(Note: This article was written by an expert in response to the Journal of Cardiovascular Surgery, and is now slightly modified for the benefit of our patients) Congenital heart disease (CHD) has become the number one birth defect disease in China. There is no doubt that surgery is the preferred treatment option for CHD. In the last decade, the level of congenital heart disease surgery in China has made great progress, and some difficult procedures have been popularized and innovated on this basis, while the success rate of some common CHD treatments has reached the level of western developed countries. However, it should not be ignored that pulmonary artery hypertension (PAH) in combination with CHD is still a great challenge in China’s precardiac surgery. There is a consensus that cardiac anomalies are contraindicated in children with combined organic PAH (i.e., Eisenmenger syndrome). With the popularization of precordial surgery and the improvement of the national health insurance system, the proportion of such patients has been decreasing. The use of targeted therapeutic agents for PAH in recent years has made it possible to operate on patients with severe PAH who are in a borderline state. However, PAH after CHD is still a blind spot in China’s precardiac surgery. During the early postoperative hospitalization of Zhang Hao in the Department of Pediatric Cardiac Surgery, Fu Wai Hospital, Beijing, PAH is often controlled by ventilator management, nitric oxide inhalation and other treatments under close monitoring. The present writing is more concerned with persistent PAH after patient discharge and the proportion of such patients is not low. In a study by Indian scholars, postoperative cardiac catheterization follow-up of patients with preoperative combined PAH revealed that even if there was only moderate PAH preoperatively, 21% of patients still had PAH six months after surgery. in a postoperative follow-up of 887 patients with ventricular septal defect combined with severe PAH in China, their survival rate at 10 years after surgery was 90%, and the expected survival rate at 18 years after surgery was only 62% to 67%. Almost all of these patients with combined severe PAH did not receive postoperative treatment to control pulmonary hypertension, and only 3% of them received medication to reduce PAH and only 6% received anticoagulation. This shows that postoperative PAH is potentially very dangerous because it is often ignored by families and physicians. One of the main causes of long-term persistent postoperative PAH includes two points, one of which is increased pulmonary vascular bed resistance due to massive left-to-right shunts in patients with preoperative multi-pulmonary blood, such as the aforementioned ventricular septal defect combined with severe PAH. Although the intracardiac shunt is blocked after surgery, the malignant remodeling of the pulmonary vascular bed caused by PAH requires a longer period of time to recover, and even the plexiform vasculopathy cannot be reversed in individual patients. The second is the patient with cyanotic precordial disease with preoperative oligopulmonary blood. Due to the long-term lack of normal pulmonary blood flow perfusion, their pulmonary vascular bed is often poorly developed. For example, in patients with pulmonary atresia, although the development of the intrinsic pulmonary arteries on both sides can be sufficient for radical surgery, there are arterial defects in the lobar segments of the lung, so the poorly developed pulmonary vascular bed can hardly accommodate the sudden increase in pulmonary blood flow after radical surgery, resulting in a persistently high PAH, leading to high right ventricular pressure or even forcing the removal of the patch of the septal defect or opening the window. We need to deal with it holistically and comprehensively. Firstly, the concept of “Treat-Repair-Treat” for PAH should be established, which means not only aggressive pressure lowering before surgery, but also close follow-up after surgery, adequate communication with the patient’s family, and aggressive pharmacological treatment. Secondly, we should develop individualized surgical plan, not to force perfection, but to achieve ideal balance of pulmonary blood flow after surgery by means of pulmonary artery bundling, septal defect patch opening, etc., so as to improve long-term survival rate.