Sinus node syndrome causes. Effective treatment of sick sinus syndrome

Well-coordinated work of the heart is a sign of health. This body experiences incredible loads during life, and, despite this, it works non-stop. Due to physiological characteristics, changes in the hormonal background of the body, various diseases, the work of the heart becomes uncoordinated, arrhythmic and inefficient. The appearance of sick sinus syndrome becomes a serious problem for a person. This disease is accompanied by pain behind the sternum, arrhythmia, and in severe cases, frequent episodes of fainting. Treatment tactics depend on the form of the disease, comorbidities and severity of symptoms.

Physiology of the heart

Sick sinus syndrome (SSS) is characterized by a rare pulse due to disturbances in the functioning of the sinoatrial node of the heart.

The conduction system of the heart consists of autonomous nerve fibers and is responsible for the formation of impulses, the latter "turn on" and force the myocardium to contract in a certain rhythm. There are the following divisions of the conducting system:

Sinoatrial node (center of automatism of the 1st order). Placed between the mouth of the inferior vena cava and the ear of the right atrium. The sinus node generates a heart rate in the range of 60-80 beats/min.
Atrioventricular node (center of automatism of the 2nd order). Located in the lower part of the interatrial septum. Can generate a heart rate of 40-60 beats per minute.
Hiss bundle and Purkinje fibers (Center of automatism of the 3rd order). These fibers pass through the thickness of the myocardium, dividing into the right and left branches. They provide heart rate in the range of 20-30 beats per minute.

The conduction system of the heart is completely autonomous. However, a number of factors can influence it. For example, vagus nerve activation during sleep dramatically lowers heart rate to 55-60 beats/minute. The influence of thyroid hormones, adrenal glands can also cause pulse jumps.

In sick sinus syndrome, the pulse may be so weak and rare that the person may pass out in full health. In this case, the generation of impulses by the automatism center of the 1st order is lost, its role is taken over by the atrioventricular node. Such changes are typical for the elderly, however, sick sinus syndrome in children is also not uncommon.

SSSU classification

Cardiologists classify sick sinus syndrome as follows:

latent flow. In this case, there are no clinical and ECG manifestations. The disease can be detected only with electrophysiological studies. There are no restrictions on physical activity.
stage of compensation. Separate two options. The first is bradysystolic, in which patients complain of short periodic dizziness, general weakness, and headaches. The second option is bradytachysystolic, when attacks of paroxysmal tacharythmia join the signs of bradysystole.
stage of decompensation. In the case of the bradisitolic variant, patients are concerned about pronounced sinus bradycardia (heart rate less than 60 beats per minute), constant dizziness during exercise or at rest, rare episodes of fainting, convulsions, shortness of breath. The bradytachysystolic variant, in addition to signs of bradycardia, is characterized by the addition of atrial fibrillation, atrial flutter, and tachycardia. In this case, the patient's ability to work is completely lost.
Constant atrial fibrillation with a bradysystolic variant of the course.

Important! During the bradysitolic variant of SSS, the heart may stop for 3-4 seconds. This is the reason for fainting.

Depending on the course of the disease, the following forms are distinguished:

chronic;
acute;
recurrent.

During the daily registration of electrical impulses of the heart, the following variants of the course of the disease can be determined:

latent (ECG signs are absent);
intermittent (ECG signs are detected at night, after exercise, stress);
manifesting (ECG signs are present regularly, at different times of the day).

Sick sinus syndrome can greatly affect a person's ability to work, so the disease should be diagnosed as early as possible and treated by an experienced cardiologist.

Internal causes of sinus node weakness

The work of the heart can be influenced by both external and internal factors. The causes of primary weakness of the sinus node are:

Cardiac ischemia. Blockage of the coronary vessels leads to ischemia of the conduction system. If a sinus node is in this zone, then it completely or partially loses the ability to generate nerve impulses, and the atrioventricular node takes over this function.
Inflammatory diseases of the myocardium, cardiomyopathies, congenital and acquired heart defects also put a high load on the conduction system.
Heart transplantation, surgical interventions on the myocardium, valves.
Systemic connective tissue diseases (rheumatism, scleroderma, lupus erythematosus) contribute to the formation of dense growths on the mitral, aortic, tricuspid valves. In this case, there is a dysfunction in the work of the myocardium, and then there are problems with the leading system.
Hypothyroidism appears with thyroid insufficiency, when a lack of hormones contributes to the deterioration of myocardial nutrition, a decrease in heart rate, the deposition of fats in the tissues of the heart, and a change in vascular tone.
Diabetes mellitus, especially insulin-dependent, is associated with a number of serious complications. At high levels of blood glucose, edema of the vascular wall occurs, myelination of nerve fibers is disturbed. As a result, the conduction of impulses is gradually disturbed, the sinus node loses the ability to automatism, there are periodic jumps in heart rate (paroxysmal tachyarrhythmia), atrial fibrillation.
Oncopathology always leads to weight loss, dehydration. The loss of fats, trace elements affects the work of the conduction system of the heart.

Doctor's advice. If a person begins to feel pain and interruptions in the work of the heart, dizziness, frequent fainting after exertion, you should immediately contact a good cardiologist

Internal factors affect the myocardium very strongly, causing structural changes in the cells of the conducting system.

External causes of weakness in the sinus node

Doctors identify several external causes of sinus node weakness:

Influence of the parasympathetic nervous system (responsible for the autonomous work of internal organs). Activation of the vagus nerve inhibits the generation and conduction of impulses in the heart, reduces heart rate, minute blood volume. This condition can occur as a result of nervous experiences, neoplasms of the brain, head trauma with hemorrhages under the meninges.
Violation of the balance of blood electrolytes. For example, an excess of potassium causes deep ischemia of the myocardium, the structures of the conduction system, and helps to reduce the frequency of heart contractions up to a stop (asystole). Such a condition may appear after a transfusion of non-uniform blood, kidney failure, excessive administration of keel mixtures.

Do not forget about the effect of drugs. Each of them can cause heart dysfunction, unpleasant symptoms and side effects:

A drug	Action
b-blockers	Used for hypertension. Reduce pressure, heart rate, inhibit the conduction and generation of impulses by the sinus node
Calcium channel blockers	Use with caution in angina pectoris. Drugs increase the time of conduction of impulses along the conduction system, dilate blood vessels, reduce myocardial contractility
cardiac glycosides	Drugs are dangerous because of the possible cumulative effect. Increase the strength of myocardial contractions, slow down conduction through the atrioventricular node, slow down the heart rate

Important! The appointment of any drugs for the heart requires a careful approach and consultation with a cardiologist

By eliminating the causes of sinus node weakness, heart problems can be avoided.

Symptoms of sinus node weakness

Problems with the conduction system of the heart can manifest themselves in different ways. To summarize, SSSU suffers from the heart and brain, and then other minor organs.

Doctors describe the following symptoms:

Important! During an attack of weakness of the sinus node, asystole can occur, which often causes sudden cardiac death.

Knowing the symptoms of the disease helps to suspect and eliminate conditions that threaten a person's life in time.

