Atrial fibrillation: causes, symptoms, treatment

• Symptoms of AF
• Pathogenesis and general clinical picture
• Causes of AF and risk factors
• Diagnostic methods
• AF treatment strategies
• Use of the drug Propanorm for AF

Atrial fibrillation (AF) is a synonym for the more applicable term “Atrial Fibrillation” in the CIS countries.
Atrial fibrillation is the most common heart rhythm disorder. AF is not associated with a high risk of sudden death, so it is not classified as a fatal rhythm disorder, such as ventricular arrhythmias.

Atrial fibrillation

One of the most common types of supraventricular tachyarrhythmias is atrial fibrillation (AF). Fibrillation is a rapid, irregular contraction of the atria, with a frequency exceeding 350 beats per minute. The onset of AF is characterized by irregular contraction of the ventricles. AF accounts for more than 80% of all paroxysmal supraventricular tachyarrhythmias. Atrial fibrillation is possible in patients of all age categories, but in elderly patients the prevalence of the syndrome increases, which is associated with an increase in organic heart pathology.

Causes of development and risk factors

Cardiac pathology

• AMI (impaired conductivity and excitability of the myocardium).
• Arterial hypertension (LA and LV overload).
• Chronic heart failure (impaired myocardial structure, contractile function and conductivity).
• Cardiosclerosis (replacement of myocardial cells with connective tissue).
• Myocarditis (structural disorder due to inflammation of the myocardium).
• Rheumatic diseases with damage to the valves.
• SU dysfunction (tachy-brady syndrome).

Extracardiac pathology

• Diseases of the thyroid gland with manifestations of thyrotoxicosis.
• Drug or other intoxication.
• Overdose of digitalis preparations (cardiac glycosides) in the treatment of heart failure.
• Acute alcohol intoxication or chronic alcoholism.
• Uncontrolled treatment with diuretics.
• Overdose of sympathomimetics.
• Hypokalemia of any origin.
• Stress and psycho-emotional stress.

Age-related organic changes.

With age, the structure of the atrial myocardium undergoes changes. The development of small focal atrial cardiosclerosis can cause fibrillation in old age.

Classification of atrial fibrillation

According to the duration of clinical manifestations.

The following forms of AF are distinguished:

• Paroxysmal (paroxysmal).
  Single episodes of AF lasting no more than 48 hours in the case of cardioversion, or up to 7 days in the case of spontaneous restoration of rhythm.
• Persistent form.
  Episodes of atrial fibrillation lasting more than 7 days without spontaneous recovery, or atrial fibrillation amenable to cardioversion (medical or electrical) after 48 hours or more.
• Permanent form (chronic).
  Continuous AF not amenable to cardioversion, if the physician and patient decide to abandon attempts to restore sinus rhythm.

By heart rate

• Tachysystolic.
  Atrial fibrillation with a ventricular rate of more than 90–100 beats. per minute
• Normosystolic.
  The AV node allows the ventricles to contract at a rate of 60–100 beats/min.
• Bradysystolic.
  Heart rate with this form of fibrillation does not reach 60 beats/min.

Types of atrial fibrillation (AF)

The term “atrial fibrillation” can refer to the following two types of supraventricular tachyarrhythmia.

Fibrillation (atrial fibrillation).

Normally, an electrical impulse arises in the sinus node (in the wall of the right atrium), spreads throughout the myocardium of the atria and ventricles, causing their successive contraction and ejection of blood. In AF, the electrical impulse travels chaotically, causing the atria to “flicker” as the myocardial fibers contract uncoordinatedly and very quickly. As a result of the chaotic transmission of excitation to the ventricles, they contract irregularly and, as a rule, not efficiently enough.

Atrial flutter.

In this case, contraction of myocardial fibers occurs at a slower pace (200–400 beats/min.). Unlike AF, with flutter the atria still contract. As a rule, due to the refractory period of the atrioventricular node, not every electrical impulse is transmitted to the ventricles, so they do not contract at such a rapid pace. However, as with fibrillation, with flutter the pumping function of the heart is disrupted, and the myocardium experiences additional stress.

Complications of atrial fibrillation

According to the latest data, patients with atrial fibrillation are at risk not only for the development of thromboembolic stroke, but also for myocardial infarction. The mechanisms of damage are as follows: with atrial fibrillation, full contraction of the atria is impossible, so the blood stagnates in them and blood clots form in the parietal space of the atria. If such a thrombus enters the aorta and smaller arteries with the blood flow, then thromboembolism occurs in the artery supplying any organ: the brain, heart, kidneys, intestines, lower extremities. The cessation of blood supply causes infarction (necrosis) of a section of this organ. A cerebral infarction is called an ischemic stroke. The most common complications are:

• Thromboembolism and stroke.
  Most often, the target is the brain (through the straight carotid arteries, the thrombus quite easily “shoots” in this direction). According to statistics, every fifth patient with a stroke has a history of atrial fibrillation.
• Chronic heart failure.
  Atrial fibrillation and flutter can cause increased symptoms of circulatory failure, including attacks of cardiac asthma (acute left ventricular failure) and pulmonary edema.
• Dilated cardiomyopathy.
  The tachysystolic form of AF, when the frequency of ventricular contractions constantly exceeds 90 beats, quickly leads to pathological expansion of all cardiac cavities.
• Cardiogenic shock and cardiac arrest
  . In rare cases, an attack of atrial fibrillation or flutter with severe hemodynamic disturbances can lead to arrhythmogenic shock, a life-threatening condition.

