaged liver is unable to inactivate aldosterone, and secondary aldosteronism contributes to the accumulation of fluid. Chronic venous congestion in internal organs can cause anorexia, malabsorption syndrome and protein loss (with diarrhea and significant hypoalbuminemia), constant blood loss through the gastrointestinal tract and (sometimes) ischemic infarction of the intestine.

Changes in cardiac activity. With worsening of the pumping function of the ventricles of the heart, the increase in preload is intended to maintain CB. As a result, remodeling of the left ventricle takes place for a long time: it becomes more elliptical, expands and hypertrophies. Being initially compensatory, these changes ultimately increase diastolic rigidity and wall tension (myocardial stress), disrupting the heart, especially during exercise. Increased cardiac wall tension increases the need for oxygen and accelerates apoptosis (programmed cell death) of myocardial cells.

Hemodynamic changes. With a decrease in CB, tissue maintenance with oxygen is maintained by increasing the production of O2 from atmospheric air, which sometimes leads to a shift in the oxyhemoglobin dissociation curve to the right to improve the release of O2.

Reduced CB with reduced systemic BP activates arterial baroreceptors, increasing sympathetic and decreasing parasympathetic tone. As a result, there is an increase in heart rate and contractility of the myocardium, arterioles in the corresponding parts of the vascular bed narrow, venoconstriction joins and sodium and water retention occurs. These changes compensate for decreased ventricular function and help maintain hemodynamic homeostasis in the early stages of heart failure. However, these compensatory mechanisms increase the work of the heart, preload and afterload; reduce coronary and renal blood flow; cause accumulation of fluid leading to swelling; increase the excretion of potassium, and also can cause necrosis of myocytes and arrhythmia.

Changes in kidney function. As a result of worsening of the heart, there is a decrease in renal blood flow and glomerular filtration, as well as redistribution of renal blood flow. The filtration function and elimination of sodium decrease, but there is an increase in reabsorption in the tubules, which leads to a delay in sodium and water. Subsequently, the blood flow is redistributed with its decrease in the kidneys under physical stress, but increase during rest, which, perhaps, contributes to the development of nocturia.

Reduced renal perfusion (and, possibly, reduced arterial systolic pressure secondary to a decrease in ventricular function) activates the renin-angiotensin-aldosterone system, increasing the retention of sodium, water and increasing the tone of renal and peripheral vessels. These effects are intensified by intense sympathetic activation accompanying heart failure.

The system of renin-angiotensin-aldosterone-vasopressin causes a cascade of potentially negative effects. Angiotensin II enhances heart failure, causing vasoconstriction, including renal arterioles, and increasing the synthesis of aldosterone, which not only increases sodium reabsorption in the distal areas of the nephron, but also leads to the deposition of collagen in myocardial vessels and fibrosis. Angiotensin II increases the release of noradrenaline, stimulates the synthesis of antidiuretic hormone (ADH) and causes apoptosis. Angiotensin II can participate in the development of vascular and myocardial hypertrophy, thus contributing to the remodeling of the heart and peripheral vasculature, potentially exacerbating heart failure. Aldosterone can be synthesized in the heart and vascular network irrespective of angiotensin II (possibly stimulated by corticotropin, nitric oxide, free radicals and other stimulants) and have negative effects in these organs.

Neurohumoral response. Under stress, neurohumoral activation promotes cardiac function, maintenance of blood pressure and blood supply to organs, but the constant activation of these reactions leads to a disruption of the normal balance between influences that increase myocardial function and cause vasoconstriction and factors that cause myocardial relaxation and vasodilation.

In the heart there is a large number of neurohumoral receptors (angiotensin type 1 and type 2, muscarinic, endothelial, serotonin, adenosine, cytokine). The role of these receptors has not yet been fully determined. In patients with heart failure, receptors (comprising 70% of the heart receptors) are depressed, probably in response to intense sympathetic stimulation, which results in a worsening of the contractility of cardiomyocytes.

The content of norepinephrine in the blood plasma is increased, which largely reflects the excitation of the sympathetic nervous system, while the amount of epinephrine does not change. Negative effects include vasoconstriction with increased preload and postload, direct damage to the myocardium, including apoptosis, decreased renal blood flow and activation of other neurohumoral systems, including the renin-angiotensin-aldosterone-ADH cascade.

ADH is released in response to a decrease in blood pressure due to various neurohormonal stimulation. An increase in the amount of ADH causes a decrease in the release of free water through the kidneys, possibly contributing to hyponatremia in heart failure. The content of ADH in patients with heart failure and normal BP varies.

The atrial natriuretic peptide is released in response to an increase in volume and pressure in the atria. Brain natriuretic peptide (type B) is released in the ventricle in response to its dilatation. These peptides (NUP) increase the secretion of sodium by the kidneys, but in patients with heart failure the effect is reduced due to a decrease in perfusion renal pressure, low receptor sensitivity and, possibly, excessive enzymatic degradation of NPM.

