Arteriovenous ductus arteriosus is a relatively common congenital cardiovascular malformation, accounting for 12-15% of all congenital heart disease. It is approximately twice as common in women as in men. Other cardiovascular malformations coexist in about 10% of cases. The ductus arteriosus is a duct located between the base of the left pulmonary artery and the beginning of the aorta. During fetal life, the lungs are atrophied and the resistance of the pulmonary vasculature is high. After birth, the lungs expand and contract with respiration, and the resistance of the pulmonary circulation decreases, so that the blood discharged from the right ventricle enters the lungs on both sides for gas exchange. When the pulmonary arterial pressure is equal to the aortic pressure, the arterial conduit is functionally closed. The ducts then gradually close histologically to form the arterial ligament due to physiologic abandonment, changes in the angular position of the ducts as the lungs expand, and certain unexplained factors. Statistically, 88% of infants have their ducts closed within 2 months of birth and 98% within 8 months. If the duct is still open at 1 week of age, it has less chance of closing on its own later, i.e., it forms an unclosed duct (syndrome). The diameter and length of the unclosed ductus arteriosus generally varies from a few millimeters to 2 cm, sometimes as thick as its adjacent descending aorta and as short as a few lengths that can be measured as a direct communication between the aorta and the wall of the pulmonary artery, so-called window-shaped ductus arteriosus. The amount of shunt flow depends on the thickness of the catheter caliber and the pressure step difference between the aorta and the pulmonary artery. Shortly after birth, the resistance of the pulmonary artery is still high and the pressure is high, so the left-to-right shunt is low or only present during systole. Thereafter, the resistance of the pulmonary artery gradually decreases, the pressure is significantly lower than that of the aorta, and the shunt flow increases. As the pulmonary artery receives both right ventricular drainage and catheter shunts, the amount of blood returning from the pulmonary veins to the left ventricle increases, increasing the load on the left ventricle and leading to enlargement, hypertrophy, and even failure of the left ventricle. If too much blood flows through the mitral orifice, relative stenosis of the mitral valve may occur. Interstitial pulmonary edema can result from obstruction of pulmonary venous blood drainage and increased pressure. The lumen of the ascending aorta and aortic arch is enlarged due to increased blood flow through them; this is also reflected by increased pulmonary artery blood flow. Long-term increase in pulmonary blood flow may cause reflex spasm of the small pulmonary arteries, which may lead to thickening and sclerosis of the walls of the small pulmonary arteries, thinning of the lumen, and increased resistance to pulmonary circulation. As the pulmonary resistance increases and pulmonary hypertension develops, the left-to-right shunt gradually decreases and eventually a reverse (right-to-left) shunt occurs, reducing the oxygen content of the arteries in the lower part of the body and causing cyanosis at the toes. Long-term blood flow impingement can cause the duct walls to become thin and brittle to the point of aneurysm or calcification. It is also susceptible to infection and endarteritis. The proximal pulmonary artery may show aneurysmal enlargement due to increased intraluminal pressure. The clinical manifestations of ductus arteriosus depend on the amount of blood flow from the aorta to the pulmonary artery and the degree of secondary pulmonary hypertension. In mild cases, there may be no obvious symptoms, while in severe cases, heart failure may occur. Common symptoms include palpitations after exertion, shortness of breath, weakness, susceptibility to respiratory infections and dysplasia. Since the widespread use of antibiotics, bacterial endarteritis has become rare. In advanced pulmonary hypertension severe enough to produce a reverse shunt, lower body cyanosis is seen. On physical examination, the typical sign is a loud, continuous machine-like murmur with tremor heard between the second ribs at the left sternal border. The second pulmonary artery sound is hyperactive, but is often masked by the loud murmur. The diastolic murmur due to relative mitral stenosis can be heard in the apical region with high fractional flow. Blood pressure measurements show that systolic pressure is mostly in the normal range, while diastolic pressure decreases, resulting in a widening of pulse pressure and a watery pulse and gunshot sound in the vessels of the extremities. In infants and children, only systolic murmurs may be heard. In advanced pulmonary hypertension, the murmur may be more variable and may be replaced by a systolic murmur or by a diastolic murmur with incomplete pulmonary valve closure. After the diagnosis of arterial catheter failure is established, if there are no contraindications, surgery or catheter intervention should be performed opportunistically to interrupt the blood flow at the catheter. In the past, it was recommended that the procedure be performed before school age, but this year it is recommended that the procedure be performed as early as possible, especially since the development of interventional therapy has made the treatment of small infants very safe. If the shunt flow is large and the symptoms are severe, the procedure should be performed earlier. The risk of surgery increases and the outcome is poor when the age is too old and pulmonary hypertension occurs. In cases of bacterial endarteritis, surgery should be withheld, but if the infection is not adequately controlled by medication, surgery should still be sought, and the infection is often quickly controlled by continuing pharmacotherapy after surgery. In recent years, for premature infants with respiratory distress syndrome caused by unclosed ductus arteriosus, surgical treatment is also advocated, and less often the use of catheter closure drugs (prostaglandin synthase inhibitor – anti-inflammatory pain) treatment, because the latter drug dose is difficult to grasp, the effect of a small amount is not obvious, a large amount of side effects, or discontinuation of the drug catheter reopening. Catheter interventions have developed rapidly in recent years, and tens of thousands of cases have been treated with catheter interventions nationwide since 1997. With the advantages of easy operation, precise efficacy, minimal trauma and no incision, catheter interventions are widely welcomed by parents of children and have replaced surgery as the preferred treatment option. Prognosis The operative mortality rate due to hemorrhage during arterial catheterization depends on the texture of the catheter wall, the surgical method used to close the catheter, and the skill of the surgeon, but should generally be less than 1%.