Among all congenital cardiac malformations in live-born infants, ventricular septal defect (ventricular defect for short) has the highest incidence. According to statistics published in the United States in 2002 (a compendium analysis of 62 groups of reports after 1955), simple ventricular defects account for more than one-third of all cardiac malformations (excluding simple aortic diastolic malformations) and have a prevalence of approximately 3.6 per 1,000 live births. At the same time, ventricular defects are one of the few cardiac malformations that can be cured to allow the patient to achieve normal cardiac function and maintain it for life, with minimal medical costs. If properly treated and managed, ventricular defects can have lifelong benefits for many patients. The human heart is a mammal with a four-chambered structure. Thanks to this structure, our body circulation and pulmonary circulation are connected in series. The blood circulation in the human body is divided into two parts, namely, the physical circulation and the pulmonary circulation. From the heart, arterial blood flows through the arteries of the body to each organ, releasing the oxygen it carries and taking away the carbon dioxide produced by the organs, and is summed up in stages by the veins of the body, finally flowing back to the right atrium of the heart. The oxygen-depleted blood that reaches the right atrium passes through the right ventricle and is pumped into the pulmonary artery. The blood flows through the pulmonary artery into the lung tissue, where it exchanges gases with the air in the alveoli, releasing carbon dioxide and recombining oxygen to become oxygenated blood. The oxygenated blood flows back to the left atrium through the pulmonary veins, enters the left ventricle, is pumped by the left ventricle into the aorta, and so on in an endless cycle. In terms of blood flow, the blood flow of the body circulation is equal to that of the pulmonary circulation. In the reptilian heart with two chambers, the oxygen-deprived venous blood mixes with the oxygenated arterial blood in the heart and its efficiency is low. When a ventricular septal defect exists, the lower pressure in the right ventricle compared to the left ventricle results in a portion of the oxygenated blood in the left ventricle that should have all drained into the aorta being shunted through the ventricular defect to the right ventricle and subsequently into the pulmonary circulation. This part of the blood flow is an inefficient circulation for human metabolism and blood gas exchange, increasing the volume load on the heart and decreasing the efficiency of the heart’s work. The size of this blood flow depends on the size of the ventricular defect and the level of pulmonary vascular resistance, and in some patients it can reach 3-4 times or more the blood flow in the body circulation. This abnormal blood flow poses several problems. The first is an increased volume load on the heart. The patient’s heart enlarges and over time eventually develops congestive heart failure, a condition that is particularly evident in infants with massive ventricular defects. The child always asks to be held and prefers to remain in a head-high position to reduce the amount of blood returned to the heart. Children with heart failure do not feed well because the burden on the heart increases after feeding and stasis of blood in the gastrointestinal tract and portal system leads to impaired digestion and absorption, so the child does not like to eat. Secondly, the lungs are congested. Patients are highly susceptible to respiratory infections, which manifest as recurrent respiratory and pulmonary inflammation, and some children are forced to be hospitalized non-stop due to respiratory infections. The third is the increased pulmonary blood flow, which leads to protective constriction of the small pulmonary arteries, increasing the resistance of the pulmonary vascular bed and decreasing the shunt flow. Continuous constriction of the small pulmonary arteries can lead to lesions in the walls of the small pulmonary arteries, producing an irreversible increase in pulmonary vascular resistance. The pressure in the pulmonary artery is equal to the product of the resistance of the pulmonary vascular bed and the pulmonary blood flow. The ability to reduce pulmonary artery pressure to normal levels after ventricular defect repair depends on who is the dominant factor in pulmonary hypertension: resistance, or flow. Increased pulmonary blood flow alone can lead to pulmonary hypertension, but if the defect disappears and pulmonary blood flow decreases to normal levels, pulmonary artery pressure will also decrease to normal. Once the factor of increased resistance in the pulmonary vascular bed becomes a major factor in pulmonary hypertension, pulmonary hypertension will remain even if the shunt disappears and resistance does not decrease. When the resistance of the pulmonary circulation approaches or exceeds that of the body circulation, the systolic pressures of the left and right ventricles are equal, a bidirectional shunt or right-to-left shunt is generated through the ventricular ischemia, and some of the blue, oxygen-deprived venous blood flows through the ventricular ischemia into the body circulation, and the patient develops cyanosis. This is clinically referred to as Eisenmenger’s syndrome (ESS). The fourth is that the valves of the heart become insufficiently closed due to the enlargement of the heart and the ventricular ischemic flow. This further burdens the heart and greatly