Since endothelial dysfunction occurs in heart failure, synthesis of endogenous vasodilators (eg, nitric oxide, prostaglandins) decreases and the formation of endogenous vasoconstrictors (eg, endothelin) increases.

The altered heart and other organs produce a tumor necrosis factor alpha (TNF). This cytokine increases catabolism and, possibly, is responsible for cardiac cachexia (loss of more than 10% of body weight), which can exacerbate manifestations of heart failure and other adverse changes.

[23], [24], [25], [26], [27], [28], [29], [30], [31]

Symptoms of the heart failure

Symptoms of heart failure vary depending on which ventricle is affected primarily - right or left. The severity of clinical manifestations varies considerably and is usually determined by the classification of the New York Heart Association (NYHA). Lack of the left ventricle leads to the development of pulmonary edema.

With left ventricular failure, the most common symptoms are shortness of breath, reflecting stagnation in the lungs, and fatigue as a manifestation of low CB. Dyspnea usually occurs with physical exertion and disappears at rest. As the heart failure worsens, shortness of breath can develop at rest and at night, sometimes causing a night cough. Frequent shortness of breath occurs immediately or soon after taking a lying position and rapidly declining in the sitting position (orthopnea). Paroxysmal nocturnal dyspnoea (PDO) awakens the patients a few hours after they lie down and decreases only after they sit for 15-20 minutes. With severe heart failure, both at night and during the day, periodic cyclic respiration (Cheyne-Stokes breathing) can occur-a brief period of rapid breathing (hyperpnoea) is replaced by a brief period of absence of breath (apnea); The sudden phase of hyperpnoea can awaken the patient from sleep. In contrast to paroxysmal nocturnal dyspnoea with this respiration, the phase of hyperpnoea is short, lasts a few seconds and passes for 1 min or earlier. Paroxysmal nocturnal dyspnoea is due to stagnation in the lungs, and Cheyne-Stokes respiration is due to low CB. Sleep-related breathing disorders, such as nocturnal sleep apnea, are common in heart failure and can aggravate it. The pronounced decrease in cerebral blood flow and hypoxemia can cause chronic irritability and impair mental activity.

Classification of heart failure in the New York Heart Association 

Class by NYHA	Definition	Restriction of physical activity	Examples
I	Normal physical activity does not lead to fatigue, shortness of breath, palpitations or angina	No	Can perform any workload that requires 7 МЕТ *: moving a cargo of 11 kg by 8 steps, lifting weights of 36 kg, cleaning snow, digging, skiing, playing tennis, volleyball, badminton or basketball; running / walking at a speed of 8 km / h
II	Normal physical activity leads to fatigue, shortness of breath, palpitations or angina	Lungs	Can perform any workload that requires 5 MET: continuous sexual intercourse, gardening, roller-blading, walking on a flat surface at a speed of 7 km / h
III	Good health at rest. A small physical load leads to the appearance of fatigue, shortness of breath, palpitations or angina	Moderate	Can perform any workload that requires 2 MET: taking a shower or dressing without rest, restyling or bedding, washing windows, playing golf, walking at a speed of 4 km / h
IV	Presence of symptoms at rest. The slightest physical stress increases the discomfort	Expressed	Can not or can not complete any of the activities listed above, requiring 2 MET. Can not cope with any of the above loads

"MET is a metabolic equivalent.

With right ventricular failure, the most common symptoms are swelling in the ankle and fatigue. Sometimes patients feel an overflow in the abdominal cavity or neck. Liver swelling can cause discomfort in the upper right quadrant of the abdomen, and edema of the stomach and intestines is accompanied by anorexia and bloating.

Less specific symptoms of heart failure include coldness of hands and feet, acrocyanosis, postural dizziness, nocturia and a reduced daily urine volume. Reducing the mass of skeletal muscles can occur with severe failure of both ventricles and reflect some reduction in diet, but also enhanced catabolism associated with increased synthesis of cytokines. A significant loss of body weight (cardiac cachexia) is a threatening sign associated with high mortality.

In general, you can find signs of systemic disorders that cause or worsen heart failure (eg, anemia, hyperthyroidism, alcoholism, hemochromatosis).

With insufficient left ventricular tachycardia and tachypnea are possible, in patients with severe left ventricular failure - obvious shortness of breath or cyanosis, arterial hypotension; they may experience drowsiness or agitation due to hypoxia and reduced cerebral blood flow. The general cyanosis (of the entire body surface, including areas warm to the touch, such as tongue and mucous membranes) reflects severe hypoxemia. Peripheral cyanosis (lips, fingers) reflects low blood flow with increased oxygen consumption. If vigorous massage improves the color of the nail bed, cyanosis can be considered peripheral; If cyanosis is central, increasing local blood flow does not improve color.

With systolic dysfunction of the left ventricle in the heart, a spaced, strengthened, laterally displaced apical impulse is revealed; audible and sometimes palpable II (S2) and IV (S4) heart tones, an accent of tone II over the pulmonary artery. Pansystolic murmur of mitral regurgitation may appear at the apex. In the study of the lungs, rales in the lower lungs are found on inhalation and in the presence of pleural effusion, dullness with percussion and weakening of respiration in the lower parts of the lung.

