Atrial fibrillation (atrial fibrillation) is a rapid arrhythmia characterized by the deterioration of atrial mechanical function due to the uncoordinated activity of the atria. Atrial fibrillation often occurs in patients with organic heart disease, but is also seen in normal individuals with other diseases and in those with no detectable cardiac lesions. Atrial fibrillation can occur in isolation or in combination with other arrhythmias, the most common combined arrhythmia being atrial flutter or atrial tachycardia. Fang Pihua, Department of Cardiovascular Medicine, Fu Wai Hospital, Beijing, China Atrial fibrillation can cause the following hazards to patients: (1) whether it is persistent or paroxysmal atrial fibrillation, due to the extremely uneven beat of the ventricles, it brings great discomfort to patients, manifesting as panic and weakness, which affects patients’ quality of life to varying degrees; (2) atrial fibrillation loses its pumping effect and reduces cardiac output, which can worsen cardiac function and cause heart failure in patients with organic heart disease; (3) atrial fibrillation can cause heart failure. (3) potential thromboembolism, the complications caused by thrombus dislodgement are 5-15 times higher than those without atrial fibrillation, and can cause embolism in various organs of the body, while embolism in the body circulation is mainly cerebral embolism, resulting in a high disability rate. In cases of ischemic stroke, atrial fibrillation is one of the most common causes; (4) atrial fibrillation with rapid ventricular response can lead to tachycardia cardiomyopathy for a long time, occasionally metamorphosing into ventricular fibrillation. (i) Epidemiology and etiology According to the information in the Guidelines for the Treatment of Atrial Fibrillation published by the American College of Cardiology (ACC) and the American Heart Association (AHA) in 2006, the incidence of atrial fibrillation accounts for 0.4%-1% of the overall population and increases with age. The average age of patients with atrial fibrillation is approximately 75 years, with approximately 70% of patients between the ages of 65-85 years. The number of male and female AF patients was about equal, but 60% of patients >76 years of age were female. Population studies have shown that the incidence of AF without a history of cardiopulmonary disease (isolated AF) accounts for less than 12% of all AF. A large domestic epidemiological study conducted in 13 provinces, 14 natural populations, and 29,079 individuals showed that the prevalence of AF in China was 0.77%, with a higher prevalence in men (0.9%) than in women (0.7%). The prevalence tends to increase significantly with age, reaching 7.5% in people over 80 years of age 1. Acute causes Atrial fibrillation may be associated with acute, transient causes. These include alcohol consumption (holiday heart syndrome), surgery, electric shock, myocardial infarction, pericarditis, myocarditis, pulmonary embolism or other pulmonary disease, and hyperthyroidism or other metabolic disorders. Atrial fibrillation can also be associated with atrial flutter, WPW syndrome, and atrioventricular or AV nodal regressive tachycardia 2. Cardiovascular disease Specific cardiovascular diseases associated with the development of atrial fibrillation include heart valve disease (primarily mitral valve disease), heart failure (congestive), coronary artery disease, and hypertension, especially in the presence of left ventricular hypertrophy. In addition, atrial fibrillation can be associated with hypertrophic cardiomyopathy, dilated cardiomyopathy, congenital heart disease, and especially atrial septal defect in adults. Etiologies also include restrictive cardiomyopathies (e.g., amyloidosis, hemochromatosis, and endomyocardial fibrosis), cardiac tumors, constrictive pericarditis, and age-related atrial fibrosis. Other cardiac diseases, such as mitral valve prolapse, mitral annular calcification, pulmonary heart disease, and idiopathic dilatation of the right atrium, are also associated with a high incidence of AF. Atrial fibrillation also often occurs in patients with sleep apnea syndrome. 3. other etiologies Obesity is an important risk factor for the development of atrial fibrillation. The etiology of atrial fibrillation also includes autonomic dysfunction (sympathetic or parasympathetic hyperfunction), endocrine disorders (pheochromocytoma), drug (alcohol or caffeine) or chemical agent intoxication, surgery (after cardiac, pulmonary or esophageal surgery) and genetic factors (familial atrial fibrillation). The incidence of atrial fibrillation increases with age, not only because of the disease, but also because of the aging changes that may occur in the heart with age, the substitution of fibers and adipose tissue in the sinus node cells and inter-nodal myocardium, and the decrease in ventricular compliance leading to varying degrees of atrial enlargement, all of which are triggers for the development of atrial fibrillation. (ii) Mechanism of occurrence The mechanism of atrial fibrillation was studied in 1914, but it has not been fully elucidated to date. The onset and maintenance of tachyarrhythmias require predisposing factors and anatomical basis. For atrial fibrillation, the onset and maintenance substrate is usually more complex, and the available data on the Guidelines for the Treatment of Atrial Fibrillation published by the ACC and AHA in 2006 concluded that the available data support a focal autoregulatory increase and multiple subwave foldback mechanism for atrial fibrillation. In 1947, scherf applied aconitine and stimulation to induce atrial fibrillation in rabbits and proposed the hypothesis of a complete “focal mechanism” of atrial fibrillation, i.e., focal