Atrial fibrillation (atrial fibrillation): causes, symptoms, diagnosis, treatment

Atrial fibrillation (AF) is a rapid, irregular atrial rhythm. Symptoms include palpitations, sometimes weakness, shortness of breath, and near-syncope. Blood clots often form in the atria, creating a high risk of ischemic stroke. Diagnosis is made using ECG data. Treatment includes pharmacological control of heart rate, prevention of thromboembolic complications with anticoagulants, and sometimes restoration of sinus rhythm with drugs or cardioversion.

Atrial fibrillation (atrial fibrillation) occurs due to a large number of small impulses with chaotic re-entry in the atria. At the same time, in many cases, the occurrence of ectopic foci at the sites of the venous trunks entering the atria (usually in the area of the pulmonary veins) can provoke the development and, probably, maintain atrial fibrillation (atrial fibrillation). In atrial fibrillation, the atria do not contract, and the atrioventricular (AV) conduction system is stimulated by a large number of electrical impulses, which leads to incorrect, disordered conduction of impulses and an irregular ventricular rhythm, often with a high frequency (tachycardic type).

Atrial fibrillation (AF) is one of the most common arrhythmias, affecting 2.3 million adults in the United States. Atrial fibrillation is more common in Caucasian men than in women and blacks. The incidence increases with age. Almost 10% of people over 80 years of age have AF. Atrial fibrillation is more common in people with heart disease, sometimes leading to heart failure because the absence of atrial contraction impairs cardiac output. The absence of atrial contractions also suggests the formation of blood clots, with an annual risk of cerebrovascular embolic events of about 7%. The risk of stroke is higher in patients with rheumatic valve disease, hyperthyroidism, hypertension, diabetes, left ventricular systolic dysfunction, or a history of embolic events. Systemic embolism can also lead to necrosis of other organs (eg, heart, kidneys, gastrointestinal tract, eyes) or extremities.

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

Causes of atrial fibrillation (atrial fibrillation)

The most common causes of atrial fibrillation are hypertension, cardiomyopathy, mitral or tricuspid valve defects, hyperthyroidism, and alcohol abuse (Sunday heart). Less common causes include pulmonary embolism, septal defects, and other congenital heart defects, COPD, myocarditis, and pericarditis. Atrial fibrillation without an identified cause in people under 60 is called isolated atrial fibrillation.

• Acute atrial fibrillation is a paroxysm of atrial fibrillation that occurs and lasts less than 48 hours.
• Paroxysmal atrial fibrillation is a recurring atrial fibrillation that usually lasts less than 48 hours and spontaneously converts to sinus rhythm.
• Persistent atrial fibrillation lasts more than 1 week and requires treatment to restore sinus rhythm.
• Permanent atrial fibrillation cannot be restored to sinus rhythm. The longer atrial fibrillation exists, the less likely it is to be restored spontaneously and the more difficult cardioversion becomes due to atrial remodeling.

Symptoms of atrial fibrillation

Atrial fibrillation is often asymptomatic, but many patients experience palpitations, chest discomfort, or signs of heart failure (eg, weakness, dizziness, shortness of breath), especially if the ventricular rate is very high (often 140-160 beats per minute). Patients may also have symptoms of acute stroke or damage to other organs due to systemic embolism.

The pulse is irregular, with a lost a-wave (when examining the pulse on the jugular veins). Pulse deficit (HR at the apex of the heart is greater than at the wrist) may be present because the stroke volume of the left ventricle is not always sufficient to create a peripheral venous wave with a rapid ventricular rhythm.

Diagnosis of atrial fibrillation

The diagnosis is made on the ECG. Changes include absent R waves, waves (fibrillations) between QRS complexes (irregular in timing, variable in shape; baseline oscillations greater than 300 per minute are not always visible in all leads), and irregular intervals. Other irregular rhythms may mimic atrial fibrillation on the ECG, but they can be distinguished by the presence of a distinct wave or flutter waves, which can sometimes be better seen with vagal maneuvers. Muscle tremors or external electrical stimuli may resemble R waves, but the rhythm is regular. A phenomenon mimicking ventricular extrasystole and ventricular tachycardia (Ashman phenomenon) is also possible with AF. This phenomenon usually occurs when a short interval follows a long RR interval. A longer interval increases the refractory period of the conduction system below the bundle of His, and the resulting QRS complex is conducted aberrantly, usually changing to a right bundle branch conduction pattern.

An echocardiogram and thyroid function tests are important in the initial examination. Echocardiography is performed to detect structural heart disease (e.g., left atrial enlargement, left ventricular wall motion abnormalities suggesting past or present ischemia, valvular defects, cardiomyopathy) and additional stroke risk factors (e.g., atrial stasis or thrombi, atherosclerotic aortic disease). Atrial thrombi are more common in the atrial appendages, where they are more easily detected using transesophageal echocardiography rather than transthoracic echocardiography.

[ 6 ], [ 7 ], [ 8 ], [ 9 ]

Treatment of atrial fibrillation

If a significant etiologic cause is suspected, a patient with newly developed atrial fibrillation should be hospitalized, but patients with recurrent episodes do not require mandatory hospitalization (in the absence of severe symptoms). Treatment tactics consist of monitoring the ventricular rate, monitoring the heart rhythm, and preventing thromboembolic complications.