Symptoms of right ventricular failure include unstrained peripheral edema (when pressed with a finger, visible and palpable impressions, sometimes very deep) remain on the legs; enlarged and sometimes pulsating liver palpable to the right below the costal edge; abdominal enlargement, ascites and visible swelling of the jugular veins, an increase in venous pressure in the jugular veins, sometimes with high waves of a or v, which are visible even when the patient is sitting or standing. In severe cases, peripheral edema can spread to the hips or even the sacrum, the scrotum, the lower part of the anterior abdominal wall, and sometimes even higher. Extensive edema in many areas is called anasarka. Edema can be asymmetric if the patient lies mostly on one side.

With edema, the liver can be enlarged or compacted. When pressing on the liver, the appearance of a hepato-yugular reflex can be detected. When palpation of the heart, you can identify swelling in the parasternal area to the left, associated with the expansion of the right ventricle, and when listening - to detect the noise of tricuspid regurgitation or S2 of the right ventricle along the left edge of the sternum.

[32], [33], [34], [35], [36], [37], [38]

Diagnostics of the heart failure

Clinical signs (for example, dyspnoea with exercise, orthopnea, swelling, tachycardia, pulmonary wheezing, swelling of the jugular veins), which indicate heart failure, appear late. Similar symptoms can occur in COPD or during pneumonia, sometimes they are mistakenly attributed to old age. Suspicion of heart failure should occur in patients with a history of myocardial infarction, hypertension or valvular disorders and the presence of additional tones and heart murmurs. Suspect a moderate degree of heart failure in elderly patients or patients suffering from diabetes.

To clarify the diagnosis, it is necessary to perform a chest X-ray, an ECG and a study that allows an objective evaluation of the heart's functioning (usually echocardiography). Blood tests, with the exception of natriuretic peptide type B, are not used for diagnosis, but they are useful for clarifying the cause and common manifestations of heart failure.

Chest X-ray findings that support heart failure include enlargement of the heart shadow, pleural effusion, fluid in the main interlobar gap, and horizontal lines in the peripheral parts of the lower posterior pulmonary fields (Curly B lines). These findings reflect a constant increase in pressure in the left atrium and a chronic thickening of the interlobar septum due to edema. It is also possible to detect venous congestion in the upper lobes of the lungs and interstitial or alveolar edema. A careful study of the shadow of the heart in the lateral projection allows us to identify a specific increase in the ventricle or atrium. X-ray examination allows a differential diagnosis with other diseases accompanied by shortness of breath (eg, COPD, idiopathic pulmonary fibrosis, lung cancer).

ECG results are not considered diagnostic, but a pathologically altered electrocardiogram, especially showing a previous myocardial infarction, left ventricular hypertrophy, left bundle branch blockade or tachyarrhythmia (eg, tachycystolic form of atrial fibrillation), increases the likelihood of having heart failure and can help identify the cause.

Echocardiography allows you to assess the size of the heart chambers, the function of the valves, the ejection fraction, the movement of the walls, left ventricular hypertrophy and effusion in the pericardial cavity. It is also possible to detect intracardiac thrombi, tumors and calcifications in the area of the heart valves, mitral ring pathology and aortic wall. Restricted or segmental disorders of the movement of the walls clearly indicate the underlying underlying cause of IHD, but may also be present in focal myocarditis. Doppler or color Doppler study can reliably identify the flaws of the valves and the discharge of blood. A Doppler study of the mitral and pulmonary venous flow often helps to detect and quantify the diastolic dysfunction of the left ventricle. Measurement of the left ventricular ejection helps to distinguish the prevailing diastolic dysfunction (PV> 0.40) from the systolic (PV <0.40), which may require a different treatment. Three-dimensional echocardiography can be an important method of research, but at present it is available only in specialized centers.

Radioisotope scanning allows us to evaluate systolic and diastolic functions, to detect a transferred myocardial infarction, ischemia or hibernation of the myocardium. MRI of the heart allows you to get accurate images of its structures, but it is not always available and costs more.

Recommended blood tests include a general clinical blood test, determination of blood creatinine, urea, electrolytes (including magnesium and calcium), glucose, protein, and functional liver tests. Functional examination of the thyroid gland is recommended for patients with atrial fibrillation and some, mostly elderly, patients. The concentration of urea in the blood serum increases with heart failure; this study can help in those cases where the clinical manifestations are unclear or other diagnosis (eg COPD) must be ruled out, especially if there is a history of diseases and lungs and heart.

Cardiac catheterization and coronarography are prescribed for suspected coronary artery disease or when the diagnosis and etiology are questionable.

An endocardial biopsy is usually performed only if there is a suspicion of infiltrative cardiomyopathy.