Diagnostics

Diagnosis of sick sinus syndrome consists in the appointment and evaluation of the following studies:

Blood test for thyroid hormones, adrenal glands.
Blood cholesterol and its fractions.
Glucose, creatinine, blood urea.
Blood electrolytes - potassium, calcium.
The ECG shows an increased distance between the P waves, heart rate below 60 beats per minute.
24-hour Holter ECG monitoring. In this case, the ECG recording is performed within 1-3 days. Using this method, you can detect any changes in the rhythm during the period of sleep and wakefulness, immediately after taking antihypertensive drugs. With SSSU, a decrease in heart rate is clearly visible, an increase in the RR interval to 2-3 seconds or more.
EchoCG (in other words, ultrasound of the heart) allows you to assess the thickness of the myocardium, the volume of the ventricles and atria, to identify areas of infarction.
The treadmill test (on a treadmill) and bicycle ergometry (on an exercise bike) are stress tests. During exercise, the patient's ECG is recorded by adding or decreasing exercise. With weakness of the sinus node, an increase in heart rate is not observed, even with excessive work on the simulator.
Electrophysiological examination through the esophagus is carried out with a thin probe, which is inserted through the nose. The electrode in the esophagus is stopped at the level of the heart and light electrical impulses are applied. At this time, the reaction of the sinus node is observed.
Massage of the carotid sinus, which is located at the site of the bifurcation of the common carotid artery into the internal and external branches on the neck. The test is carried out under the supervision of a doctor, a light massage is performed with the tips of two fingers of the indicated zone for 5-10 seconds. If during this time there was an asystole for 3 seconds or more, or the pressure dropped by 50 mm Hg. Art., then the patient has no signs of SSSU. This is how carotid sinus syndrome manifests itself.

Important! Normally, massaging the carotid sinus cannot lead to asystole, in this case, you can only reduce the heart rate

The diagnostic program should include all methods, because the omission of one of the causes of the disease can lead to the wrong path in the treatment of the disease.

Treatment of sick sinus syndrome

Heart problems dramatically complicate a person's life, leading to unpleasant symptoms: shortness of breath, chest pain, fatigue, dizziness, sleep problems. To eliminate such manifestations, it is necessary to clearly know the cause of their appearance. With sick sinus syndrome, the treatment of the disease is as follows:

Treatment method

Description of the method

Withdrawal from certain drugs

Some of the following drugs should be stopped immediately to avoid episodes of asystole and loss of consciousness:

b-blockers (Atenolol, Bisoprolol, Metoprolol, Concor and others).
Calcium channel antagonists (verapamil).
Potassium-sparing diuretics (Veroshpiron).

Installing a pacemaker (EX)

The method is considered vital for patients with decompensated SSSU. The procedure is invasive - a thin electrode is inserted through the skin on the chest into the right atrium. And the stimulator itself is placed under the skin at the level of 2-3 ribs on the left or right. Indications for the setting of the EX are:

Morgagni-Adams-Stokes attack;
bradycardia less than 40 beats per minute;
asystole for 3 seconds or more;
constant episodes of dizziness, angina pectoris, heart failure;
the appearance of arrhythmia, which requires the appointment of antiarrhythmics

Important! Morgagni-Adams-Stokes syndrome is characterized by a sudden loss of consciousness, a rare heart rate, as a result of insufficient blood circulation in the myocardium and brain

Conservative treatment of SSSU is ineffective, and is used only in the initial stages of the disease. Setting a pacemaker is considered the only method that can save patients from sudden death. In this case, the device generates a normal heart rhythm, depending on the needs of the body.

Sick sinus syndrome (SSS) combines in its concept some types of cardiac arrhythmias, the cause of which is a pathological change in the functioning of the sinus node. This disease is characterized by the obligatory presence of bradycardia. Often, against the background of pathologists, ectopic foci of arrhythmia occur.

Along with the true syndrome of weakness of the sinus node, in which organic cell damage occurs, 2 more forms of the disease can be distinguished. These include impaired autonomic function and drug dysfunction of the node. The last two variants of the pathology are eliminated when the function of the corresponding part of the nervous system is restored or the drug that caused the decrease in heart rate (HR) is canceled.

The disease is accompanied by weakness, dizziness or fainting. The diagnosis is made on the basis of electrocardiography (ECG) or Holter monitoring. The course of the SSSU is very diverse. With a proven diagnosis, the installation of an artificial pacemaker (IVR) is indicated - a permanent pacemaker.

Sinus node pathology most often occurs in the elderly. The average age is 60-70 years. A study by scientists from the United States showed that the disease occurs in 0.06% of the population over 50 years of age. By gender, there is no predisposition to the disease. SSSU can also manifest in childhood.

Causes of the disease

The syndrome of weakness of the sinus node usually leads either to an organic pathology, which is the culprit of structural changes in cells, or to external etiological factors. The latter lead to a violation of only the function of the source of the heart rhythm. Sometimes the causes of SSS are both factors at the same time.

Organic pathology causing SSSU:

degenerative disorders. The most common cause of sinus node disease is its fibrosis. In this case, the automaticity of the rhythm source and the degree of conduction of the nerve signal through it are reduced. There is evidence of a genetic predisposition to such changes. Fibrosis can be caused by:
- sarcoidosis;
- heart tumors.
Ischemic heart disease (CHD). This disease rarely leads to SSS, however, its role is quite large. Here we are talking about both acute ischemia (myocardial infarction) and the chronic form. The main reason for the development of the pathology of the sinus node in this case is its insufficient blood supply:
- atherosclerosis of the right coronary artery, which feeds the node;
- thrombosis of vessels that bring blood to the source of rhythm (observed with lateral or lower myocardial infarction).
It is for this reason that heart attacks with such localization are often accompanied by bradycardia (up to 10% of cases).
Arterial hypertension (hypertension) is chronically high blood pressure.
Heart injury due to heart transplant.
Hypothyroidism is a deficiency of thyroid hormones in the body.

External factors leading to dysfunction of the sinus node:

Violation of the autonomic nervous system:
- increased activity of the vagus nerve (causes a decrease in heart rate);
- physiological increase in its tone (observed during urination, vomiting, swallowing, defecation and coughing);
- with diseases of the digestive tract and urinary system of the body;
- increased tone of the vagus nerve with sepsis (blood infection), elevated levels of potassium in the blood, or hypothermia.
The effect of drugs that can reduce the function of the sinus node:
- beta-blockers (Anaprilin, Metoprolol);
- some calcium channel blockers (Diltiazem and Verapamil);
- cardiac glycosides (Strophanthin, Digoxin);
- various antiarrhythmic drugs (Amiodarone, Sotalol, etc.)

The pathogenesis of sick sinus syndrome

For a complete understanding of the mechanism of development of SSSU, it is necessary to know and understand the anatomical and physiological features of the cells of the sinus node.

Sinus node in the diagram of the adductor system of the heart This node, which is the main source of heart rhythm, is located in the right atrium and consists of cells that regularly generate a nerve impulse. Further, the latter spreads along the conduction system of the myocardium, causing its contraction.

Due to the fact that the sinus node is a constant source of rhythm, it is forced to work in various conditions. For example, during physical activity, human organs and systems require a larger amount of oxygen. This causes the heart to beat faster. The frequency is set by the sinus node. The change in heart rate is achieved by switching the work of the centers of the node. Thus, some structural elements are able to generate impulses with a minimum frequency, and some are tuned to a maximum heart rate.