increases the complexity of the procedure. The management of ventricular defect repair combined with valvular lesions is surgically complex, more costly, had greater risk, and the long-term outcome may become worse. The fifth is the local endocardial damage and turbulence caused by the high velocity motion of the trans-septal blood flow. These factors contribute to the aggregation and adhesion of platelets, which form fine redundancies and microthrombi on the tissue adjacent to the ventricular defect. When bacteria or mycobacteria enter the bloodstream because of infection or breakage elsewhere in the body, they tend to adhere to these areas, leading to infective endocarditis. Infective endocarditis has a high rate of misdiagnosis, many complications and serious consequences, and is complicated and expensive to treat. Sixth is the distress caused by heart murmurs. In many cases, if a person has a heart murmur, regardless of the nature of the murmur and whether or not his or her heart function is affected, he or she is considered to be a heart patient and will have great trouble getting into daycare, getting vaccinated, going to school, getting a job, joining the military, and buying commercial insurance. This problem has nothing to do with heart disease, but is a result of the lack of medical knowledge among people, and is also a characteristic of China. When and how to treat a ventricular defect has a lot to do with the location and size of the defect. Patients should undergo ventricular defect repair surgery as early as possible, regardless of their age, when: 1) a non-restrictive ventricular defect (i.e., the size of the defect is close to or larger than the area of the patient’s aortic valve opening, and blood flows through the defect without resistance) should, in principle, be completed within 2 years of age; 2) severe heart failure; 3) significant mitral or aortic regurgitation; 4) the presence of moderate or higher pulmonary hypertension. Delay may result in the patient losing the opportunity to operate surgery. All ventricular defects should be repaired in one stage, with the exception of large myocardial multiple ventricular defects (also known as Swiss-Cheese Defect, with high fractional flow, significant heart failure, high potential for pulmonary vasculopathy, and difficult repair in infancy), which require elective surgical repair after pulmonary artery annuloplasty in infancy. The risk of cardiac surgery in infants and children is inversely proportional to the age of the patient; the younger the child, the greater the risk of surgery. After the age of half a year, the risk of surgery is much less than in infancy. Both physicians and parents should truly look at the patient’s interests, consider the increased surgical risks associated with a small child and the adverse consequences of delayed surgery, and weigh the pros and cons to choose the right time for surgery. Subpulmonary ventricular defects (also known as substem ventricular defects) have the potential to lead to aortic valve leaflet prolapse followed by aortic valve insufficiency, and these ventricular defects do not heal on their own. No matter how small the sub-stem ventricular defect is, it should be treated surgically as soon as it is detected. The lifelong impact of aortic valve insufficiency due to aortic valve prolapse is enormous. In moderate-sized ventricular defects, surgery should be done before school age. This ventricular defect will not lead to heart failure and pulmonary vasculopathy like a large ventricular defect, but it may affect the child’s physical development. Furthermore, as the child becomes more aware, this defect can create a sense of “illness” in the child. Even after surgery is completed and the heart is functioning normally, the child may still feel that he or she is a sick person and is unwilling to hold himself or herself to normal standards, even though his or her body is already normal. Very small ventricular defects, especially those in the perimembranous region, have the potential to close spontaneously, but this possibility decreases significantly after the age of 5-7 years. A group of 229 patients in the United States who were followed up for nonoperative treatment of small ventricular defects, with patients aged 14-18 years at entry and 30 ± 10 years at the end of follow-up, had a spontaneous closure rate of only 6% of ventricular defects. This defect results in a small fractional flow with minimal cardiac and pulmonary vascular effects. It causes problems for the patient, firstly, the trouble with heart murmurs and secondly, the increased probability of developing infective endocarditis. The above are the general principles of surgical treatment of ventricular defect. The conditions and technical level of each hospital in China vary, so the timing of surgery should take into account the specific local conditions, but the principles should not be violated arbitrarily. Ventricular defect repair surgery is usually performed with artificial patch (polyester patch, PTFE patch, treated bovine pericardial patch or patient’s own pericardial patch) as the repair material, and the patch is sutured to the edge of the ventricular defect with special surgical sutures; very small membrane or myocardial ventricular defects can also be sutured directly with sutures with spacers. After the onset of Eisenmenger syndrome, the pathological changes in the heart are significantly altered compared to the period of massive shunting. This is when the end-diastolic internal diameter of the left ventricle shrinks and even