[39], [40], [41], [42], [43], [44], [45], [46], [47], [48], [49], [50]

Treatment of the heart failure

Patients with heart failure associated with certain causes (eg, acute myocardial infarction, atrial fibrillation with a fast ventricular rhythm, severe arterial hypertension, acute valvular regurgitation) are shown with emergency hospitalization, as well as patients with pulmonary edema, severe manifestations, heart failure, identified for the first time or resistant to outpatient treatment. Patients with mild exacerbations diagnosed with heart failure can be treated at home. The main goal is to diagnose and eliminate or treat the pathological process that led to heart failure.

The immediate tasks include reducing clinical manifestations, correcting hemodynamics, eliminating hypokalemia, renal dysfunction, symptomatic arterial hypotension, and correction of neurohumoral activation. Long-term goals include the treatment of hypertension, the prevention of myocardial infarction and atherosclerosis, a reduction in hospital admissions and an improvement in survival and quality of life. Treatment involves changes in the nature of nutrition and lifestyle, drug therapy (see below) and (sometimes) surgery.

Limiting sodium supplied with food helps reduce fluid retention. All patients should not salivate food during cooking and at the table, and avoid salty foods. The heaviest patients should limit the intake of sodium (<1 g / day) by consuming only food with a low content of sodium. Controlling body weight every morning helps to detect the delay of sodium and water in the early periods. If the weight has increased by more than 4.4 kg, the patients themselves can adjust the dose of the diuretic, however, if the weight gain continues or other symptoms join, they need to seek medical help. Patients with atherosclerosis or diabetes should strictly follow the appropriate diet. Obesity can be the cause of heart failure and always worsens its symptoms; patients should strive to achieve a BMI of 21-25 kg / m ².

Regular light physical activity (for example, walking), according to the degree of severity, is encouraged. Activity prevents the deterioration of skeletal muscle physical fitness (reducing functional status); whether this recommendation affects survival, is currently being investigated. When exacerbations, it is necessary to observe rest.

Treatment is selected taking into account the cause, symptoms and reactions to drugs, including adverse effects. Treatment of systolic and diastolic dysfunction has some differences, although there are general purposes. The patient and his family should participate in the choice of treatment. They need to explain the importance of adherence to medication, describe the signs of severe exacerbation and the importance of using drugs that do not have a quick effect. Careful observation of the patient, especially when the patient adheres to treatment, taking into account the frequency of unscheduled visits to the doctor or emergency calls and hospitalizations help determine the time when medical intervention is necessary. Specialized nurses are very important for teaching patients, monitoring and regulating the dose of drugs according to existing protocols. Many centers (for example, specialized outpatient facilities) have combined practitioners from various disciplines (for example, nurses specializing in heart failure, pharmacists, social workers, rehabilitation specialists) in multidisciplinary teams or outpatient programs for heart failure. This approach can improve the results of treatment and reduce the number of hospitalizations, it is most effective in the most severe patients.

If arterial hypertension, severe anemia, hemochromatosis, uncontrolled diabetes mellitus, thyrotoxicosis, beriberi, chronic alcoholism, Chagas disease or toxoplasmosis successfully treated, the condition of patients can significantly improve. Attempts to correct extensive ventricular infiltration (for example, in amyloidosis and other restrictive cardiomyopathies) remain unsatisfactory.

Surgical treatment of heart failure

Surgical intervention can be indicated in certain diseases underlying heart failure. Usually, surgical intervention in patients with heart failure is performed in specialized centers. Therapeutic intervention may be a surgical correction of congenital or acquired intracardiac shunts.

Some patients with ischemic cardiomyopathy can benefit from CABG, which allows to reduce the degree of ischemia. If heart failure develops due to the pathology of the valve apparatus, consider the possibility of plasty or replacement of the valve. The best effect is observed in patients with primary mitral regurgitation compared to patients with mitral regurgitation due to dilatation of the left ventricle, in whom myocardial functions probably will not improve after the operation. It is preferable to perform surgical correction before the onset of irreversible dilatation of the ventricle.

Heart transplantation is the method of choice for patients younger than 60 years with severe refractory heart failure without other life-threatening conditions. Survival is 82% in the first year and 75% within 3 years; However, the death rate during the donor's waiting is 12-15%. Accessibility of human organs remains low. Auxiliary systems of prosthetics of left ventricular function can be used before transplantation or (in some selected patients) permanently. Artificial heart can not yet become a real alternative. Surgical interventions at the research stage include the implantation of limiting devices to reduce the progressive expansion of the heart chambers and a modified aneurysmectomy, called surgical ventricular remodeling. Dynamic cardiac myoplasty and excision of segments of the enlarged myocardium (Operation Batista - partial ventricullectomy) are now not recommended.

Arrhythmias

Sinus tachycardia, a usual compensatory reaction in heart failure, is usually stopped with the effective treatment of heart failure. If this does not occur, it is necessary to eliminate the attendant causes (eg, hyperthyroidism, pulmonary embolism, fever, anemia). With the preservation of tachycardia, despite the correction of the reasons, it is necessary to consider the possibility of prescribing a beta-adrenoblocker with a gradual increase in its dose.

