Atrial septal defect (ASD) is a congenital heart disease that causes blood communication between the left and right ventricles due to partial atrial septal tissue defects, accounting for about 13% of all heart malformations. Secondary ASD is the most common type of ASD and can generally be treated with minimally invasive closure. At present, the commonly used minimally invasive methods in clinical practice mainly include X-ray-guided percutaneous occlusion, transesophageal ultrasound-guided transthoracic occlusion and ultrasound-guided percutaneous occlusion. This review focuses on the basic research process of occluder materials, and advantages and disadvantages of three different surgical methods.
A solid-liquid two-phase finite element model of articular cartilage and a microscopic finite element model of chondrocytes were established using the finite element software COMSOL in this study. The purpose of the study is to investigate the mechanics environment and the liquid flow field of the host cartilage chondrocytes in each layer by multi-scale method, under physiological load, with the different elastic modulus of artificial cartilage to repair cartilage defect. The simulation results showed that the uniform elastic modulus of artificial cartilage had different influences on the microenvironment of different layer chondrocytes. With the increase of the elastic modulus of artificial cartilage, the stress of the shallow surface layer and the intermediate layer chondrocytes increased and the stress of deep layer chondrocytes decreased. The flow field direction of the middle layer and the bottom layer of cartilage can also be changed by artificial cartilage implantation, as well as the ways of nourishment supply of the middle layer and underlying chondrocytes change. A barrier to underlying chondrocytes nutrition supply may be caused by this, thus resulting in the uncertainty of the repair results. With cross-scale finite element model simulation analysis of chondrocytes, we can quantitatively evaluate the mechanical environment of chondrocytes in each layer of the host cartilage. It is helpful to assess the clinical effect of cartilage defect reparation more accurately.