Diet as arrhythmia prevention

Food can be not only beneficial, but also harmful if it contains toxic substances or an excess of certain elements. An unhealthy diet can sometimes cause high cholesterol levels in the blood. With this disorder, atherosclerosis of the vascular system develops.

This disease causes various pathological changes in the heart, disturbances in its functioning, and the development of arrhythmia. Prevention of cardiac arrhythmia should include eating natural and healthy food, which is prepared mainly by steaming or in the oven. Food should not be too spicy, fatty, hot or salty. It is also recommended to eliminate or reduce the consumption of sweets, pickles, strong tea and coffee. It is necessary to include a sufficient amount of fresh herbs, cereals, fruits, vegetables, and low-fat dairy products.

Drug therapy

The following areas of drug therapy for atrial fibrillation are distinguished: cardioversion (restoration of normal sinus rhythm), prevention of repeated paroxysms (episodes) of supraventricular arrhythmias, control of the normal frequency of contractions of the ventricles of the heart. Another important goal of drug treatment for MA is the prevention of complications - various thromboembolisms. Drug therapy is carried out in four directions.

Treatment with antiarrhythmics.

It is used if a decision has been made to attempt drug cardioversion (restoring the rhythm with the help of drugs).
The drugs of choice are propafenone, amiodarone.
Propaphenone

is one of the most effective and safe drugs used to treat supraventricular and ventricular heart rhythm disorders. The action of propafenone begins 1 hour after oral administration, the maximum concentration in the blood plasma is reached after 2–3 hours and lasts 8–12 hours.

Heart rate control.

If it is impossible to restore the normal rhythm, it is necessary to bring the atrial fibrillation back to normal form. For this purpose, beta-blockers, non-dihydropyridine calcium antagonists (verapamil group), cardiac glycosides, etc. are used.

Beta blockers

. Drugs of choice for controlling heart function (frequency and strength of contractions) and blood pressure. The group blocks beta-adrenergic receptors in the myocardium, causing a pronounced antiarrhythmic (heart rate reduction) as well as hypotensive (blood pressure reduction) effect. Beta blockers have been shown to statistically increase life expectancy in heart failure. Contraindications for use include bronchial asthma (since blocking beta 2 receptors in the bronchi causes bronchospasm).

Anticoagulant therapy.

To reduce the risk of thrombosis in persistent and chronic forms of AF, blood thinning drugs must be prescribed. Anticoagulants of direct (heparin, fraxiparin, fondaparinux, etc.) and indirect (warfarin) action are prescribed. There are regimens for taking indirect (warfarin) and so-called new anticoagulants - antagonists of blood clotting factors (Pradaxa, Xarelto). Treatment with warfarin is accompanied by mandatory monitoring of coagulation parameters and, if necessary, careful adjustment of the drug dosage.

Metabolic therapy.

Metabolic drugs include drugs that improve nutrition and metabolic processes in the heart muscle. These drugs purport to have a cardioprotective effect, protecting the myocardium from the effects of ischemia. Metabolic therapy for MA is considered an additional and optional treatment. According to recent data, the effectiveness of many drugs is comparable to placebo. Such medicines include:

• ATP (adenosine triphosphate);
• K and Mg ions;
• cocarboxylase;
• riboxin;
• mildronate;
• preductal;
• mexico.

Diagnosis and treatment of any type of arrhythmia requires considerable clinical experience, and in many cases, high-tech hardware. In case of atrial fibrillation and flutter, the main task of the doctor is, if possible, to eliminate the cause that led to the development of the pathology, preserve heart function and prevent complications.

These include:

1. Rhythm control/pulse rate control
If rhythm disturbances occur more than once or twice a year, constant use of antiarrhythmic drugs is necessary.

Tactics to actively restore and maintain normal (sinus) rhythm using AAP are called rhythm control tactics. It is preferable in those patients with paroxysmal, permanent and persistent forms of the disease who lead an active lifestyle and do not have solid concomitant pathology. With fairly frequent, prolonged episodes of AF, ongoing planned antiarrhythmic therapy is also mandatory. Often, an increase in paroxysms is a natural course of the disease. But in some cases, this form of MA is caused by improper treatment, when the patient takes medications in insufficient doses or is not treated at all. It is the arrhythmologist who is called upon to select the treatment regimen that will help the patient cope with the disease. If it is unsuccessful, the patient may be recommended to consult a cardiac surgeon - arrhythmologist for surgical treatment of AF.