With ischemia of the arteries supplying the sinus node, or with its other lesions, there is a lack of nutrition and some cells of the node are replaced by connective tissue. Extensive death and structural changes in the elements of the rhythm source are isolated into a separate disease - idiopathic dystrophy.

The affected centers responsible for the minimum frequency begin to work incorrectly - they are excited less often and cause bradycardia (a decrease in the frequency of heart contractions).

Clinical manifestations of SSSU

The initial stages of the course of the disease are often completely asymptomatic. This can be even if there are pauses between contractions reaching 4 seconds.

In some patients, there is a shortage of blood supply to various organs, which leads to corresponding symptoms. Not always a decrease in heart rate leads to a lack of tissue nutrition, because. when this condition occurs, compensatory mechanisms are activated that promote adequate blood circulation.

The progression of the disease is accompanied by symptoms associated with bradycardia. The most common manifestations of SSS are:

dizziness;
fainting;
pain in the region of the heart;
labored breathing.

The above manifestations are of a transient nature, i.e. arise spontaneously and cease in the same way. The most common symptoms:

Cerebral. These include irritability, feeling tired, memory impairment, and mood swings. With the progression of the disease, loss of consciousness, tinnitus, convulsions occur. In addition, SSSU is often accompanied by a decrease in blood pressure (BP), cold sweat. Over time, signs of dyscirculatory encephalopathy appear: dizziness, sharp “lapses” in memory, speech impairment.
Cardiac (heart). The very first complaints patients present are the sensation of an irregular slow heartbeat. Due to the lack of blood circulation of the heart, pain behind the sternum appears, shortness of breath develops. Heart failure, ventricular tachycardia and fibrillation may occur. The last two manifestations often significantly increase the risk of sudden coronary (cardiac) death.
Other symptoms. Among the manifestations of SSS, not related to circulatory disorders of the brain and heart, there are signs of kidney failure (oliguria - low urine output), gastrointestinal manifestations and muscle weakness (intermittent claudication).

Diagnostics

In view of the fact that 75 out of 100 people suffering from sick sinus syndrome have severe bradycardia, this symptom can be considered as the main symptom for suggesting pathology. The basis of diagnosis is the removal of the electrocardiogram (ECG) at the time of the attack. Even in the presence of a pronounced decrease in heart rate, it is unambiguously impossible to speak of SSSU. Any bradycardia can be a manifestation of a violation of its autonomic function.

Methods used to determine sick sinus syndrome:

Holter monitoring.
Medical tests and tests with physical activity.
Electrophysiological intracardiac study.
Definition of clinical manifestations.

To choose a treatment it is important to determine the clinical form of pathology.

Bradyarrhythmic. The main manifestations are associated with impaired hemodynamics. Morgagni-Edems-Stokes attacks may occur (due to lack of cerebral circulation). The ECG shows an abnormal rhythm with a reduced heart rate. However, this sign is not always a consequence of SSSU. Similar electrocardiographic changes occur when atrial fibrillation is combined with atrioventricular block.
Tachy-bradyarrhythmic. Before an attack of tachycardia and after it, pauses are recorded on the ECG (an increase in the R-R interval). This variant of SSSU is characterized by a protracted course and often turns into a permanent replacement atrial fibrillation.
Bradycardic. With this form of SSSU, bradycardia with a rhythm source in the sinus node is determined first at night. Along with this, replacement rhythms are recorded. The initial stages of this variant of the disease are recognized only with the help of Holter monitoring.
Posttachycardic. This option differs from the previous ones by longer pauses that occur after an attack of atrial fibrillation or tachycardia.

Sometimes the initial symptom of SSS is a violation of sinoatrial conduction, as a result of which the transmission of a nerve impulse to the atria is blocked. The ECG clearly shows an increase in the P-P interval by two, three or more times.

The disease progresses in the form of one of the above options. Further, SSSU develops into an expanded form, when any symptoms of the pathology begin to be undulating. Separately allocated three variants of the course of the disease:

Latent.
Intermittent.
Manifesting.

The latent variant is not determined even with repeated Holter monitoring. It is diagnosed using an intracardiac electrophysiological study. To do this, medical denervation is performed (artificial disruption of the conduction of nerve signals to the sinus node from the autonomic nervous system). Such a course in most cases is observed in violation of sinoatrial conduction.

The intermittent variant is characterized by the occurrence of a decrease in heart rate at night. This is due to a decrease in sympathetic influence and an increase in the parasympathetic function of the autonomic nervous system.

The manifesting course develops with the progression of the disease. In this case, the manifestations of SSS can also be determined using Holter monitoring, because. they occur more than once a day.

Treatment

SSSU therapy begins with the elimination of various factors that theoretically can lead to impaired conduction. To do this, the first step is to cancel such drugs.

If the patient has an alternation of tachycardia with bradycardia, but the decrease in heart rate is not critical, then under the control of Holter monitoring, Allapinin is prescribed at a minimum dosage several times a day. Disopyramide is used as an alternative drug. Over time, the progression of the disease still reduces the heart rate to the minimum allowable. In this case, the drug is canceled and a pacemaker is implanted.

When deciding whether to install a pacemaker (IVR-artificial pacemaker), it is imperative to exclude hypothyroidism and hyperkalemia in a patient. In these conditions, a functional occurrence of bradycardia is possible.

With the acute development of SSSU, it is advisable to treat the cause that caused the pathology:

In case of suspicion of inflammatory changes in the sinus node, therapy is started with Prednisolone.
A pronounced decrease in heart rate with impaired hemodynamics (blood circulation of the whole body) is stopped by the introduction of an Atropine solution.
In the absence of heart contractions (asystole), resuscitation is immediately carried out.
To prevent the dangerous manifestations of sick sinus syndrome, an endocardial pacemaker is sometimes installed.

Basic principles of treatment of sick sinus syndrome:

In the case of minimal manifestations - observation.
With a moderately severe clinic, conservative drug therapy is indicated, aimed at preventing manifestations.
In a severe case, surgical therapy (IVR implantation).

A pacemaker is inserted below the skin under the collarbone and connected to the heart Indications for the installation of a permanent pacemaker:

bradycardia less than 40 beats per minute;
Morgagni-Edems-Stokes attacks in history. Even in the presence of a single case of loss of consciousness;
pauses between heartbeats for more than 3 seconds;
the occurrence of dizziness, fainting, heart failure or high blood systolic pressure due to SSS;
cases of a disease with rhythm disturbances in which it is impossible to prescribe antiarrhythmic drugs.

In the modern world, the vast majority of people with installed artificial pacemakers suffer from SSSU. This method of treatment does not increase life expectancy, but significantly improves its quality.

The choice of pacing method should provide not only adequate ventricular systolic function. To prevent the formation of blood clots and the corresponding complications, it is imperative to organize a normal rhythmic contraction of the atria.

SSSU forecast

Since the disease almost always progresses over time, patients' symptoms worsen. According to statistics, SSSU increases the level of total mortality by 4-5%.

