Only some of the atrial septal defects, ventricular septal defects and patent ductus arteriosus can heal on their own, but the rest, especially complex precardiac disease, not only cannot heal on their own, but also will progressively worsen, and many children must be operated on within 2 years, 1 year, half a year, or even within a month, otherwise there is a risk of losing the opportunity to operate due to deterioration. The mechanism of natural closure of atrial septal defects is that the heart continues to develop after birth. The rate of natural closure is approximately 20% to 39% and occurs basically within 1 year of age, with little possibility of closure after 1 year of age. There are three mechanisms for natural closure of ventricular septal defects: 1) continued development of the heart; 2) adhesion of the tricuspid valve leaflets and tendons to the ventricular defect; 3) high velocity blood shunts causing proliferation and fibrosis of the tissue surrounding the ventricular defect, resulting in gradual reduction of the notch. Although spontaneous closure of larger defects has been reported, membranous defects less than 0.5 cm in diameter are most likely to close spontaneously, and small muscular ventricular defects may also close spontaneously, while subdural ventricular defects are almost impossible to heal spontaneously. Spontaneous closure usually occurs within 4 years of age or before school age, and rarely later. The ductus arteriosus is a normal structure in the fetus. During fetal life, high local circulating prostaglandin E (PGE) levels and low oxygen levels cause spiral smooth muscle relaxation and keep the ductus open, allowing most of the right ventricular blood to flow from the high resistance pulmonary circulation into the descending aorta to the low resistance placental tissue. After birth, there is a significant decrease in PGE and an increase in the partial pressure of oxygen in the blood passing through the duct, causing contraction of the ductal smooth muscle and protrusion of the thickened endothelium into the lumen to fill the duct, with the majority of the ducts closing functionally within 24 hours, and after 2 to 3 weeks, the endothelial fibrous tissue proliferates and closes permanently after fibrosis, forming the ductal ligament. Failure of the ductus arteriosus to close properly after birth is called ductus arteriosus. The mechanism of self-closing is the continuation of the closure mechanism described above, and 85% of them close within 2 months, with rare self-closing after the age of half a year. If respiratory distress and heart failure occur in preterm or neonatal infants, administration of oxygen and intragastric infusion of anti-inflammatory pain, 0.2 mg/kg for the first dose and 0.1 mg/kg for the next three doses every 8 hours, along with fluid restriction, cardiac, diuretic, vasoactive drugs and mechanical ventilation support, may induce ductal closure.