Ventricular rate control

Patients with atrial fibrillation of any duration require ventricular rate control (usually less than 80 beats per minute at rest) to prevent the development of symptoms and tachycardia-induced cardiomyopathy.

In acute paroxysms with a high frequency (for example, 140-160 per minute), intravenous blockers of conduction through the AV node are used.

CAUTION! AV node conduction blockers should not be used in Wolff-Parkinson-White syndrome, when an accessory bundle is involved in conduction (manifested by prolongation of the QRS complex); these drugs increase the rate of conduction via the bypass tract, which can lead to ventricular fibrillation.

Beta-blockers (such as metoprolol, esmolol) are considered preferable if high levels of catecholamines in the blood are expected (e.g. in thyroid pathology, in cases provoked by excessive physical exertion), non-hydropyridine calcium channel blockers (verapamil, diltiazem) are also effective. Digoxin is the least effective, but may be preferable in heart failure. These drugs can be taken orally for a long time to control heart rate. If beta-blockers, non-hydropyridine calcium channel blockers and digoxin (as monotherapy and in combination) are ineffective, amiodarone may be prescribed.

Patients who do not respond to these treatments or who cannot take rate-controlling medications may undergo radiofrequency ablation of the AV node to induce complete AV block, which requires implantation of a permanent pacemaker. Ablation of only one conduction pathway, the AV junction (AV modification), can reduce the number of atrial impulses reaching the ventricles and avoid the need for pacemaker implantation, but is considered less effective than complete ablation.

Rhythm control

In patients with heart failure or other hemodynamic disorders directly related to atrial fibrillation, restoration of normal sinus rhythm is necessary to increase cardiac output. In some cases, conversion to normal sinus rhythm is optimal, but antiarrhythmic drugs capable of providing such conversion (la, lc, III classes) have a risk of side effects and may increase mortality. Restoration of sinus rhythm does not eliminate the need for permanent anticoagulant therapy.

Synchronized cardioversion or drugs can be used for emergency rhythm restoration. Before rhythm restoration, the heart rate should be < 120 beats per minute, and if atrial fibrillation has been present for more than 48 hours, the patient should be given anticoagulants (irrespective of the method of conversion, it increases the risk of thromboembolism). Anticoagulant therapy with warfarin is carried out for at least 3 weeks (until the rhythm is restored), and if possible, it is continued long-term, since atrial fibrillation can recur. Alternatively, treatment with sodium heparin can be possible. Transesophageal echocardiography is also indicated; if an intra-atrial thrombus is not detected, cardioversion can be performed immediately.

Synchronized cardioversion (100 J, then 200 J and 360 J if needed) converts atrial fibrillation to normal sinus rhythm in 75% to 90% of patients, although the risk of recurrent attacks is high. The effectiveness of maintaining sinus rhythm after the procedure is increased by administering Ia, Ic, or class III drugs 24 to 48 hours before cardioversion. This procedure is more effective in patients with short-term atrial fibrillation, isolated atrial fibrillation, or atrial fibrillation due to reversible causes. Cardioversion is less effective in patients with left atrial enlargement (>5 cm), decreased flow in the atrial appendages, or significant structural changes in the heart.

Drugs used to restore sinus rhythm include Ia (procainamide, quinidine, disopyramide), Ic (flecainide, propafenone), and class III (amiodarone, dofetilide, ibutilide, sotalol) antiarrhythmic drugs. All are effective in approximately 50% to 60% of patients but have varying side effects. These drugs should not be used until heart rate can be controlled with beta-blockers and nonhydropyridine calcium channel blockers. These rhythm-restoring drugs are also used for long-term maintenance of sinus rhythm (with or without prior cardioversion). The choice depends on the patient's tolerance. At the same time, in paroxysmal atrial fibrillation, which occurs only or predominantly during rest or sleep, when there is high vagal tone, drugs with a vagolytic effect (for example, disopyramide) may be especially effective, and exercise-induced atrial fibrillation may be more sensitive to beta-blockers.

ACE inhibitors and angiotensin II receptor blockers may reduce myocardial fibrosis, which creates a substrate for atrial fibrillation in patients with heart failure, but the role of these drugs in the routine treatment of atrial fibrillation has not yet been established.

Prevention of thromboembolism

Thromboembolism prophylaxis is necessary during cardioversion and during long-term treatment in most patients.

The dose of warfarin is gradually increased until an INR of 2 to 3 is achieved. It should be taken for at least 3 weeks before electrical cardioversion in case of isolated atrial fibrillation lasting more than 48 hours, and for 4 weeks after effective cardioversion. Anticoagulant treatment should be continued in patients with recurrent paroxysmal, persistent, or permanent atrial fibrillation in the presence of risk factors for thromboembolism. Healthy patients with a single episode of atrial fibrillation receive anticoagulants for 4 weeks.

Aspirin is less effective than warfarin but is used in patients with risk factors for thromboembolism who are contraindicated for warfarin. Ximelagatran (36 mg twice daily), a direct thrombin inhibitor that does not require INR monitoring, has an equivalent effect to warfarin in preventing stroke in high-risk patients, but further studies are needed before it can be recommended instead of warfarin. In the presence of absolute contraindications to warfarin or antiplatelet drugs, surgical ligation of the atrial appendages or catheter closure may be an option.