Concomitant pathology of the heart of an organic nature has an adverse effect on the general condition of the human cardiovascular system. In view of the fact that thromboembolism is a frequent (about 40-50%) cause of death in cardio-diseases, the prognosis of CVD depends on the degree of risk of thrombi in the heart cavities.

With sinus bradycardia without cardiac arrhythmia, the risk of complications is minimal. The variant of SSS with sinus pauses slightly increases the risk of thrombi. The worst prognosis is with alternating bradycardia with tachyarrhythmias. In this case, the highest probability of developing thromboembolism.

Despite the prescribed treatment, sudden coronary death can occur at any time in SSSU. The level of risk depends on the severity of diseases of the cardiovascular system. If left untreated, patients with sick sinus syndrome can live for absolutely any amount of time. It all depends on the form of the disease and its course.

Prevention

To prevent SSSU, like all heart diseases, lies the right lifestyle and the rejection of bad habits. Specific prevention consists in the timely diagnosis of abnormalities in the work of the heart and the correct prescription of drugs.

Thus, it can be said that the standard of living and its duration in sick sinus syndrome depends on various factors. With the right choice of treatment, the risk of coronary death can be reduced to a minimum.

Sick sinus syndrome is an electrocardiographic clinical syndrome that displays dysfunction of the affected structures of the Keyes-Fleck node and disorders in ensuring regular conduction of automatic impulses to the walls of the atrium.

To understand the danger of this phenomenon, you need to know the etiology of its development, classification, main clinical symptoms, as well as modern methods of examination and treatment.

The main reason leading to the formation of pathological changes in the heart is organic lesions of the walls of the right atrium.

This pathology is observed in patients of all age categories. The majority of people (80-85%) with sinus node dysfunction syndrome are aged 50-60 years. The remaining 15-20% are children under 16 years of age.

Among the factors provoking weakness syndrome in a child or adolescent, there are:

Myocarditis. Inflammatory foci in viral infections are able to capture the area of the right atrium, as a result of which the patient develops CVD.
Amyloidosis with the formation of destructive changes in the heart muscle. With this disease, a protein called amyloid is deposited in the patient's myocardium. As a result, signs of blockade of the pacemaker are observed.
Toxic damage to the heart. Reception, calcium channel antagonists and organophosphorus compounds can lead to weakness of the Keyes-Fleck sinoatrial node. Often, pathological changes are eliminated after discontinuation of the drug and a complex of symptomatic treatment.
Autoimmune diseases affecting the myocardium. These include: scleroderma, systemic lupus erythematosus and rheumatism.

Pacemaker dysfunction in adults in most cases develops after 60 years of age.

In addition to the above pathologies, the development of weakness of the sinus node may be due to:

Ischemic heart disease. In the presence of coronary artery disease, the patient has a deterioration in blood flow and trophism of the right atrium, which is the main factor in the development of the syndrome in the elderly.
Myocardial infarction. During this pathology, the formation of cicatricial changes in the lesions, which can affect the sinoatrial node, is noted.

The secondary reasons for the decrease in the performance of the pacemaker include:

disruption of the endocrine glands;
severe exhaustion of the body;
age-related changes;
changes in electrolytes in the blood;
overdoses of calcium channel blockers or cardiac glycosides;
disorders in the work of autonomic regulatory levers of automatism.

Classification

The distribution of disorders of the Keyes-Fleck node occurs based on the characteristics of the development of the pathology:

Manifesting current. Disorders of the node function have a pronounced character. When performing daily monitoring using an electrocardiogram, the syndrome of weakness of the sinoatrial pacemaker is registered.
latent flow. Symptoms of insufficiency of the node are not actually noted. Multi-day observation using Holter monitoring does not reveal violations. Deterioration is diagnosed by electrophysiological examination.
intermittent flow. Clinical manifestations of SSSU are observed mainly during the patient's sleep. This indicates the influence of the autonomic system in the implementation of the transmission of cardiac impulses.

According to the mechanism of the occurrence of pathology, doctors distinguish the following types of syndrome:

Primary. Its presence is due to pathogenic processes that are localized in the sinus node.
Secondary. The pathogenesis of this type is the failure of the regulation of the activity of the heart.

Based on the form of the pathology, cardiologists distinguish the following types:

Blockade of the Kees-Fleck node. In cases of the presence of this form of pathology, changes during the work of the heart are not noted. Failure of functions occurs during the transmission of cardiac impulses, some of which do not pass further.
Stopping the sinoatrial node. This variant of the syndrome is characterized by interruptions in the creation of impulses.
Syndrome of bradycardia-tachycardia. This is a type of SSSU, in which a rapid heartbeat is replaced by slowdowns in the work of the myocardium. In some patients, it contributes to the disappearance of breaks between beats, which is the reason for the development of arrhythmia and extrasystole.
sinus bradycardia. Reducing the number of conducted impulses contributes to a drop in the level of heart rate.

The classification of Keyes-Fleck node dysfunctions is based on the factors that caused the disorders.

Among them are:

organic factors affecting the performance of the pacemaker;
external causes that can lead to disruptions in the functioning of the node.

Symptoms

Clinical features for all types of sinus node disorders are represented by three syndromes:

Cardiac - cardiac symptoms.
Astheno-vegetative - common signs.
Cerebral - disorders in the brain.

The main symptoms of pathological syndromes are in this table:

The main variants of the clinical manifestation of SSSU include:

Chronic course of pathology with periodic deterioration of the human condition and constant slowing of the rhythm during physical exertion. The patient complains of general weakness, frequent migraines, dizziness, shortness of breath and slow pulse. Often in the pathogenesis, the development of severe complications is noted as atrial fibrillation, paroxysmal tachycardia and ventricular extrasystoles.
In cases of a normal rhythm, sudden attacks of loss of consciousness, acute bradycardia and a drop in blood pressure are possible. This form of pathology is called Morgagni-Adams-Stokes syndrome.
Manifestations due to heavy loads or at rest without pathological precursors from the work of the Keyes-Fleck node. They are accompanied by squeezing retrosternal pain, difficulty breathing, wheezing in the lungs and bradycardia.
latent flow. This means that heart rate drops are periodically noted during the patient's sleep.

SSS with a pronounced slowing of the rhythm is the cause of the development of acute myocardial infarction, stroke, pulmonary edema and complete cardiac arrest.

Diagnostics

The standard research plan, in cases of suspected pathology of the sinoatrial node, includes:

Electrocardiogram. This method is informative for pronounced changes in the conductivity of the Kees-Fleck node.
. With the help of it, the cardiologist fixes dysfunctions of the pacemaker, among which paroxysms with further pauses in heartbeats are most often noted.
ECG after dosed physical activity. Their examples are and. The doctor evaluates the increase in heart rate, after which he compares them with a normal indicator and establishes a diagnosis.
Endocardial electrophysiological study. This is an invasive diagnostic method, which consists in introducing a special electrode into the right atrium through the vessels with further stimulation of myocardial contractions. After that, an assessment of the level of heart rate and the degree of delay in the conduction of impulses along the sinoatrial node is carried out, which appear on the ECG as pauses lasting more than three seconds.
Transesophageal EFI. When it is carried out, the microelectrode is inserted through the upper parts of the patient's esophagus, in places closest to the wall of the right atrium.
Auxiliary methods of examination. Among them, the most effective are: ultrasound, a blood test to determine the indicators of electrolytes, as well as a cardiac tomography.