If this arrhythmia becomes permanent, active rhythm restoration is not indicated due to ineffectiveness. Under the influence of a long-term arrhythmia, the structure and function of the heart change and it “gets used” to living with it; it is no longer possible. In such patients, pulse control tactics are used, that is, with the help of medications, a heart rate that is comfortable for the patient is achieved. But no active attempts are made to restore the rhythm.

The following are currently used as antiarrhythmic drugs:

• beta blockers (metoprolol, bisoprolol, carvedilol)
• propafenone
• amiodarone
• sotahexal
• allapinin
• digoxin
• drug combination

2.Prevention of complications:
prevention of stroke and thromboembolism

With AF, there is no single, coordinated ejection of blood from the heart; some of the blood stagnates in its chambers and, in the form of blood clots, can enter the vessels. Most often, the blood vessels of the brain are affected and a stroke develops.

In order to prevent it, drugs that affect blood clotting are prescribed - warfarin, rivaroxaban, dabigatran, apixaban, which reliably (more than 90%) protect against stroke.

While taking these drugs, the patient should monitor for bleeding and monitor the complete blood count and creatinine quarterly. (when taking rivaroxaban, dabigatran and apixaban)., or test the INR (international normalized ratio) at least once a month when taking warfarin. This is necessary in order to correctly calculate the dose of the drug and monitor its safety.

Acetylsalicylic acid (aspirin, cardiomagnyl, thromboass) is not routinely used for the prevention of thromboembolism, since the degree of protection against venous thrombosis when used is only 25%.

prevention of heart failure

Heart failure (HF)

– a complication of many heart diseases, including AF. This condition is caused by the lack of full pumping function of the heart, as a result of which the liquid part of the blood stagnates in the tissues and organs, which is manifested by shortness of breath and edema.

For the prevention and treatment of heart failure, ACE inhibitors (enalapril, lisinopril, perindopril, etc.), veroshpiron (eplerenone), and diuretics (torasemide, furosemide, hypothiazide) are used.

3. Surgical treatment is used if there is no effect from medications and is carried out in specialized cardiac surgery clinics.

Types of surgical treatment of MA:

• implantation of a pacemaker for bradyform MA
• radiofrequency ablation of the pulmonary veins and other arrhythmogenic areas
• with paroxysmal tachyform of atrial fibrillation and flutter

Surgery for arrhythmias in general and AF in particular is the “last cartridge” used when drug therapy is unsuccessful.

After surgical treatment, in order to prevent recurrence of arrhythmia, patients are prescribed planned antiarrhythmic therapy.

Thus, treatment of atrial fibrillation is a way of life that involves the patient “working on himself.” And an arrhythmologist helps him with this.

A patient with MA should avoid colds, lead a healthy lifestyle, get rid of bad habits and avoid factors leading to its development, and strictly follow all the recommendations of his doctor. The doctor will help you choose an individual treatment regimen and recommend what to do if a recurrence of arrhythmia develops, and will also promptly refer you to a cardiac surgeon - arrhythmologist, if indicated.

It is important to understand that the selection of antiarrhythmic therapy takes some time, requires repeated examinations by a doctor and a number of dynamic studies (general clinical tests, study of thyroid hormone levels, cardiac ultrasound and Holter ECG monitoring, electrocardiogram registration) and this should be treated with understanding. In some cases, it is necessary to replace one drug with another.

Living with atrial fibrillation is not an easy process and it is very important that the patient feels supported and helped by the doctor. We are happy to help you with this and are ready to offer follow-up programs for a cardiologist, arrhythmologist and cardiac surgeon in our clinic.

Symptoms of AF

Depending on the form of arrhythmia (constant or paroxysmal) and the patient’s susceptibility, the clinical picture of AF varies from the absence of symptoms to the presence of signs of heart failure. Patients may complain of:

• interruptions in heart function;
• “bubbling” and/or chest pain;
• a sharp increase in heart rate;
• darkening of the eyes;
• general weakness, dizziness (against the background of hypotension);
• lightheadedness or fainting;
• a feeling of lack of air, shortness of breath and a feeling of fear.

Atrial fibrillation and atrial flutter may be accompanied by increased urination caused by increased production of natriuretic peptide. Attacks that last several hours or days and do not go away on their own require medical intervention.

Causes of AF and risk factors

Diseases of various origins

Most often, AF occurs in patients with diseases of the cardiovascular system - arterial hypertension, coronary artery disease, chronic heart failure, heart defects - congenital and acquired, inflammatory processes (pericarditis, myocarditis), heart tumors. Among the acute and chronic diseases not related to heart pathology, but affecting the occurrence of atrial fibrillation, there are dysfunctions of the thyroid gland, diabetes mellitus, chronic obstructive pulmonary disease, sleep apnea syndrome, kidney disease, etc.

Age-related changes

Atrial fibrillation is called “grandfather arrhythmia” because the incidence of this arrhythmia increases sharply with age. Electrical and structural changes in the atria may contribute to the development of this cardiac arrhythmia. However, experts note that atrial fibrillation can occur in young people who do not have heart pathology: up to 45% of cases of paroxysmal and up to 25% of cases of persistent fibrillation.

