The left atrium and left atrial appendage have unique genetic anatomical and physiological features. Recently, advances in diagnostic imaging technology have provided much new knowledge. Clinically, the risk of developing atrial fibrillation increases with age. In order to reduce the public health burden such as cerebral infarction caused by atrial fibrillation, we need to find some predictive risk factors and preventive strategies for cerebral infarction and more effective treatments. The new concept of atrial myopathy has emerged, and animal models and human studies have revealed close interactions between atrial myopathy, atrial fibrillation, and stroke through various mechanisms. Structural and electrical remodeling such as fibrosis and deterioration of the balance of autonomic nerves and complicated interactions between these mechanisms lead to deterioration of atrial fibrillation and a continuous vicious cycle, and finally thrombosis in the left atrial appendage. Although anticoagulant therapy for patients with atrial fibrillation is strongly recommended, it is difficult for many patients to continue optimal treatment. In the nearly future, it will be important to understand the anatomy and physiology of the left atrial appendage and to understand the shape changes, size and the changes of autonomic function, and thrombus formation conditions associated with LAA remodeling during atrial fibrillation, and then we should provide early therapeutic intervention.