Treatment

Therapeutic measures, in the presence of a syndrome of weakness of the sinoatrial node, have two goals:

The elimination of factors that led to the development of pathology.
Normalization of the pacemaker by medication or surgery.

After establishing the etiology, as a result of which the syndrome developed, patients are prescribed a complex of medical procedures. They are aimed at eliminating the underlying disease and its complications.

Medical

Refusal to take certain drugs will avoid the disappearance of the bioelectric activity of the heart muscle:

B1-blockers - Atenolol, Carvedilol, Nebivolol.
Potassium-sparing diuretics - Spironolactone, Decriz, Eridanus.
Calcium channel antagonists - Gallopamil, Diltiazem, Bepridil.

Timely adequate therapy of SSSU makes it possible to prevent death from asystole.

The main group of drugs that are used to maintain the patient's condition are coronary lytics:

Atropine.
Theotard.
Teopak.

To reduce myocardial oxygen demand, the following are prescribed:

Nitroglycerine.
Nitrosorbide.
Nitrong.
Nifedipine.
Diltiazem.

In order to increase the supply of oxygen to the heart muscle, the following are used:

Eufillin.
Carbocromen.
Pentoxifylline.

To increase the resistance of the heart to hypoxia, you can use:

potassium chloride;
vitamins A, C, E;
cytochrome C;
phosphadena;
riboxin.

With node weakness, which is accompanied by concomitant cardiac pathologies and rhythm disorders, antiarrhythmic drugs are used with extreme caution. In patients with SSSU associated with their overdose, the drug is completely canceled.

Installing a pacemaker

The main surgical technique for eliminating the syndrome is the implantation of a pacemaker.

All types of indications for the procedure are divided into 2 classes:

Class I. It is diagnosed in patients with persistent changes in the functioning of the node, which are accompanied by a decrease in heart rate and the presence of pauses between myocardial contractions lasting more than three seconds.
Class IIa. This type is accompanied by dysfunctions of the Keyes-Fleck node, in which the heart rate is less than 50 beats per minute, as well as classic clinical symptoms.
Class IIb. Slightly pronounced signs of pathology with a heart rate after an exercise test of less than 50 beats per minute.

Normal rhythmic atrial contraction also avoids the formation of blood clots and the development of related complications.

Forecast

Pathology has a progressive course. Keyes-Fleck node weakness syndrome is a factor that increases mortality from diseases of the heart and blood vessels by 5-6%. Pathologies that provoke the development of organic myocardial lesions also adversely affect the prognosis.

Successful recovery of the patient depends on the severity of the clinical symptoms of sinoatrial node weakness. The most unfavorable prognosis includes patients with atrial tachyarrhythmias, sinus pauses and bradycardia. This is due to the high probability of blood clots, which are the cause of half of all deaths in cardiovascular pathologies. These people have a disability.

The possibility of death due to a complication of the syndrome, as well as the underlying disease, can occur at any stage of the course of the disease. In the absence of adequate therapy, patients with SSS live from two weeks to ten years.

Sinus node weakness syndrome in cardiology is referred to as clinical and pathogenetic concepts that combine rhythm disturbances provoked by a decrease in the functional ability of the sinus node. ICD-10 code I49.5. Consider the leading provocateurs of the development of SSSU, what it is, symptoms, and describe the features of the manifestation of the disorder in children. Let us dwell in more detail on the diagnosis, features of therapy and prevention of a pathological condition.

The sinus node (SN) is represented by a section of the muscle that produces impulses aimed at regulating the functioning of the heart. The weakness syndrome of the zone in question often accompanies, ectopic arrhythmias.

Experts identify true SSSU, which occurs as a result of an organic lesion of the node. In a separate group are allocated: vegetative dysfunction of the sinus node, medication type of malfunction. They are eliminated with drug denervation of muscle fibers, the abolition of medications that have an overwhelming effect on the creation and conduction of a sinus impulse.

Symptoms may practically not manifest themselves or consist in weakening, feeling a strong heartbeat, fainting ().

Diagnostics includes Holter ECG monitoring, stress tests, invasive studies, ECG, TPEFI. The therapeutic course is prescribed taking into account the type of pathology. If there are signs of pathology, patients are recommended to implant artificial pacemakers.

SSSU classification

Taking into account the specificity of the clinic, the variants of the course of the pathological condition, doctors distinguish the following forms of SSSU:

Latent. The specificity of this form is the absence of manifestations on the ECG, other symptoms. Determine the dysfunction in the electrophysiological study. The patient is not provided with disability restrictions, he does not need to install a pacemaker.

2. Compensated. It has 2 options:

bradysystolic. There is a failure of cerebral blood flow, this condition is accompanied by transient paresis, spinning in the head, fainting. Heart failure occurs due to bradyarrhythmia. The patient's ability to work is severely limited. Implantation is needed in case of asystole, the recovery rate of the SU is more than 3 seconds;
bradytachysystolic. The signs described above are supplemented by paroxysmal tachyarrhythmias. Patients are considered completely disabled. The need for an implant is as described above.

4. Permanent (bradysystolic) form of atrial fibrillation. It has the following types:

Given the manifestations of SSSU during ECG monitoring, doctors determine the following courses:

latent (there are no manifestations of the disease);
intermittent (manifestation of SSSU in the case of an increase in parasympathetic tone, a decrease in sympathetic;
manifesting. Symptoms are noticeable with daily 24-hour ECG monitoring.

Given the course of the pathology, there are:

acute;
recurrent.

According to the etiological indicator, the forms are distinguished:

primary. Provoked by organic damage to the sinoatrial zone (SAD);
secondary. It is provoked by failure of autonomic regulation of SPZ.

Causes

Specialists separate several causes that provoke damage to the SU and can activate the pathology in question. Among them:

Of the external factors that cause dysfunction of the considered part of the organ, there are several:

Symptoms

SSSU has a different clinic. Doctors explain this nuance by the fact that pathology is included in heterogeneous failures. The initial stages are asymptomatic. SSSU can proceed without visible manifestations even when the patient has a heart rhythm pause of 4 or more seconds. Only a certain part of the sick feel a deterioration in the condition due to a malfunction in the blood flow of the brain, peripheral blood flow, and slowing of the rhythm.

With the development of the disease, signs of weakness of the sinus node appear, which are associated with bradycardia. There are complaints about:

When brady- and tachycardia alternate, the following symptoms occur:

head spinning;
feeling of increased heart rate;
fainting.

We indicate separately the cerebral signs of pathology:

With a mild clinic, patients develop fatigue, some forgetfulness, emotional lability, inexplicable irritability. Older people notice a decrease in memory, intellectual level. There are fainting, pre-fainting states.
The progression of the pathology, failures in the circulatory system contribute to the fact that cerebral symptoms manifest themselves more noticeably.
Pre-fainting in sick people is sometimes accompanied by tinnitus, rapidly emerging weakness. Fainting with a cardiac nature is distinguished by the absence of an aura and convulsions in a sick person.
Patients do not always feel the previous slowing of the heartbeat, stop of the organ.
There may be a sharp drop in blood pressure, blanching, cooling of the dermis, cold sweat. Fainting causes a rapid turn of the head, coughing, wearing a tight collar. Usually, fainting recedes on its own. Only in exceptional cases are resuscitation measures required.
With the progression of bradycardia, it is possible to increase dizziness, paresis, irritability, memory lapses, insomnia, memory loss.