Other risk factors

Atrial fibrillation can develop due to alcohol consumption, electric shock, and open heart surgery. Paroxysms can be triggered by factors such as physical activity, stress, hot weather, and drinking too much. In rare cases, there is a hereditary predisposition to the occurrence of AF.

Why do you need to control your lifestyle?

Because it affects the size of the left atrium. The more severe the obesity, the larger the size of the left atrium. If a person is overweight, the pressure in the heart increases, the volume of circulating blood increases, and the left atrium stretches. The larger the left atrium is from normal (400 mm), the higher the risk of developing atrial fibrillation.

Situations

With normal left atrium size, the effectiveness of radiofrequency ablation can reach 70%. The larger the size of the left atrium, the lower the effectiveness of RFA.

● If a patient is undergoing radiofrequency ablation, it is important to remember: the more abnormal the atrial function is, the higher the risk of recurrent atrial fibrillation. ● When a person’s heart rhythm is lost, during an ultrasound they pay attention to the size of the left atrium: if it is slightly dilated, it makes sense to try to restore this rhythm using medications or electrical pulse therapy. But if the left atrium is significantly dilated, there is no particular point in restoring the rhythm - sooner or later it will break down again.

What to do?

● Control your weight. ● Avoid alcohol - alcohol increases the risk of bleeding and aggravates the course of the arrhythmia or increases the frequency of breakdowns of this arrhythmia. ● Stop smoking. ● Stop taking dietary supplements - most of them can enhance the effect of anticoagulants. ● Increase physical activity. ● Monitor the condition of the thyroid gland by an endocrinologist.

Diagnostic methods

First you need to determine your individual risk of stroke:

Determination of stroke risk during primary* (if no previous stroke) prevention (J Am Coll Cardiol 2001;38:1266i-1xx).

Obtaining required data

Studying the patient's medical history and complaints. It is necessary to find out the specific symptoms that manifest atrial fibrillation, determine its clinical form, the date of appearance of the first signs, the frequency and duration of paroxysms, determine the predisposing factors and provoking diseases, and the effectiveness of the treatment.

Carrying out ECG, EchoCG. These examinations make it possible to determine the type of heart rhythm disturbances, assess the size of the heart chambers and the condition of the valves, and changes in myocardial contractility.

Blood test. To determine the function of the thyroid gland (T3, T4) and pituitary gland (TSH), to identify a lack of electrolytes (potassium) and signs of acute rheumatism or myocarditis.

Getting More Data

Holter monitoring ECG. 24-hour ECG recording allows you to monitor and evaluate heart rate at different times of the day (including sleep) during the patient’s normal daily routine, and to record attacks of AF.

Record AF paroxysms online. This type of Holter monitoring allows you to record electrocardiogram signals transmitted by telephone directly at the time of an attack.

Bicycle ergometry, treadmill test and other stress tests. These methods are used in cases where adequate control of heart rate is not established (in chronic AF), to provoke arrhythmia caused by exercise, as well as to exclude cardiac ischemia before treatment with class 1C antiarrhythmics.

Transesophageal echocardiography. This test helps identify the presence of a thrombus in the left atrium before cardioversion.

Electrophysiological study. EPI is performed to explain the mechanism of tachycardia, identify and surgically treat predisposing arrhythmia (radiofrequency ablation).

Diagnosis of arrhythmias

Diagnostic techniques: general (history collection, examination) and specific (non-invasive and invasive) techniques. Non-invasive research methods include:

• ECG;
• ergometry (physical stress tests);
• surface ECG mapping;
• echocardiography;
• magnetic resonance imaging.

Invasive diagnostics is an electrophysiological study in which special sensors are inserted into the heart cavity, which record the frequency and regularity of contractions of different parts of the myocardium.

AF treatment strategies

There are two main strategies used to treat patients with atrial fibrillation:

• rhythm control – restoration of sinus rhythm (drug or electrical cardioversion with subsequent prevention of relapse;
• rate control – heart rate control combined with anticoagulant or antiplatelet therapy (if AF persists).

The treatment strategy for a particular patient is chosen depending on many factors, and, first of all, the form of the disease - paroxysmal or persistent atrial fibrillation. So, in the first case, the attack must be stopped (this is especially true for the very first manifestation of AF). With a persistent form of atrial fibrillation, constant medication is prescribed to control heart rate and prevent stroke.

According to the results of recent studies, the use of propafenone provides high efficiency in restoring and maintaining sinus rhythm. Following the VNOK recommendations for the diagnosis and treatment of fibrillation, this drug is classified as the first line of drugs used for persistent AF for pharmacological cardioversion (class I, level of evidence A).