Atrial fibrillation with uncontrolled ventricular rhythm is an indication for drug correction. The drugs of choice are beta-blockers, but with preserved systolic function with caution, it is possible to use lowering heart rate blockers of calcium channels. Sometimes the addition of digoxin is effective. With moderate heart failure, restoring sinus rhythm may not have advantages over normalizing heart rate, but some patients with heart failure feel better with sinus rhythm. If, with tachysystolic form of atrial fibrillation, drug therapy does not work, in some cases, a permanent two-chamber pacemaker is implanted with complete or partial ablation of the AV node.

Isolated ventricular extrasystoles, characteristic of heart failure, do not require special treatment. Persistent ventricular tachycardia, which persists despite optimal treatment of heart failure, may be an indication for the appointment of an antiarrhythmic drug. Means of choice - amiodarone and b-adrenoblockers, since other antiarrhythmic drugs can have adverse proarrhythmic effects in the presence of systolic dysfunction of the left ventricle. Since amiodarone contributes to increased digoxin concentration, the dose of digoxin should be reduced by half. Since long-term use of amiodarone may be accompanied by adverse effects, use as low a dose as possible (200-300 mg once a day). Blood tests for the study of liver function and thyroid-stimulating hormone are performed every 6 months, and also in those cases when pathological changes are detected on the roentgenogram of the chest or dyspnea is aggravated. Chest X-ray and lung function tests are performed annually to exclude the development of pulmonary fibrosis. With stable ventricular arrhythmias, amiodarone may be prescribed 400 mg once a day.

An implantable cardioverter defibrillator (ICDF) is recommended for patients with a good predicted lifespan if they have symptomatic persistent ventricular tachycardia (especially leading to syncope), ventricular fibrillation or LVEF <0.30 after myocardial infarction.

[51], [52], [53],

Refractory heart failure

After the treatment, the symptoms of heart failure may persist. The reasons may be the persistence of the underlying pathology (eg, arterial hypertension, ischemia, valvular regurgitation), irrational treatment of heart failure, failure to adhere to prescription medications, excessive sodium intake from food or alcohol, undiagnosed thyroid disease, anemia or arrhythmia (eg, Atrial fibrillation with a high conductivity to the ventricles, unstable ventricular tachycardia). In addition, drugs used to treat other diseases may undesirably interact with drugs used to treat heart failure. NSAIDs, antidiabetic agents, dihydropyridine and nondihydropyridine calcium channel blockers of short action can worsen the course of heart failure, so they are usually not used. Biventricular pacemakers reduce the severity of clinical manifestations in patients with heart failure, severe systolic dysfunction and an extended QRS complex.

Medications for heart failure

Drugs that reduce the manifestations of heart failure include diuretics, nitrates and digoxin. ACE inhibitors, beta-blockers, aldosterone receptor blockers and angiotensin II receptor blockers are effective for long-term administration and improve survival. In the treatment of systolic and diastolic dysfunction, various strategies are used. For patients with severe diastolic dysfunction, diuretics and nitrates should be administered at lower doses, as these patients do not tolerate a reduction in blood pressure or plasma volume. In patients with hypertrophic cardiomyopathy, digoxin is ineffective and may even cause harm.

Diuretics

Diuretics are prescribed to all patients with systolic dysfunction, accompanied by symptoms of heart failure. The dose is selected, starting with the minimum, able to stabilize the patient's body weight and reduce the clinical manifestations of heart failure. Preference is given to loop diuretics. Furosemide is used most often, starting from 20-40 mg once a day with an increase in the dose to 120 mg once a day (or 60 mg twice a day) if necessary, taking into account the effectiveness of treatment and functioning of the kidneys. An alternative is bumetanide and especially torasemide. Torasemide has better absorption and may be used for longer (dose ratio with furosemide 1: 4). In addition, due to the antialdosterone effects, the use of torasemide results in a less electrolyte imbalance. In refractory cases, furosemide can be administered at a dose of 40-160 mg intravenously, ethacrylic acid 50-100 mg intravenously, bumetanide 0.5-2.0 mg or 0.5-1.0 mg intravenously. Loop diuretics (especially when used with thiazides) can cause hypovolemia with arterial hypotension, hyponatremia, hypomagnesemia and severe hypokalemia.

At the beginning of treatment, serum electrolytes are monitored daily (when diuretics are administered intravenously), subsequently as needed, especially after increasing the dose. Potassium-sparing diuretics - spironolactone or eplerenone (are blockers of aldosterone receptors) - can be added to prevent loss of potassium when high doses of loop diuretics are prescribed. Hyperkalemia may develop, especially with simultaneous administration of ACE inhibitors or angiotensin II receptor blockers, thus the electrolyte composition should be monitored regularly. Thiazide diuretics are commonly used with concomitant arterial hypertension.