Among the cardiac symptoms of SSSU, we list the main ones:

The occurrence of chest pain. Doctors explain this condition by organ hypoperfusion.
Irregular, slow pulse (usually noted early in the disease).
The emergence of slipping rhythms. It is manifested by a feeling of palpitations, malfunctions of the organ.
Due to the limited chronotropic reserve during exercise, shortness of breath, weakness occur, and heart failure (chronic form) may develop.
The later stages of the pathology are accompanied by ventricular tachycardia, fibrillation. These conditions are dangerous for the likelihood of cardiac death, which occurs unexpectedly.

Among the additional features of the SSSU, we note:

Diagnostics

The study of the pathological condition under consideration consists in carrying out a number of activities:

Features of the disease in children

In younger patients, SSSU is considered an irreversible process of failure of the SU, underlying accumulations of cardiomyocytes that form electrical impulses. This reduces the number of beats of the heart muscle. In children, pathology is dangerous for their lives, so doctors recommend timely detection of the disease and surgical treatment.

In babies, the symptoms of the disease in question are of 3 types:

Transient. You can observe them with inflammation of the myocardium.
Permanent. Observed in the presence of defects of the heart muscle.
Progressive. Manifested in the case of primary myocardial damage, asynchronous repolarization of the organ.

Often covers the pathology of the conductive cardiac system. It is difficult to diagnose the disease in childhood due to the lack of symptoms. The syndrome is usually diagnosed in half of the children quite by accident.

The second half has:

fainting states;
arrhythmia;
head spinning;
weakness;
head pain.

Sinus node dysfunction (sinus node weakness)

The sinus node (SN) normally automatically generates electrical impulses with an "intrinsic frequency". The method of its determination and the calculation formula are described in the section "Special examination of patients with cardiac arrhythmias". The autonomic nervous system modulates this frequency so that parasympathetic influences (acetylcholine) decrease it and sympathetic influences (norepinephrine) increase it. The balance of these influences is constantly changing depending on the time of day, body position, level of physical and emotional stress, ambient temperature, factors triggering reflex reactions, etc. Therefore, the frequency of sinus rhythm during the day varies widely, decreasing at rest, especially during sleep, and increasing during the daytime in the waking state. At the same time, along with normosystole, both sinus tachycardia (heart rate more than 100 imp/min) and sinus bradycardia (heart rate less than 50 imp/min) can be observed. To characterize these conditions from the point of view of the norm and pathology (sinus node dysfunction), it is important not only to determine the permissible limits for the severity of bradycardia, but also to assess the adequacy of the increase in the frequency of the sinus rhythm in response to the loads.
Physiological sinus bradycardia can be observed during the daytime at rest and at night as the predominant heart rhythm. It is believed that the maximum decrease in the frequency of the rhythm during the day at rest is determined by the value of 40 imp/min, at night - 35 imp/min and does not depend on sex and age. They also allow the development of sinus pauses, the duration of which is up to 2000 ms, which is not uncommon in healthy individuals. But their duration cannot normally exceed 3000 ms. Often in highly qualified athletes, as well as in hard physical labor, in young men, bradycardia is recorded with a frequency below those indicated, possibly in combination with other manifestations of sinus node dysfunction. These conditions can only be classified as normal if they are asymptomatic and there is an adequate increase in sinus rate in response to exercise.
Assessment of the adequacy of the sinus rate increase in response to exercise often causes difficulties in clinical practice. This is due to the lack of universal methodological approaches to the definition of chronotropic failure and agreed criteria for its diagnosis. The most widespread is the so-called chronotropic index, which is calculated from the results of a test with physical activity according to the protocol of maximum tolerance for symptom-limited physical activity. The chronotropic index is the ratio (%) of the difference between peak heart rate at maximum exercise and resting heart rate (chronotropic response) to the difference between age-predicted maximum heart rate calculated by the formula (220 - age) (imp/min) and resting heart rate (chronotropic reserve ). It is believed that the normal value of the chronotropic index is ≥80%. Improved formulas are also proposed, adapted to gender, the presence of cardiovascular disease (CHD) and the use of beta-blockers, but the discussion about the appropriateness of their clinical use continues.
The normal function of the sinus node is carried out due to the spontaneous depolarization of its pacemaker N-cells (automatism) and the conduction of emerging impulses by transient T-cells to the atrial myocardium through the sino-atrial (SA) zone (sino-atrial conduction). Violations of any of these components lead to sinus node dysfunction (SNS). They are based on numerous reasons, some of which, internal, lead to structural damage to the tissue of the node and the perinodal zone (often extending to the atrial myocardium) or are reduced to a primary dysfunction of the ion channels. Other, external causes, are due to the action of drugs, autonomous influences or the impact of other external factors that lead to dysfunction of the SU in the absence of its organic damage. The relative conditionality of such a division is determined by the fact that external factors are always present in the presence of internal causes, enhancing the manifestations of sinus node dysfunction.
The most important internal cause of DSU is the replacement of sinus node tissue with fibrous and adipose tissue, and the degenerative process usually extends to the perinodal zone, the atrial myocardium, and the atrioventricular node. This defines comorbidities that are inextricably linked to DSS. Degenerative changes in SU can be caused by myocardial ischemia, including myocardial infarction, infiltrative (sarcoidosis, amyloidosis, hemochromatosis, tumors) and infectious processes (diphtheria, Chagas disease, Lyme disease), collagenoses (rheumatism, systemic lupus erythematosus, rheumatoid arthritis, scleroderma) and other forms of inflammation (myocarditis, pericarditis). In addition, there are reasons to believe that damage to the artery of the sinus node of various nature can also lead to dysfunction of the sinus node. But in most cases, there is idiopathic degenerative fibrosis, which is inextricably linked with aging. In young people, a common cause of SU lesions is trauma after surgery for congenital heart defects. Family forms of sinus node dysfunction are also described, in which there are no organic lesions of the heart, and the pathology of SU, designated as isolated, is associated with mutations in the genes responsible for sodium channels and pacemaker current channels (If) in SU cells.
Among the external causes, first of all, is the influence of drugs (beta-blockers, calcium current blockers, cardiac glycosides, class I, III and V antiarrhythmic drugs, antihypertensive drugs, etc.). A special place is occupied by syndromes mediated by autonomic influences, such as neurocardial syncope, hypersensitivity of the carotid sinus, reflex influences caused by coughing, urination, defecation and vomiting. Electrolyte imbalances (hypo- and hyperkalemia), hypothyroidism, rarely hyperthyroidism, hypothermia, increased intracranial pressure, hypoxia (sleep apnea) lead to DSU. In idiopathic forms of DSU, a possible mechanism is increased vagal tone or deficiency of atrial cholinesterase, as well as the production of antibodies to M2-cholinergic receptors that have stimulating activity.
The prevalence of DSU cannot be adequately assessed due to the inability to account for asymptomatic cases and the difficulty of differentiating physiological and pathological bradycardia in population studies. The frequency of detection of DSU increases with age, but in the group over 50 years old it is only 5/3000 (0.17%). The frequency of symptomatic cases of DSU is estimated by the number of implantations of artificial pacemakers (IVR), but these figures vary greatly in different countries, which is associated not only with demographic characteristics and the prevalence of the disease, but also with material security and characteristics of indications for implantation. However, DSU accounts for about half of all pacemaker implantations, and the frequency of their distribution by age is bimodal with peaks in the intervals of 20-30 and 60-70 years.
Rice. 1. Electrocardiographic manifestations of sinus node dysfunction associated with impaired automatism function. A - sinus bradycardia. B - stops the sinus node. B - long sinus pause. D - post-tachycardic arrest of the sinus node with escape rhythm from the AV junction. E - post-tachycardic stop of the sinus node with escape impulses from the AV junction and recurrence of atrial fibrillation.Disorders of the SU function have a variety of electrocardiographic manifestations. The most common form is sinus bradycardia (SB). In this case, a rare atrial rhythm is characterized by excitation of the atria from the SU region (see the chapter "Special examination of patients with cardiac arrhythmias"), and in the presence of arrhythmia, the R-R intervals change smoothly from cycle to cycle (Fig. 1A). The SB is based on a decrease in the automatism function of the SS.
More pronounced violations of the automatism of the SU lead to the cessation of the SU, manifested by a sinus pause of various durations. A characteristic feature of this pause is that it is never a multiple of the duration of the previous sinus cycle, even with allowance for arrhythmia. There are obvious difficulties in qualifying such pauses as SS stops. There are no generally accepted quantitative criteria in this regard, and the solution of the issue largely depends on the severity of sinus arrhythmia and the average frequency of the previous rhythm. Regardless of the frequency and severity of the arrhythmia, a pause lasting more than twice the previous sinus cycle definitely indicates SU stop (Fig. 1B). If the pause is shorter than this value, then to ascertain the stop of the SS, it is required, based on the limiting normal frequency of 40 imp/min, that it be more than 2 s, which is equivalent to exceeding the previous cycle by 25% or more. Such pauses, however, may not have clinical significance, and then the criterion for stopping the SU is proposed to be longer than 3 s, which excludes its physiological nature.
Difficulties of a different kind arise when diagnosing SU stops during very long pauses, when there is no complete certainty that only the mechanism for suppressing the automatism of SU in the absence of a simultaneous blockade of SA conduction is the basis (Fig. 1C). The use of the multiplicity criterion here is difficult to apply, firstly, due to the ambiguity of the choice of the reference cycle (Fig. 1B), secondly, due to its absence in cases of post-tachycardic pause development, and, thirdly, due to the interference of escape impulses and rhythms (Fig. 1D, E). Although it is believed that post-tachycardic pauses are based on the suppression of automatism of SU by frequent atrial impulses (overdrive suppression), the involvement of CA conduction disturbances is also not ruled out. Therefore, when designating prolonged asystole, they prefer to avoid terms that indicate the mechanism of the phenomenon, often using the term sinus pause.
Another cause of sinus pauses is a violation of SA conduction. Prolongation of SA conduction time (SA blockade of the 1st degree) has no electrocardiographic manifestations and can only be detected by direct recording of the SU potential or by indirect methods using atrial electrical stimulation. In SA blockade II degree Mobitz type I (with Wenckebach periodicity) there is a progressive increase in the time of conduction of successive sinus impulses in the SA zone until a complete blockade of the next impulse develops. On the ECG, this is manifested by cyclic changes in the P-P intervals with their progressive shortening, followed by a pause, the duration of which is always less than twice the P-P interval (Fig. 2A). In second-degree Mobitz type II SA block, blocking of the sinus impulses occurs without a preceding prolongation of SA conduction time, and on the ECG this is manifested by pauses whose duration is almost exactly (taking into account the arrhythmia tolerance) a multiple of the duration of the previous P-P interval (Fig. 2B). With further inhibition of SA conduction, the frequency of pulse conduction in the periodicals decreases until the development of SA blockade II degree 2:1 (Fig. 2C). With its stable preservation, the ECG picture is indistinguishable from sinus bradycardia (Fig. 2D). In addition, blocked atrial extrasystole in the form of bigeminia, not related to DSU, mimics both sinus bradycardia and CA block II degree 2:1 (Fig. 2E). T wave distortions, indicating the possible presence of premature atrial excitation, cannot always be correctly interpreted, since a notch on the T wave may be a natural manifestation of repolarization disorders against a background of a rare rhythm. The problem of differential diagnosis is solved by long-term ECG recording with the capture of transients. In the case of blocked atrial premature beats, esophageal electrocardiography may be required.