Diagnostics

It is possible to diagnose atrial fibrillation during a physical examination. Pathology is indicated by an orderly pulse, irregular heart sounds, and significant fluctuations in their volume. Having discovered these deviations, the doctor refers the patient for instrumental studies. In the cardiology center of the Federal Scientific and Clinical Center of the Federal Medical and Biological Agency, diagnostics are carried out using:

• taking an ECG during an attack of arrhythmia;
• daily HM-ECG with recorded arrhythmia (ECG using the Holter method);
• data from electrophysiological studies of the heart;
• MRI or MSCT of the heart.

Use of the drug Propanorm for AF

Relief of paroxysms

The strategy, called the “pill in the pocket,” is based on taking a loading dose of Propanorm, which allows you to restore the heart rhythm both in hospital and outpatient treatment. According to many placebo-controlled studies, the effectiveness of a single oral dose of 450-600 mg of propafenone ranges from 56 to 83% (Boriari G, Biffi M, Capucci A, et al., 1997). According to the all-Russian study "PROMETHEUS", which involved 764 patients with recurrent atrial fibrillation, the effectiveness of the loading dose of the drug was 80.2%.

Prevention of paroxysms

The strategy is based on taking the drug daily to prevent paroxysms. The multicenter, open-label, randomized, prospective comparative study "Prostor" provided the following preliminary results.

1. Propanorm® does not lead to a deterioration in hemodynamic parameters in patients with arterial hypertension, coronary heart disease and chronic heart failure with preserved systolic function. The use of the drug for atrial fibrillation for prophylactic purposes helps reduce the number of hospitalizations associated with circulatory decompensation by 72.9%.
2. The antiarrhythmic effectiveness of Propanorm after 12 months from the start of administration is almost equal to the indicators when using Cordarone - 54.2% and 52.9%, respectively.
3. In the absence of post-infarction cardiopathy (ejection fraction less than 40%), Propanorm® can be used as an antiarrhythmic drug, including in combination with beta-blockers, if necessary.
4. Propanorm® has a better safety profile compared to Cordarone.

To maintain sinus rhythm in patients diagnosed with recurrent atrial fibrillation, the recommended daily dose for continuous use of Propanorm is 450 mg (3 times a day) or 600 mg (2 times a day). With frequent occurrence of paroxysms, it is possible to increase the dose to 900 mg (3 times a day).

Treatment of atrial fibrillation and flutter

What are the recommendations for antithrombotic therapy? How to choose a drug for preventive antiarrhythmic therapy?

Atrial fibrillation (AF) is one of the most common tachyarrhythmias in clinical practice, its prevalence in the general population ranges from 0.3 to 0.4% [1]. The detection of AF increases with age. Thus, among people under 60 years of age it is approximately 1% of cases, and in the age group over 80 years of age it is more than 6%. About 50% of patients with atrial fibrillation in the United States are over 70 years of age, and more than 30% of those hospitalized for cardiac arrhythmias are patients with this arrhythmia [2]. Atrial flutter (AFL) is a significantly less common arrhythmia compared to AF. In most countries, AF and AFL are considered different rhythm disorders and are not combined under the common term “atrial fibrillation.” In our opinion, this approach should be considered correct for many reasons.

Prevention of thromboembolic complications and relapses of atrial fibrillation and flutter

Atrial fibrillation and flutter worsen hemodynamics, aggravate the course of the underlying disease and lead to an increase in mortality by 1.5-2 times in patients with organic heart disease. Non-valvular (non-rheumatic) AF increases the risk of ischemic stroke by 2-7 times compared to the control group (patients without AF), and rheumatic mitral disease and chronic AF - by 15-17 times [3]. The incidence of ischemic stroke in non-rheumatic atrial fibrillation averages about 5% of cases per year and increases with age. Cerebral emboli recur in 30-70% of patients. The risk of another stroke is highest during the first year. The risk of stroke is low in patients with idiopathic AF under 60 years of age (1% per year), slightly higher (2% per year) at the age of 60-70 years. In this regard, most patients with frequent and/or prolonged paroxysms of atrial fibrillation, as well as its permanent form, should be prevented from thromboembolic complications. A meta-analysis of all studies on primary and secondary prevention of strokes showed that indirect anticoagulants reduce the risk of developing the latter by 47-79% (on average by 61%), and aspirin by a little more than 20%. It should be noted that when using aspirin, a statistically significant reduction in the incidence of ischemic stroke and other systemic embolisms is possible only with a fairly high dose of the drug (325 mg/day) [4]. At the same time, in the Copenhagen AFASAK Study [5], the number of thromboembolic complications in the groups of patients receiving aspirin 75 mg/day and placebo did not differ significantly.

In this regard, patients with AF who are at high risk for thromboembolic complications: heart failure, EF 35% or less, arterial hypertension, ischemic stroke or transient ischemic attack in history, etc., should be prescribed indirect anticoagulants (maintaining the International Normalized ratio - INR - on average at the level of 2.0-3.0). For patients with non-valvular (non-rheumatic) atrial fibrillation who are not at high risk, continuous use of aspirin (325 mg/day) is advisable. There is an opinion that in patients under 60 years of age with idiopathic AF, in whom the risk of thromboembolic complications is very low (almost the same as in people without rhythm disturbances), preventive therapy may not be required. Antithrombotic therapy in patients with AFL should obviously be based on taking into account the same risk factors as in AF, since there is evidence that the risk of thromboembolic complications in AFL is higher than in sinus rhythm, but somewhat lower than in AF [ 6].

