Atrial fibrillation is the most common clinically significant heart rhythm disorder. It can be seen in various cardiac diseases, in diseases other than cardiovascular (e.g., hyperthyroidism), and in normal subjects. The abnormal hemodynamic forces and thromboembolism caused by atrial fibrillation increase the morbidity p mortality and health care costs. The physiological basis for the development of atrial fibrillation consists of two processes: 1. Increased autoregulation of one or more foci of rapid depolarization excitation. This foci of excitation have now been shown to be located in 90-95% of the right and left superior pulmonary veins, with a few located in the right atrium, superior vena cava, or coronary sinus. This focal origin has important implications for paroxysmal AF. By ablating these foci of excitation, a cure for these AFs can be expected. Moe and colleagues first proposed the “multiple subwave theory” of atrial fibrillation folding, in which the wavefront conduction in the atrial myocardium splits into multiple self-sustaining “subwaves”. The number of subwaves depends on the size of the atrium and the wave loop, the atrial myocardial stress period and the conduction speed. According to Prof. Qi Wenhang of Ruijin Hospital in Shanghai, AF can be maintained only when there are at least three or more multi-source folds in the atria. Atrial fibrillation is no longer maintained if the number of foldbacks is reduced to less than three. Short atrial action potential (APD) and delayed atrial conduction and enlarged atrial cavity are important factors in the formation and persistence of atrial folding. Linear ablation can interrupt the foldback loop. Non-pharmacological treatment of atrial fibrillation includes: 1, surgery 2, catheter ablation therapy (including radiofrequency ablation p cryoablation p cryogenic perfusion ablation p saline perfusion ablation) 3, pacemaker prevention of atrial fibrillation (AAI pacemaker preferred) 4, intraatrial resuscitation defibrillator 5, extracorporeal electric shock resuscitation 6, left auricular occlusion to prevent atrial fibrillation embolism. We will mainly review the pharmacological treatment of atrial fibrillation. Therapeutic goals: to revert and maintain sinus rhythm, control ventricular rate, and prevent embolism. Paroxysmal AF (paroxysmal AF) has no apparent structural heart disease, AF can be self-reversing, 90% persists at age 65, hypertension, coronary artery disease, hyperthyroidism, hypertrophic cardiomyopathy, diabetes, large left atrium, emboli found in the left atrium, low left ventricular function, previous embolism or transient cerebral ischemia. There are two broad types of thrombus formation. One type occurs under conditions of slow blood flow, such as venous thrombosis, and its formation requires activation of clotting factors, so the corresponding treatment is with anticoagulant drugs such as warfarin. Slow blood flow in the atria is the same type as venous thrombosis, so Warfarin is also appropriate. Another type of thrombosis occurs in the case of fast blood flow, such as intra-arterial thrombosis, which is mainly related to platelet activation mechanism. Therefore, antiplatelet agents, such as aspirin, can be used for treatment. Warfarin is significantly better than aspirin in preventing embolism, but it is still widely accepted because bleeding complications during antiplatelet therapy are significantly less than with warfarin, it is easy to use, and it is not necessary to observe blood coagulation indicators. Those who receive anticoagulation therapy must be tested regularly for the International Standard Ratio (INR). Extensive foreign data suggest that an INR of 2-3 provides the best anticoagulation and minimizes intracranial hemorrhage. The requirements are higher for prosthetic valve replacements. The following conditions should be anticoagulated: 1. Chronic atrial fibrillation with high-risk factors. However, it should be noted that people >75 years old are prone to complications of intracranial hemorrhage. 2, valvular atrial fibrillation 3, frequent paroxysmal atrial fibrillation 4, before and after resuscitation therapy. 5, atrial fibrillation lasting >2 days with a history of embolism.