delivery of high-frequency electrical excitation originating in the atria could lead to atrial fibrillation. In the last decade, with the advent of more refined calibrations and catheter ablation techniques, this theory gained attention when focal points of origin were identified in the human heart and ablation of this point led to the cure of AF. Although the pulmonary veins are the most common focal point of origin for tachyarrhythmias, focal points of origin can also be located in the superior vena cava, the border crest, Marshall’s ligament, the left posterior free wall of the left atrium, and the coronary sinus. In 1959, Moe et al. first proposed the “multiple subwave hypothesis” as the mechanism of fibrillation based on the results of a study of a canine vagal-mediated model of atrial fibrillation, suggesting that the forward waves form their own extended subwaves as they pass through the atria and that the maintenance of atrial fibrillation depends on a certain number (at least 3-5) of folding subwaves in the atria. The maintenance of AF depends on the simultaneous presence of a certain number (at least 3-5) of foldback subwaves in the atria. These folding subwaves run randomly and are distributed spatially, and their folding loops are not determined by the atrial anatomy but by the effective atrial local nonstop and excitability. Because of this, collisions, annihilation, splitting, and fusion can occur between these foldback subwaves, resulting in changes in the number of foldback subwaves, the size and speed of the foldback loops, etc. at any time. (iii) Classification In the classification proposed in the Guidelines for the Treatment of Atrial Fibrillation published by ACC and AHA in 2006, AF is classified into paroxysmal AF, persistent AF, and permanent AF for clinical practicality and to be able to show the different treatment characteristics of different types of AF. The first episode of atrial fibrillation is primary atrial fibrillation of variable duration; patients with ≥2 episodes are considered to have recurrent atrial fibrillation. If the AF is self-terminating, recurrent AF is called paroxysmal AF, which usually lasts ≤7 days and most of them <24 hours. If AF occurs continuously for >7 days, it is called persistent AF. Persistent AF can be restored and maintained in sinus rhythm with medication or electrical resuscitation. Atrial fibrillation that cannot be restored or maintained in sinus rhythm with medication or electrical resuscitation is called permanent AF. It can occur for the first time in either primary or persistent AF. Persistent AF also includes longer-term AF that has not been reversed (e.g., >1 year) and usually becomes permanent AF. Based on clinical features, AF can also be classified as isolated AF, familial AF, and non-valvular AF. Isolated atrial fibrillation is generally defined as patients (age <60 years) without cardiopulmonary disease other than simple atrial fibrillation. These patients have a better prognosis in terms of thromboembolism and mortality. < p=""> Familial atrial fibrillation refers to isolated atrial fibrillation that occurs in a family. Patients whose parents have AF are more likely to develop AF, suggesting a familial susceptibility to AF, but whether there is an inherited molecular defect is not known. Several domestic studies on familial AF have shown that even a single genetic mutation can lead to shortened atrial expiration. Non-valvular atrial fibrillation refers to atrial fibrillation that occurs in patients without a history of rheumatic mitral valve disease or valve replacement. （Most patients complain of palpitations, chest tightness, dyspnea, fatigue, dizziness, or syncope. The severity of clinical symptoms of atrial fibrillation depends on the degree of irregular heart rhythm and fast or slow ventricular rate, the status of underlying cardiac function, the duration of atrial fibrillation and the patient’s own factors. Some patients have symptoms only during paroxysmal atrial fibrillation episodes or during long intervals of persistent atrial fibrillation. Patients with permanent atrial fibrillation often feel that the palpitations become less and less symptomatic until they eventually become clinically inactive, especially in older patients. The most distinctive features of atrial fibrillation on the ECG are: (1) disappearance of P waves; (2) complete irregularity in the frequency of ventricular beats (QRS waves); (3) irregular low-amplitude rapid oscillations and fibrillation waves in the baseline in all leads, which are f waves of different sizes and shapes with uneven intervals, with frequencies of 350-600 bpm; the f wave pattern is easier to recognize in leads V1 or II (right-hand leads). (Figure 1) (v) Treatment The treatment of atrial fibrillation has three main goals: (1) heart rate control, (2) prevention of thromboembolism, and (3) rhythm control. The initial treatment strategies include heart rate control and rhythm control. The heart rate control strategy refers to controlling the ventricular rate while the rhythm is not converted and sinus rhythm is maintained. A rhythm control strategy is an attempt to revert and maintain sinus rhythm. Theoretically, rhythm control should be superior to heart rate control, but the AFFIRM study showed no significant differences between the two treatment strategies in terms of mortality and stroke rates, impact on patients’ quality of life, or on the onset and progression of heart failure. the RACE trial found that the heart rate control group was no less effective than the rhythm control group in preventing mortality and reducing morbidity. Heart rate control therapy is a reasonable treatment for older patients with less symptomatic atrial fibrillation. However, either strategy requires anticoagulation therapy to prevent thromboembolic complications. 