International experts offer the following specific recommendations for antithrombotic therapy for various groups of patients with atrial fibrillation, depending on the level of risk of thromboembolic complications [7]:

• age less than 60 years (no heart disease - lone AF) - aspirin 325 mg/day or no treatment;
• age less than 60 years (heart disease, but no risk factors such as congestive heart failure, EF 35% or less, arterial hypertension) - aspirin 325 mg/day;
• age 60 years or more (diabetes mellitus or coronary artery disease) - oral anticoagulants (INR 2.0-3.0);
• age 75 years or more (especially women) - oral anticoagulants (INR up to 2.0);
• heart failure - oral anticoagulants (INR 2.0-3.0);
• LVEF 35% or less - oral anticoagulants (INR 2.0-3.0);
• thyrotoxicosis - oral anticoagulants (INR 2.0-3.0);
• arterial hypertension - oral anticoagulants (INR 2.0-3.0);
• rheumatic heart defects (mitral stenosis) - oral anticoagulants (INR 2.5-3.5 or more);
• artificial heart valves - oral anticoagulants (INR 2.5-3.5 or more);
• history of thromboembolism - oral anticoagulants (INR 2.5-3.5 or more);
• the presence of a thrombus in the atrium, according to TPEchoCG, - oral anticoagulants (INR 2.5-3.5 or more).

The international normalized ratio should be monitored with indirect anticoagulants at the beginning of therapy at least once a week, and subsequently monthly.

In most cases, patients with recurrent paroxysmal and persistent atrial fibrillation in the absence of clinical symptoms of arrhythmia or their insignificant severity do not need to be prescribed antiarrhythmic drugs. In such patients, prophylaxis of thromboembolic complications (aspirin or indirect anticoagulants) and heart rate control are carried out. If clinical symptoms are pronounced, anti-relapse and relief therapy is required, combined with heart rate control and antithrombotic treatment.

In case of frequent attacks of atrial fibrillation and flutter, the effectiveness of antiarrhythmics or their combinations is assessed clinically; in case of rare attacks, TES or VEM is performed for this purpose after 3-5 days of taking the drug, and when using amiodarone - after saturation with it. To prevent relapses of AF/AFL in patients without organic heart disease, antiarrhythmic drugs of classes 1A, 1C and 3 are used. In patients with asymptomatic LV dysfunction or symptomatic heart failure, and possibly with significant myocardial hypertrophy, therapy with class 1 antiarrhythmics is contraindicated due to the risk of worsening life prognosis.

To prevent paroxysms of atrial fibrillation and atrial flutter, the following antiarrhythmics are used: quinidine (kinylentine, quinidine durules, etc.) - 750-1500 mg/day; disopyramide - 400-800 mg/day; propafenone - 450-900 mg/day; allapinin - 75-150 mg/day; etacizin - 150-200 mg/day; flecainide - 200-300 mg/day; amiodarone (maintenance dose) - 100-400 mg/day; sotalol - 160-320 mg/day; dofetilide - 500-1000 mcg/day. Verapamil, diltiazem and cardiac glycosides should not be used for anti-relapse therapy of AF and AFL in patients with Wolff-Parkinson-White syndrome (WPU), since these drugs reduce the refractoriness of the accessory atrioventricular conduction pathway and can cause aggravation of the arrhythmia.

In patients with sick sinus syndrome and paroxysms of atrial fibrillation and flutter (bradycardia-tachycardia syndrome), there are expanded indications for implantation of an electrical pacemaker (pacemaker). Permanent pacing is indicated in such patients both for the treatment of symptomatic bradyarrhythmia and for the safe administration of preventive and/or curative antiarrhythmic therapy. To prevent and relieve attacks of AF and AFL in patients without pacemakers, class 1A antiarrhythmics with anticholinergic effects (disopyramide, procainamide, quinidine) can be used. In hypertrophic cardiomyopathy, amiodarone is prescribed to prevent tachyarrhythmia paroxysms, and beta-blockers or calcium antagonists (verapamil, diltiazem) are prescribed to reduce the frequency of ventricular contractions.

As a rule, treatment with antiarrhythmics requires monitoring the width of the QRS complex (especially when class 1C antiarrhythmics are used) and the duration of the QT interval (when treated with class 1A and 3 antiarrhythmics). The width of the QRS complex should not increase by more than 150% of the initial level, and the corrected QT interval should not exceed 500 ms. Amiodarone has the greatest effect in preventing arrhythmia [14, 15, 16, 17]. A meta-analysis of published results from placebo-controlled studies involving 1465 patients showed that the use of low maintenance doses of amiodarone (less than 400 mg/day) did not cause an increase in lung and liver damage compared with the placebo group [8]. Some clinical studies have demonstrated a higher preventive effectiveness of class 1C drugs (propafenone, flecainide) compared to class 1A antiarrhythmics (quinidine, disopyramide). According to our data, the effectiveness of propafenone is 65%, ethacyzine - 61% [9, 10].

