Atrial fibrillation (AF) is one of the most common arrhythmias. It is characterized by the loss of regular, orderly atrial electrical activity, replaced by rapid, disordered fibrillatory waves, representing the most severe atrial electrical disturbance. The disorganized atrial activity leads to ineffective atrial contraction and relaxation, resulting in impaired or lost atrial pumping function. The AV node's decremental conduction of rapid atrial impulses causes a highly irregular ventricular response. Thus, irregular ventricular rhythm, impaired cardiac function, and atrial thrombus formation are the main pathophysiological features in AF patients.
Etiology
AF often occurs in patients with structural heart disease, commonly seen in coronary artery disease, hypertensive heart disease, valvular disease, cardiomyopathy, and hyperthyroidism. It can also occur in constrictive pericarditis, chronic cor pulmonale, Wolff-Parkinson-White syndrome, and older patients. AF may be idiopathic and can occur in healthy individuals during emotional stress, surgery, exercise, or heavy alcohol consumption.
Classification
AF is generally classified into paroxysmal AF, persistent AF, long-standing persistent AF, and permanent AF.
Table 1 Clinical classification of atrial fibrillation
Clinical manifestations
The severity of AF symptoms depends on the ventricular rate. When the ventricular rate exceeds 150 bpm, patients may experience angina and heart failure; when the ventricular rate is not fast, symptoms are mild or absent. During AF, effective atrial contraction is lost, reducing cardiac output by 25% or more compared to sinus rhythm.
The risk of thromboembolism is significant, particularly cerebral embolism, which can be life-threatening and severely affect quality of life. Emboli often originate from the left atrium, particularly the left atrial appendage, due to loss of atrial contraction and blood stasis. Patients with non-valvular AF have a 5 - 7 times higher risk of cerebral embolism than those without AF; this risk is even higher with mitral stenosis or mitral valve prolapse.
Cardiac auscultation reveals variable intensity of the first heart sound and an extremely irregular rhythm. A rapid ventricular rate may cause pulse deficit due to weak ventricular contractions that fail to open the aortic valve or insufficient arterial pressure waves that do not reach peripheral arteries.
If the ventricular rhythm becomes regular, the following possibilities can be considered:
- Reversion to sinus rhythm
- Transition to atrial tachycardia
- Transition to atrial flutter (with a fixed AV conduction ratio)
- Development of junctional tachycardia or ventricular tachycardia
A slow, regular ventricular rhythm (30 - 60 bpm) suggests complete AV block. ECG is essential for diagnosis. AF patients with junctional or ventricular tachycardia or complete AV block often have digitalis toxicity.
Electrocardiogram features
ECG features include:
- Absence of P waves, replaced by small, irregular baseline fluctuations with varying shapes and amplitudes, known as f waves, with a frequency of 350 - 600 bpm
- Extremely irregular ventricular rate
- Normal QRS morphology, which may widen and deform with rapid ventricular rates due to intraventricular aberrant conduction
Figure 1 Atrial fibrillation
Atrial fibrillation waves (f waves) with a frequency of approximately 375 beats per minute, an average ventricular rate of about 102 beats per minute, and extremely irregular RR intervals.
Treatment
The treatment of atrial fibrillation emphasizes long-term comprehensive management. The basic principles include treating the underlying disease and triggering factors, preventing thromboembolism, restoring and maintaining sinus rhythm, and controlling the ventricular rate.
Anticoagulation therapy
Patients with AF have a higher risk of embolism, making anticoagulation therapy a crucial aspect of treatment. For non-valvular AF, the CHA2DS2-VASc score is used to assess the risk of thromboembolism. Anticoagulation is recommended for males with a score of 2 or more and females with a score of 3 or more. For males with a score of 1 or females with a score of 2, anticoagulation can be considered based on a benefit-risk assessment. Those with a score of 0 for males or 1 for females typically do not require anticoagulation. Patients with valvular AF, such as those with moderate to severe mitral stenosis or mechanical valve replacement, should directly receive warfarin without CHA2DS2-VASc scoring.
Table 2 CHA2DS2-VASc score for the risk of stroke in non-valvular atrial fibrillation
Note: TIA, transient ischemic attack. Vascular diseases include previous myocardial infarction, peripheral artery disease, and aortic plaque.
Table 3 HAS-BLED score
Note: Uncontrolled hypertension is defined as systolic blood pressure >160 mmHg; liver dysfunction is defined as chronic liver disease (liver fibrosis) or bilirubin > 2 times the upper limit of normal, alanine aminotransferase > 3 times the upper limit of normal; renal dysfunction is defined as chronic dialysis or renal transplant or serum creatinine ≥200 μmol/L; hemorrhage refers to a history of hemorrhage and/or hemorrhage tendency; INR instability refers to INR instability with time within the therapeutic window < 60%; medications refer to concomitant use of antiplatelet agents or nonsteroidal anti-inflammatory drugs.