1. pharmacological treatment (1) heart rate control In atrial fibrillation, the efficiency of pharmacological control of ventricular rate is 80%. Patients with persistent or permanent atrial fibrillation are often treated with oral beta-blockers or calcium channel blockers (verapamil, diltiazem) to control the ventricular rate in the physiological range; when rapid ventricular rate control is required or when oral medications are not appropriate, medications can be administered intravenously, with caution in cases of hypotension or combined heart failure, when calcium channel blockers can lead to further hemodynamic deterioration. Patients with heart failure should be given digitalis or amiodarone intravenously. Patients with atrioventricular bypass can be treated with intravenous procainamide and ibrit if their hemodynamic status is stable. Amiodarone has both antisympathetic and calcium channel antagonistic activity, inhibits atrioventricular conduction, and can effectively control the ventricular rate in atrial fibrillation. When other drugs are ineffective or contraindicated, intravenous amiodarone can help control the ventricular rate in atrial fibrillation. (In patients with persistent atrial fibrillation that can be converted to sinus rhythm, immediate cardioversion is required if atrial fibrillation is the primary cause of acute heart failure, hypotension, or worsening angina in patients with coronary artery disease. Resuscitation is usually achieved by pharmacologic or direct current resuscitation methods. 1) Pharmacologic resuscitation Pharmacologic resuscitation is most effective when applied within 7 days of the onset of atrial fibrillation. Guideline recommendations for resuscitation include flecainide, dofetilide, propafenone, ibrit, and amiodarone. The main risk of pharmacological resuscitation is the toxicity of antiarrhythmic drugs, for example, the adverse effects of amiodarone include bradycardia, hypotension, visual impairment, abnormal thyroid function, nausea, constipation and phlebitis, while quinidine is no longer recommended as a first-line drug due to its poor efficacy and high incidence of side effects. 2) DC electric resuscitation Atrial fibrillation with myocardial ischemia, symptomatic hypotension, angina pectoris, heart failure, pre-excitation syndrome, when rapid ventricular rate medication is ineffective, or when the patient’s hemodynamic status is unstable, or when symptoms are intolerable, electric resuscitation should be performed. The starting power of DC resuscitation for atrial flutter can be low, but resuscitation of atrial fibrillation requires high energy, usually ≥200 J. To avoid damage, the patient should be resuscitated with a high power. The main risks of DC resuscitation are embolism and various arrhythmias. < p=""> (3) Anticoagulation All patients with atrial fibrillation, especially when associated with high-risk factors such as diabetes mellitus, hypertension, obesity, and advanced age, should undergo anticoagulation to prevent thromboembolism, except for those with contraindications. When taking warfarin, the target value for monitoring INR is usually 2.0-3.0 internationally, and 1.8-2.5 is generally sufficient for national patients. Monitoring should be done at least once a week when starting treatment and at least once a month once the results are stable. For young patients without risk factors, aspirin can be taken to prevent blood clots. 2. Non-pharmacological treatment (1) Catheter ablation Early radiofrequency catheter ablation mimicking surgical labyrinthine procedures to create multiple linear scars in the atrial endocardium has a success rate of about 40-50%, but complications are high. Subsequent studies found that electrical activity originating in the pulmonary veins or near their openings often triggered atrial fibrillation and demonstrated that removal of these lesions could end atrial fibrillation, leading to the widespread implementation of catheter ablation for atrial fibrillation. With the increasing maturity of atrial fibrillation catheter ablation techniques and the continuous improvement of the calibration tools (electroanatomical and non-contact calibration systems) and ablation devices, especially the new technique of cryoballoon catheter ablation for atrial fibrillation that has been developed in recent years, the catheter ablation procedure for atrial fibrillation has become faster and safer. The success rate of this treatment has been greatly improved, and the current success rate of ablation for paroxysmal AF without organic heart disease is 80% to 90%, with a significant decrease in complication rate (<2%), so catheter ablation provides a better treatment for most patients who have failed drug therapy or have difficulty with electrical conversion of sinus rhythm. < p=""> (2) Surgical treatment In some cases of recalcitrant atrial fibrillation, surgical maze surgery can also be used. in 1989, Cox reported atrial maze surgery, which achieved more desirable results in atrial fibrillation, i.e., elimination of atrial fibrillation, preservation of atrial synchronous excitation, and preservation of atrial transmitral function. By 1996, Cox reported 178 patients with atrial fibrillation and atrial flutter who underwent the maze procedure, with a perioperative mortality rate of 2.2%, a cure rate of 93% and a recurrence rate of 7% at a follow-up of more than 3 months. For atrial fibrillation combined with other heart diseases requiring surgical correction, surgical maze surgery is an effective treatment method. In recent years, minimally invasive transthoracic radiofrequency ablation surgery has opened up another new way for the treatment of atrial fibrillation.