Choice of drug for prophylactic antiarrhythmic therapy of paroxysmal and persistent atrial fibrillation and flutter

We can agree with the opinion expressed in international recommendations for the management of patients with atrial fibrillation [7], according to which anti-relapse therapy in patients without heart pathology or with minimal structural changes should begin with class 1C antiarrhythmics (propafenone, flecainide). Let's add to them domestic drugs of the same class (allapinin and etacizin), as well as sotalol; they are quite effective and devoid of pronounced extracardiac side effects. If the listed antiarrhythmics do not prevent relapses of AF/AFL or their use is accompanied by side effects, you should proceed to prescribing amiodarone and dofetilide. Then, if necessary, class 1A drugs (disopyramide, quinidine) or non-pharmacological treatments are used. Probably, in patients with so-called “adrenergic” AF, one can expect a greater effect from therapy with amiodarone or sotalol, and in “vagal” AF it is advisable to start treatment with disopyramide.

Coronary heart disease, especially in the presence of post-infarction cardiosclerosis, and heart failure increase the risk of manifestation of the arrhythmogenic properties of antiarrhythmic drugs. Therefore, treatment of atrial fibrillation and flutter in patients with congestive heart failure is usually limited to the use of amiodarone and dofetilide. While the high efficacy and safety of amiodarone in heart failure and coronary artery disease (including myocardial infarction) has been proven for a long time, similar results for dofetilide were obtained in the recent placebo-controlled studies DIAMOND CHF and DIAMOND MI [11].

For patients with coronary heart disease, the recommended sequence of prescribing antiarrhythmics is as follows: sotalol; amiodarone, dofetilide; disopyramide, procainamide, quinidine.

Arterial hypertension, leading to hypertrophy of the left ventricular myocardium, increases the risk of developing polymorphic ventricular tachycardia “torsades de pointes”. In this regard, to prevent relapses of AF/AFL in patients with high blood pressure, preference is given to antiarrhythmic drugs that do not significantly affect the duration of repolarization and the QT interval (class 1C), as well as amiodarone, although it prolongs it, but extremely rarely causes ventricular tachycardia . Thus, the algorithm for pharmacotherapy of this rhythm disorder in arterial hypertension appears to be as follows: LV myocardial hypertrophy of 1.4 cm or more - use only amiodarone; There is no left ventricular myocardial hypertrophy or it is less than 1.4 cm - start treatment with propafenone, flecainide (bear in mind the possibility of using domestic class 1C antiarrhythmics allapinin and etacizin), and if they are ineffective, use amiodarone, dofetilide, sotalol. At the next stage of treatment (ineffectiveness or occurrence of side effects of the above drugs), disopyramide, procainamide, and quinidine are prescribed [7].

It is quite possible that with the emergence of new results from controlled studies on the effectiveness and safety of antiarrhythmic drugs in patients with various diseases of the cardiovascular system, changes will be made to the above recommendations for the prevention of relapses of paroxysmal and persistent AF, since at present the relevant information is clearly insufficient.

If there is no effect from monotherapy, combinations of antiarrhythmic drugs are used, starting with half doses. An addition, and in some cases an alternative to preventive therapy, as mentioned above, may be the prescription of drugs that worsen AV conduction and reduce the frequency of ventricular contractions during paroxysms of AF/AFL. The use of drugs that impair conduction in the AV junction is justified even in the absence of effect from preventive antiarrhythmic therapy. When using them, it is necessary to ensure that the heart rate at rest is from 60 to 80 per minute, and with moderate physical activity - no more than 100-110 per minute. Cardiac glycosides are ineffective for controlling heart rate in patients leading an active lifestyle, since in such cases the primary mechanism for reducing the frequency of ventricular contractions is an increase in parasympathetic tone. Therefore, it is obvious that cardiac glycosides can be chosen only in two clinical situations: if the patient suffers from heart failure or has low physical activity. In all other cases, preference should be given to calcium antagonists (verapamil, diltiazem) or beta-blockers. In case of prolonged attacks of atrial fibrillation or flutter, as well as in their permanent form, combinations of the above drugs can be used to reduce heart rate.

Relief of paroxysms of fibrillation and atrial flutter

The primary task during an attack of the tachysystolic form of AF/AFL is to reduce the heart rate, and then, if the paroxysm does not stop on its own, stop it. Control of the ventricular contraction rate (decrease to 70-90 per minute) is carried out by intravenous administration or oral administration of verapamil, diltiazem, beta-blockers, intravenous administration of cardiac glycosides (preference is given to digoxin), amiodarone. In patients with reduced LV contractile function (congestive heart failure or EF less than 40%), heart rate is reduced only with cardiac glycosides or amiodarone. Before stopping tachysystolic forms of atrial fibrillation and atrial flutter (especially atrial flutter) with class 1A antiarrhythmics (disopyramide, procainamide, quinidine), conduction blockade in the AV node is required, since the above-mentioned antiarrhythmic drugs have an anticholinergic effect (most pronounced with disopyramide) and can significantly increase the frequency contractions of the ventricles.