Some patients are taught the possibility of increasing the dose of diuretics outpatient, if there is an increase in body weight or peripheral edema occurs. While maintaining an increased body weight, these patients should urgently seek medical help.

Experimental preparations from the group of ADH blockers increase the excretion of water and the concentration of sodium in the blood serum, they are less able to cause hypokalemia and renal dysfunction. These drugs can be a useful adjunct to permanent diuretic therapy.

[54], [55], [56], [57], [58], [59], [60]

Angiotensin converting enzyme inhibitors

All patients with systolic dysfunction in the absence of contraindications (for example, creatinine in the blood plasma> 250 μmol / L, bilateral stenosis of the renal arteries, stenosis of the renal artery of a single kidney or Quinck's edema due to ACE inhibitors in history) are prescribed ACE inhibitors inwards.

ACE inhibitors reduce the synthesis of angiotensin II and the breakdown of bradykinin - mediators that affect the sympathetic nervous system, endothelial function, vascular tone and myocardial function. Hemodynamic effects include dilatation of the arteries and veins, a significant decrease in the filling pressure of the left ventricle during rest and exercise, a reduction in systemic vascular resistance, and a beneficial effect on ventricular remodeling. ACE inhibitors increase life expectancy and reduce the number of hospitalizations for heart failure. In patients with atherosclerosis and vascular pathology, these drugs can reduce the risk of developing myocardial infarction and stroke. In diabetic patients, they delay the development of nephropathy. Thus, ACE inhibitors can be prescribed to patients with diastolic dysfunction in combination with any of these diseases.

The starting dose should be low (1/4 - 1/2 of the target dose, depending on blood pressure and kidney function). The dose is gradually increased within 2-4 weeks before reaching the maximum tolerated, then long-term treatment. The usual target doses of the existing drugs are as follows:

• Enalapril - 10-20 mg 2 times a day;
• lisinopril - 20-30 mg once a day;
• ramipril 5 mg 2 times a day;
• Captopril 50 mg 2 times a day.

If the hypotensive effect (more often observed in patients with hyponatremia or a decrease in BCC) the patient suffers poorly, it is possible to reduce the dose of diuretics. ACE inhibitors often cause moderate reversible renal failure due to the expansion of efferent glomerular arterioles. An initial increase in creatinine by 20-30% is not considered an indication for drug withdrawal, but a slower dose increase, a decrease in the dose of a diuretic or a withdrawal from an NSAID is necessary. Potassium retention can occur due to a decrease in the effect of aldosterone, especially in patients receiving additional potassium preparations. Cough occurs in 5-15% of patients, probably due to the accumulation of bradykinin, but it is necessary to remember other possible causes of coughing. Sometimes there are rashes or dysgeusia. Angioedema develops rarely, but can threaten life; it is considered a contraindication to the appointment of this class of drugs. Alternatively, angiotensin II receptor blockers can be used, but cross-reactivity is sometimes reported. Both groups of drugs are contraindicated in pregnancy.

Before the appointment of ACE inhibitors, it is necessary to study the electrolyte composition of blood plasma and kidney function, then 1 month after the start of treatment and then after each significant increase in the dose or change in the clinical condition of the patient. If, due to an acute disease, dehydration develops or renal function worsens, the ACE inhibitor can be temporarily discontinued.

[61], [62], [63], [64], [65],

Angiotensin II receptor blockers

Angiotensin II receptor blockers (ARA II) do not have significant superiority over ACE inhibitors, but are less likely to cause cough and Quincke's edema. They can be used when these adverse effects do not allow the use of ACE inhibitors. It is still unclear whether the inhibitors of ACE and ARA II are equally effective in chronic heart failure, and the choice of the optimal dose is also in the process of the study. Ordinary target doses for oral administration for valsartan are 160 mg 2 times a day, candesartan 32 mg once a day, losartan 50-100 mg once a day. The starting doses, the regimen for their increase and control when taking ARA II and ACE inhibitors are similar. Like ACE inhibitors, APA II can cause reversible renal dysfunction. If, due to an acute disease, dehydration develops or kidney function worsens, a temporary cancellation of ARA II is possible. The addition of ARA II to ACE inhibitors, beta-blockers and diuretics is considered for patients with moderate failure while maintaining symptoms and frequent re-hospitalization. Such combination therapy requires targeted monitoring of blood pressure, electrolyte blood plasma and kidney function.

[66], [67], [68], [69], [70], [71], [72]

Aldosterone receptor blockers

Since aldosterone can be synthesized independently of the renin-angiotensin system, its adverse effects are not completely eliminated even with the maximum use of ACE inhibitors and ARA II. Thus, aldosterone receptor blockers, spironolactone and eplerenone, can reduce lethality, including sudden death. In most cases, spironolactone is prescribed in a dose of 25-50 mg once a day to patients with severe chronic heart failure, and eplerenone at a dose of 10 mg once a day for patients with acute heart failure and LVEF <30% after myocardial infarction. The additional potassium function is stopped. The concentration of serum potassium and creatinine should be monitored every 1-2 weeks during the first 4-6 weeks of use and after a dose change that is reduced if the potassium concentration is between 5.5 and 6.0 mEq / L, in addition, the drug is discontinued at digits> 6.0 mEq / L, an increase in creatinine greater than 220 μmol / L, or if there are changes in ECG data, characteristic of hyperkalemia.