Before starting anticoagulation, hemorrhage risk assessment is recommended using the HAS-BLED score. A score of 3 or more indicates high hemorrhage risk. However, reversible hemorrhage risk factors should be corrected, and a high HAS-BLED score should not be considered a contraindication for anticoagulation.
Warfarin
Warfarin is effective for anticoagulation in AF. It requires maintaining an INR between 2.0 and 3.0 to safely and effectively prevent stroke. It is the first choice for patients with moderate to severe mitral stenosis or mechanical heart valves. Due to its narrow therapeutic window and interactions with drugs and foods, regular INR monitoring is essential. Vitamin K1 can be used to treat severe hemorrhage caused by warfarin.
Novel oral anticoagulants (NOACs)
NOACs, such as dabigatran (a direct thrombin inhibitor) and factor Xa inhibitors such as rivaroxaban and apixaban, offer good efficacy and safety. Compared to warfarin, NOACs do not require routine coagulation monitoring, and have no food interactions, fewer drug interactions, and better compliance. Therefore, NOACs are preferred for non-valvular AF patients. Serious or life-threatening hemorrhage from NOACs can be reversed with idarucizumab for dabigatran and andexanet α for factor Xa inhibitors.
Cardioversion
In patients with AF lasting more than 48 hours, anticoagulation for 3 weeks is recommended or transesophageal echocardiography can be used to rule out atrial thrombus before cardioversion. Anticoagulation should continue for 4 weeks after cardioversion. For emergency cardioversion, intravenous heparin or subcutaneous low molecular weight heparin can be used.
Left atrial appendage closure
Percutaneous left atrial appendage closure is a strategy to prevent stroke or systemic embolism. It is considered for patients unsuitable for long-term anticoagulation or those who experience stroke or embolism despite adequate anticoagulation, especially with a HAS-BLED score of 3 or more.
Restoration and maintenance of sinus rhythm
Atrial fibrillation carries a risk of thromboembolism during cardioversion, so a thorough assessment of this risk is essential before proceeding. For patients with AF lasting more than 48 hours, thromboembolism risk should be evaluated, and appropriate anticoagulation therapy should be administered before cardioversion. Methods for converting AF to sinus rhythm include pharmacological cardioversion, electrical cardioversion, and catheter ablation.
The primary medications for cardioversion and maintaining sinus rhythm are Class Ic (propafenone) and Class III (amiodarone, ibutilide, dronedarone, sotalol) antiarrhythmic drugs. Patients without structural heart disease may use propafenone or ibutilide for cardioversion, and propafenone, dronedarone, or sotalol for maintaining sinus rhythm. Those with significant structural heart disease should use amiodarone for both conversion and maintenance, while considering its side effects. If pharmacological cardioversion is ineffective, electrical cardioversion can be used. Emergency electrical cardioversion is recommended for patients with AF accompanied by severe hemodynamic instability or acute heart failure. The success of cardioversion is influenced by the duration of AF, the size of the left atrium, and the age of patients.
Catheter ablation has been proven effective and safe in numerous clinical studies. It is superior to antiarrhythmic drugs in maintaining sinus rhythm, significantly reducing the risk of AF recurrence, and improving symptoms and quality of life. Catheter ablation is the first choice for symptomatic paroxysmal AF. Patients with symptomatic AF who do not respond to or cannot tolerate medication, as well as those with reduced left ventricular ejection fraction, should consider catheter ablation. Additionally, maze procedures and hybrid ablation procedures can be used to maintain sinus rhythm.
Ventricular rate control
AF with a rapid ventricular rate is a major cause of symptoms, and prolonged rapid rates can lead to hemodynamic instability or tachycardia-induced cardiomyopathy. Therefore, effective ventricular rate control is crucial in AF management. For asymptomatic AF with normal left ventricular systolic function, the resting ventricular rate should be controlled to less than 110 beats per minute. For those with significant symptoms or tachycardia-induced cardiomyopathy, the resting ventricular rate should be less than 80 beats per minute, and the ventricular rate should be less than 110 beats per minute during moderate exercise.
Medications for rate control include β-blockers, non-dihydropyridine calcium channel blockers, digitalis glycosides, and certain antiarrhythmic drugs (amiodarone), which can be used alone or in combination, but contraindications must be considered. Patients with heart failure with preserved ejection fraction may use β-blockers and/or non-dihydropyridine calcium channel blockers. For heart failure with reduced ejection fraction, β-blockers are preferred, and if ventricular rate control is inadequate or contraindicated, digitalis glycosides or amiodarone should be considered. After achieving strict rate control, a 24-hour Holter monitor should be used to assess for bradycardia and cardiac pauses.
For patients with AF and rapid ventricular rates unresponsive to medication, atrioventricular node ablation in combination with permanent pacemaker implantation may be used to control the ventricular rate.