Considering the risk of thromboembolism during prolonged paroxysm of AF, the issue of stopping it must be resolved within 48 hours, since if the duration of an attack of AF exceeds two days, it is necessary to prescribe indirect anticoagulants (maintaining the INR at the level of 2.0-3.0) for 3-4 weeks before and after electrical or drug cardioversion. Currently, the most widely used indirect anticoagulants are coumarin derivatives: warfarin and syncumar. If the duration of AF is unknown, the use of indirect anticoagulants before and after cardioversion is also necessary. Similar prevention of thromboembolic complications should be carried out in case of atrial flutter.

For pharmacological cardioversion, the following antiarrhythmics are used:

• amiodarone 5-7 mg/kg - intravenous infusion over 30-60 minutes (15 mg/min);
• ibutilide 1 mg - intravenous administration over 10 minutes (if necessary, repeated administration of 1 mg);
• novocainamide 1-1.5 g (up to 15-17 mg/kg) - intravenous infusion at a rate of 30-50 mg/min;
• propafenone 1.5-2 mg/kg - intravenous administration over 10-20 minutes;
• flecainide 1.5-3 mg/kg - intravenous administration over 10-20 minutes.

The international recommendations for cardiopulmonary resuscitation and emergency cardiac care [12] and the ACC/AHA/ECC recommendations for the treatment of patients with atrial fibrillation [7] note that it is advisable to relieve paroxysm in patients with heart failure or EF less than 40% mainly with amiodarone. The use of other antiarrhythmics should be limited due to the rather high risk of developing arrhythmogenic effects and the negative impact of these drugs on hemodynamics.

The use of verapamil and cardiac glycosides is contraindicated in patients with AF/AFL and Wolff-Parkinson-White syndrome. In the presence of the latter, AF/AFL is treated with drugs that impair conduction along the Kent bundle: amiodarone, procainamide, propafenone, flecainide, etc.

Oral relief of atrial fibrillation and flutter with quinidine, procainamide, propafenone, flecainide, dofetilide, etc. is possible.

Atrial flutter (type 1) can be relieved or converted to AF by frequent transesophageal or endocardial atrial pacemaker. Stimulation is prescribed for a duration of 10-30 seconds with a pulse frequency that is 15-20% higher than the frequency of atrial contractions, i.e. 300-350 (400) pulses per minute.

When AF/AFL is accompanied by severe heart failure (cardiac asthma, pulmonary edema), hypotension (systolic pressure less than 90 mm Hg), increased pain and/or worsening myocardial ischemia, immediate electrical pulse therapy (EPT) is indicated.

In case of atrial fibrillation, EIT begins with a discharge with a power of 200 J; for biphasic current, the energy of the first discharge is less. If it turns out to be ineffective, discharges of higher power (300-360 J) are successively applied. Atrial flutter is often relieved by a low-energy shock (50-100 J).

Electropulse therapy can also be chosen for the planned restoration of sinus rhythm in patients with prolonged paroxysms of AF/AFL. Medical cardioversion is recommended if EIT is not possible, undesirable, or fails to restore sinus rhythm. In case of an attack of AF/AFL lasting more than 48 hours, indirect anticoagulants before cardioversion can not be used for a long time if transesophageal echocardiography (TPEchocardiography) excludes the presence of thrombi in the atria (in 95% of cases they are localized in the left atrial appendage). This is the so-called early cardioversion: intravenous administration of heparin (increase in aPTT by 1.5-2 times compared to the control value) or short-term administration of an indirect anticoagulant (bringing the INR to 2.0-3.0) before cardioversion and four weeks of indirect administration anticoagulants after restoration of sinus rhythm. According to preliminary data from the ACUTE multicentre study [13], the incidence of thromboembolic complications is significantly lower when using TPEchoCG and short courses of preventive therapy with heparin or warfarin (in the absence of a thrombus) or longer-term administration of an indirect anticoagulant (if a thrombus is re-detected after three weeks of warfarin treatment) before EIT, than with traditional therapy carried out “blindly” with indirect anticoagulants for 3-4 weeks before and after electrical cardioversion, and is 1.2% and 2.9%, respectively. In patients who do not receive anticoagulants before cardioversion, thromboembolic complications develop in 1-6% of cases.

For severe paroxysms of AF and AFL, refractory to drug treatment, non-pharmacological treatment methods are used: destruction of the AV connection with implantation of an electrical pacemaker, “modification” of the AV connection, implantation of an atrial defibrillator or special pacemakers, radiofrequency catheter destruction of the impulse circulation path in the right atrium during AFL and sources ectopic impulses in patients with focal atrial fibrillation, “corridor” and “labyrinth” operations.

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