[73], [74], [75], [76], [77], [78]

Beta-blockers

Beta-blockers are an important addition to ACE inhibitors in chronic systolic dysfunction in most patients, including elderly patients, patients with diastolic dysfunction in hypertension and hypertrophic cardiomyopathy. Refusal to use BAB is possible only if there are obvious contraindications (bronchial asthma II or III degree, atrioventricular block or previous intolerance). Some of these drugs improve LVEF, survival and other major cardiovascular outcomes in patients with chronic systolic dysfunction, including severe disease. Beta-blockers are particularly effective in diastolic dysfunction, as they reduce the heart rate, prolonging the diastolic filling time, and possibly improve ventricular relaxation.

In acute decompensation of CHF beta-blockers should be used with caution. They should be prescribed only with complete stabilization of the patient's condition, which excludes even a slight fluid retention; in patients who are already taking a beta-blocker, it is temporarily withdrawn or reduced.

The starting dose should be low (from 1/8 to 1/4 of the target daily dose), with a gradual increase within 6-8 weeks (on tolerability). Usually the target doses for oral administration for carvedilol are 25 mg twice a day (50 mg twice a day for patients with a body weight of more than 85 kg), for bisoprolol 10 mg once a day, for metoprolol 200 mg 1 time per day day (metoprolol sustained action succinate). Carvedilol, a non-selective beta-blocker of the third generation, also serves as a vasodilator with the effects of an antioxidant and a-adrenoblocker. This is the preferred drug, but in many countries it costs more than other beta-blockers. Some beta-blockers (for example, bucindolol, xamoterol) have proved ineffective and can even cause harm.

After the start of treatment, there is a change in the heart rate, myocardial oxygen demand, and the shock volume and filling pressure remain the same. At a lower heart rate, the diastolic function is improved. The type of filling of the ventricles normalizes (increases in early diastole), becoming less restrictive. Improvement of myocardial functions is noted in many patients after 6-12 months of treatment, there is an increase in PV and CB and a decrease in LV filling pressure. Tolerance to physical activity increases.

After starting treatment, the appointment of beta-blockers may require a temporary increase in the dose of diuretics if acute negative inotropic effects of beta-adrenergic blockade cause a decrease in heart rate and fluid retention. In such cases, it is advisable to slowly increase the dose of the beta-blocker.

[79], [80], [81], [82]

Vasodilator funds

Hydralazine in combination with isosorbide dinitrate can be used only for the treatment of patients who do not tolerate ACE inhibitors or ARA II (usually due to severe renal dysfunction), although the long-term results of this combination do not show a pronounced positive effect. As vasodilators, these drugs improve hemodynamics, reduce valvular regurgitation, and increase resistance to physical exertion without significant changes in kidney function. Hydralazine is prescribed starting at a dose of 25 mg 4 times a day and increasing it every 3-5 days to a target dose of 300 mg per day, although many patients do not tolerate this drug at a dose above 200 mg per day due to hypotension. Isosorbide dinitrate begins to take in a dose of 20 mg 3 times a day (with a 12-hour interval without the use of nitrate) and increase it to 40-50 mg 3 times a day. It is not yet known whether lower doses (often used in clinical practice) provide a long-term effect. In general, vasodilators have been replaced with ACE inhibitors: these drugs are easier to use, they are usually better tolerated by patients, and in addition, they have a greater proven effect.

As a monotherapy, nitrates can reduce the symptoms of heart failure. Patients should be trained to use a spray with nitroglycerin (if necessary for acute manifestations) and patches (with nighttime dyspnoea). In patients with heart failure and angina pectoris, the use of nitrates is safe, effective and well tolerated.

Other vasodilators, such as calcium channel blockers, are not used to treat systolic dysfunction. Short-acting dihydropyridines (eg, nifedipine) and non-dihydropyridine preparations (eg diltiazem, verapamil) can worsen the condition. However, amlodipine and felodipine are well tolerated and can have a positive effect on patients with heart failure in combination with angina or hypertension. Both drugs can cause peripheral edema, sometimes amlodipine causes pulmonary edema. Felodipine can not be taken with grapefruit juice, which significantly increases the content of felodipine in the blood plasma and its side effects due to inhibition of the metabolism of cytochrome P450. Patients with diastolic dysfunction, calcium channel blockers can be prescribed as needed to treat hypertension or ischemia or to monitor heart rate with atrial fibrillation. Verapamil is used for hypertrophic cardiomyopathy.