Rice. 39. Electrocardiographic manifestations of sinus node dysfunction associated with impaired sino-atrial conduction. A - SA block II degree type I with a periodicity of 9:8. B - SA block II degree type II. B - SA block II degree type I with periods of 2:1 and 3:2. D - SA block II degree type I with a steady development of periodicals 2:1. E - the development of an episode of blocked atrial extrasystole in the form of bigeminy, simulating manifestations of dysfunction of the sinus node.
The development of a far-reaching CA blockade of the II degree is manifested by long sinus pauses, the duration of which is a multiple of the previous atrial cycle. But the same problems of diagnosing the mechanism of a long pause remain, which are described for stopping the SS. One of the provoking factors in the development of advanced CA block II degree is a critical increase in sinus impulses associated with physical or other stress. At the same time, a sharp decrease in heart rate from a frequency determined by metabolic needs, as a rule, is manifested by clinical symptoms.

Rice. 3. Sino-atrial blockade of the III degree with slipping rhythms from the atria. Note: asterisks on fragment B indicate sinus impulses.
The extreme degree of violation of CA conduction, - CA blockade of the III degree, is manifested by the absence of sinus impulses during the electrical activity of the atria in the form of escaped atrial rhythms (Fig. 3) or a rhythm from the AV junction. In this case, individual impulses from the SU can rarely be observed (Fig. 3B). This condition, which is difficult to differentiate from SU stop, should not be identified with the complete absence of atrial electrical activity, referred to as atrial standstill. This condition is associated with electrical non-excitability of the atrial myocardium with possibly preserved sinus mechanism (hyperkalemia).
SU dysfunction is often accompanied by a number of additional manifestations. First of all, these are escape impulses and rhythms coming from the atria or the AV junction. They occur with sufficiently long sinus pauses, and the development of clinical symptoms of DSU largely depends on the activity of their sources. Like SU, second-order pacemakers are subject to autonomic and humoral influences, as well as the phenomenon of overdrive suppression. Since DSU from internal causes is characterized by the spread of the degenerative process to the atrial myocardium, this creates the basis for the development of atrial arrhythmias, primarily atrial fibrillation. At the moment of cessation of arrhythmia, favorable conditions are created for the development of prolonged asystole, since the automatism of the SU and second-order pacemakers are in a depressed state. This, as a rule, leads to clinical symptoms, and a similar condition in the form of a tachycardia-bradycardia syndrome was first described by D. Short in 1954. .
SU dysfunction and inextricably linked clinical manifestations and concomitant arrhythmias form a clinical and electrocardiographic symptom complex. For the first time, B. Laun, observing various manifestations of DSU after electrical cardioversion of atrial fibrillation with a characteristic low ventricular rate, used the term sick sinus syndrome, translated into Russian and rooted as sick sinus syndrome (SSS). Later, under this term, both the manifestations of DSU and concomitant arrhythmias, including the tachycardia-bradycardia syndrome, and concomitant atrioventricular conduction disorders were combined. Later, chronotropic failure was added. The ongoing evolution of terminology has led to the fact that at present the preferred term for this syndrome is sinus node dysfunction, and the term SSS is proposed to be used in cases of DSU with clinical symptoms. This syndrome includes:

persistent, often severe, sinus bradycardia;
sinus node stops and sino-atrial blockade;
persistent atrial fibrillation and flutter with a low ventricular rate in the absence of drug reduction therapy;
chronotropic failure.

The natural course of DSU (SSSU) is characterized by its unpredictability: long periods of normal sinus rhythm and prolonged remission of clinical symptoms are possible. However, DSU (SSSU), primarily from internal causes, tends to progress in most patients, and SB in combination with stops of SU and SA blockades, on average, after 13 (7-29) years, reaches the degree of complete stop of SA activity. At the same time, mortality directly related to DSU (SSSU) does not exceed 2% over a 6-7 year follow-up period. Age, concomitant diseases, especially coronary artery disease, the presence of heart failure are important factors that determine the prognosis: annual mortality during the first 5 years of follow-up in patients with DSU and concomitant diseases is 4-5% higher than that in patients without DSU of the same age and with the same heart rate. vascular pathology. The mortality rate of patients with DSU without concomitant pathology does not differ from the control group. Over time, atrioventricular conduction disturbances are detected and progress, but they are not pronounced and do not affect the prognosis. Of greater importance is the increase in the number of cases of atrial fibrillation, estimated at 5-17% per year. It is with it, first of all, that the high frequency of thromboembolic complications in DSU (SSV) is associated, which account for 30 to 50% of all deaths. At the same time, it was shown that the prognosis of patients with tachycardia-bradycardia syndrome is significantly worse compared to other forms of DSU. This serves as an important indication of the direction of treatment of such patients and the need for careful identification of asymptomatic atrial arrhythmias.
In the diagnosis of DSU, the most important task is to confirm the relationship of clinical symptoms with bradycardia, i.e. detection of clinical and electrocardiographic correlation. That is why the most important elements of the examination of the patient are a thorough analysis of the patient's complaints, described in detail in the section "Differential diagnosis of syncope", and an electrocardiographic examination. Since a standard ECG can rarely be recorded at the time of the development of symptoms that are transient, long-term ECG monitoring methods play a major role. These include Holter ECG monitoring, use of event recorders with loop memory, remote (home) ECG monitoring, and implantation of ECG recorders. For indications for their use, see the section "Special examination of patients with cardiac arrhythmias". The results obtained with these methods directly guide the direction of treatment. The use of Holter monitoring alone for up to 7 days makes it possible to establish a clinical and electrocardiographic correlation in at least 48% of cases. However, in some cases, this diagnostic strategy gives a too delayed result, which may be unacceptable due to the severity of clinical symptoms. In these cases, provocative tests are used, which, unfortunately, are characterized by a fairly high frequency of false positive and false negative results.
As such methods (see the section "Special examination of patients with cardiac arrhythmias"), the exercise test is an invaluable aid in the diagnosis of chronotropic failure and in the identification of DSU associated with natural exercise. Carotid sinus massage and passive orthostatic test play an important role as provoking neuro-reflex tests. To assess the role of external and internal causes of DSU (SSSU), pharmacological tests are important. Atrial electrical stimulation for the diagnosis of DSU is limited in its use, which is associated with a low frequency of detecting a positive clinical and electrocardiographic correlation, and the indication for invasive EPS is the need to exclude other arrhythmic causes of syncope.
Treatment of patients with DSU involves the following areas: elimination of bradycardia with its clinical manifestations, elimination of concomitant cardiac arrhythmias and prevention of thromboembolic complications and, of course, treatment of the underlying disease. Asymptomatic patients with DSU in the absence of organic heart disease and concomitant arrhythmias do not require treatment. At the same time, such patients should avoid drugs that can be prescribed for reasons not related to cardiovascular pathology and that inhibit the function of the SU (lithium and other psychotropic drugs, cimetidine, adenosine, etc.). In the presence of organic cardiovascular diseases, the situation is complicated by the need to prescribe such drugs (beta-blockers, calcium channel blockers, cardiac glycosides). Particular problems may arise in connection with the prescription of antiarrhythmic drugs for the treatment of concomitant arrhythmias, primarily atrial fibrillation. If at the same time it is not possible to achieve the desired result by choosing drugs that have a lesser effect on the function of the SU, or by reducing the dose of drugs, then the aggravation of DSU with the appearance of its clinical symptoms will require the implantation of an IVR. In patients with pre-existing clinical symptoms of DSU, the issue of IVR implantation requires priority consideration.
Continuous cardiac electrical stimulation eliminates the clinical manifestations of DSU, but does not affect overall mortality. It appears that single chamber atrial pacing (AAIR) or dual chamber pacing (DDDR) have advantages over single chamber ventricular pacing (VVIR): increased exercise tolerance, reduced rate of pacemaker syndrome and, most importantly, reduced incidence of atrial fibrillation and thromboembolic events. complications. Moreover, the advantages of dual-chamber pacing over single-chamber atrial pacing have been identified, which are determined by the lower incidence of paroxysms of atrial fibrillation and the lower frequency of pacemaker reimplantation, which are required during atrial pacing due to the development of atrioventricular conduction disturbances. It has also been shown that prolonged right ventricular pacing due to excitation dyssynchrony causes impaired left ventricular contractile function, and algorithms are used to reduce the number of imposed ventricular excitations during dual-chamber pacing, which give an advantage to own impulses conducted to the ventricles. Thus, dual-chamber pacing with responsive rate and AV delay control (DDDR + AVM) is currently recognized as the first choice pacing technique. Indications for this method of treatment are presented in Table. 1.However, it should be taken into account that in the case of the development of DSU due to transient, apparently reversible causes, the issue of implanting a pacemaker should be postponed, and treatment should be aimed at correcting the causing conditions (drug overdose, electrolyte disturbances, the consequences of infectious diseases, thyroid dysfunction, etc.). .d.). Atropine, theophylline, temporary electrical stimulation of the heart can be used as means of eliminating DSU. Persistent atrial fibrillation with a low ventricular rate should be considered a natural self-healing from DSU and refrain from restoring sinus rhythm.
Antithrombotic therapy should be carried out in all cases of concomitant atrial tachyarrhythmias in full accordance with the recommendations for antithrombotic therapy for atrial fibrillation (see the appropriate section of the Guidelines).Taking into account modern treatment, the prognosis of DSU is determined by the underlying disease, age, the presence of heart failure and thromboembolic complications, the frequency of which can be affected by adequate antithrombotic therapy and an adequate choice of pacing regimen.
Table 1. Indications for continuous cardiac pacing in sinus node dysfunction