Drugs of digitalis

These drugs inhibit Na, K-ATPase. As a result, they cause a weak positive inotropic effect, reduce sympathetic activity, block the atrioventricular node (slowing the ventricular rhythm at the atrial fibrillation or extending the PR interval with a sinus rhythm), reduce vasoconstriction and improve renal blood flow. The most commonly prescribed drug digitalis is digoxin. It is excreted by the kidneys, the half-life period is 36-40 hours in patients with normal kidney function. Digitoxin is largely excreted through bile. It serves as an alternative for patients with weak renal function, but it is rarely prescribed.

Digoxin does not have a proven positive effect on life expectancy, but when used with diuretics and an ACE inhibitor it can help reduce clinical manifestations. Digoxin is most effective in patients with large end-diastolic LV volume and S ₃. Abrupt withdrawal of digoxin can increase the number of hospitalizations and aggravate the manifestations of heart failure. Toxic effects are disturbing, especially in patients with impaired renal function and predominantly in women. Such patients may need to prescribe a lower dose of the drug taken orally, as well as the elderly, low-weight patients and patients taking amiodarone simultaneously. Patients weighing more than 80 kg may need a higher dose. In general, lower doses are used now than before, and it is acceptable to consider the average content of the drug in the blood (within 8-12 hours after administration) in the range of 1-1.2 ng / ml. The method of dosing of digoxin varies considerably between different specialists and in different countries.

In patients with normal kidney function with the appointment of digoxin (0,125-0,25 mg orally once a day, depending on age, sex and body weight), complete digitalization is achieved after approximately 1 week (5 half-lives). A faster digitalization is not currently recommended.

Digoxin (and all the digitalis glycosides) has a narrow therapeutic window. The most severe toxic effects are life-threatening arrhythmias (eg, ventricular fibrillation, ventricular tachycardia, complete atrioventricular blockage). Bi-directional ventricular tachycardia, non-paroxysmal nodular tachycardia in combination with atrial fibrillation and hyperkalemia are serious signs of the toxic effects of digitalis. Nausea, vomiting, anorexia, diarrhea, confusion, amblyopia, and (rarely) xerophthalmia are also possible. With hypokalemia or hypomagnesemia (often due to the appointment of diuretics), lower doses can cause toxic effects. The electrolyte composition of blood should be frequently monitored in patients taking diuretics and digoxin, in order to prevent the development of negative effects; it is advisable to prescribe potassium-saving diuretics.

When toxic effects of digitalis appear, the drug is canceled and correction of the electrolyte deficiency is performed (intravenously with pronounced disorders and acute manifestations of toxicity). Patients with severe intoxication symptoms are hospitalized in the observation unit and a Fab fragment of antibodies to digoxin (fragments of sheep antibodies to digoxin) in the presence of arrhythmias or if an overdose is accompanied by serum potassium concentration above 5 mmol / l is prescribed. This drug is also effective in glycosidic intoxication in overdose of plant glycosides. The dose is selected depending on the plasma concentration of digoxin or the total dose taken internally. Ventricular arrhythmias are treated with lidocaine or phenytoin. Atrioventricular blockade with a slow ventricular rhythm may require the setting of a temporary pacemaker; isoproterenol is contraindicated because it increases the risk of ventricular arrhythmia.

[83], [84], [85], [86], [87], [88], [89],

Other drugs

Various drugs that have a positive inotropic effect have been investigated in patients with a moderate insufficiency, but all of them, except for digoxin, increased the risk of death. Regular intravenous injection of inotropic drugs (eg dobutamine) to outpatients increases lethality and is currently not recommended.

Forecast

In general, patients with heart failure have a pessimistic prognosis, if the cause of its development is not amenable to correction. Mortality within 1 year after the first hospitalization with heart failure is approximately 30%. In chronic heart failure, lethality depends on the severity of symptoms and ventricular dysfunction, it can vary between 10-40% per year.

Heart failure usually involves progressive deterioration with episodes of severe decompensation and eventually death. However, a lethal outcome can also be sudden and unexpected without a previous worsening of the symptoms.

Further care for patients

All patients and their family members should be warned about the progression of the disease. For some patients, improving the quality of life is just as important as increasing its duration. Thus, it is necessary to take into account the patients' opinion on this matter (for example, the need for endotracheal sounding, mechanical ventilation) if their condition worsens, especially in severe middle failure. All patients should be adjusted to the fact that the symptomatology will decrease, and they should strive for the earliest possible access to a doctor if their condition changes significantly. Involving pharmacists, nurses, social workers and clergymen who may be part of an interdisciplinary team to implement a patient care plan at home is particularly important for patient care at the end of life.

Heart failure is a consequence of ventricular dysfunction. Left ventricular failure leads to the development of dyspnea and rapid fatigue, right ventricular failure - peripheral edema and accumulation of fluid in the abdominal cavity. Typically, both ventricles are involved to some extent in the process. The diagnosis is established clinically, confirmed by chest X-ray and echocardiography. Treatment includes diuretics, ACE inhibitors, beta-blockers and therapy for the underlying disease that caused heart failure.

[90], [91], [92], [93], [94], [95], [96]