reaches normal values. However, the right ventricle and tricuspid valve, which are anatomically morphologically suited to work at low pressures, are chronically exposed to high pressures equal to those of the left ventricle, resulting in dilatation of the right ventricular and tricuspid annulus and the development of right heart failure and severe tricuspid regurgitation. Patients develop swelling of the lower extremities, abdominal distention, hepatomegaly and pleural and ascites fluid. The patient develops cyanosis due to the shunt flow of hypoxic venous blood into the left heart via ventricular ischemia. In this situation, if ventricular defect repair is performed, the right ventricular excretory load (afterload) increases, the patient’s heart failure is further aggravated, and some patients even die from the procedure. There are often patients in clinical practice whose pulmonary vascular disease has reached a certain level, between those who can be treated surgically and those who cannot. Currently, there is some debate among physicians as to whether these patients can undergo ventricular defect repair surgery and what the long-term outcome is after surgery, especially when drugs such as sildenafil and bosentan are available for the treatment of pulmonary hypertension. Some hospitals currently use a patch with a living flap to repair the ventricular defect, a technique that is only appropriate or trialed in the “borderline” cases described above, not in Eisenmenger’s syndrome. At present, the only effective treatment for ventricular defects combined with Eisenmenger’s syndrome is combined heart-lung transplantation. It is an undisputed fact that the longer the duration of pulmonary hypertension before surgery, the more severe the pulmonary vascular disease will be, and the greater the risk of surgery and the greater the likelihood that the pulmonary resistance will not decrease or will continue to increase after surgery. During surgery, the interference of the atrioventricular valve tendons and papillary muscles around the ventricular defect and the intentionally limited cardiac incision to reduce the extent of injury sometimes make the visualization of the ventricular defect so difficult that the surgeon is unable to see the entire edge of the ventricular defect the edge of the ventricular defect, resulting in a poorly repaired defect. The edges of the ventricular defect are partially composed of myocardium or thin annulus tissue, which, especially in infants, is so tender that surgical sutures can cut through it, or as the saying goes, “the sutures are pulling the flesh open. When this happens, it can also lead to residual shunting of the ventricular defect after surgery. However, if the stitches are deeper, there is a risk of damaging the cardiac conduction system at the edge of the ventricular defect, resulting in a complete AV block. Aseptic tissue inflammation due to sutures and surgical traction on the edge of the ventricular defect may also lead to complete AV block. If this complete AV block is irreversible, the patient must undergo permanent pacemaker implantation to maintain the necessary heart rate. Residual shunts and complete AV block are the main complications of ventricular defect repair surgery. From October 1996 to December 2008, a total of 8,979 simple ventricular defect repairs were performed at Beijing Fuwai Hospital, with 17 surgical deaths, 18 cases of residual shunts, 4 cases of complete AV block, and 2 cases of permanent sudden cerebral stroke after surgery. From January 2000 to December 2006, 215 simple ventricular defect repairs were performed at Texas Children’s Hospital in the United States, with a mean age of 10 months and weight of 7 Kg. No patient was reoperated for residual shunts and no central nervous system complications. There was one case of early surgical death and two cases of late death. In recent years, with the advancement of medical science, the method of percutaneous interventional occlusion for ventricular defect has emerged? The general method is to place a blocker into the heart through the patient’s femoral artery, reach the defect, release the blocker, and slowly generate a thrombus inside the blocker to finally block the defect completely. The advantage of this method is that it does not require surgery and is minimally invasive. The main problem with this method is that the edge of the blocker may come into contact with the leaflet of the heart valve, damaging it and causing it to perforate. The blocker can compress the cardiac conduction system located under the endocardium of the left ventricular surface of the defect, resulting in complete AV block. Embolism of the body circulation may occur if the thrombus formed on the surface of the blocker is dislodged. Children who are too young for the blocker to be delivered are limited by the diameter of the femoral artery. The U.S. Food and Drug Administration (FDA) restricts the use of the Amplatzer blocker to high surgical risk and anatomically appropriate types of muscular ventricular defects. Conditions that preclude its use include: 1) defects less than 4 mm from the valve; 2) severe or irreversible pulmonary vascular disease; 3) perimembranous ventricular defects or septal perforations complicated by myocardial infarction; 4) patients weighing less than 5.2 Kg; 5) sepsis or active bacterial infection; and 6) contraindications to antiplatelet aggregation drug (aspirin) therapy. The results of the phase I trial of the new Amplatzer blocker in the United States in 2006 showed that in 35 patients with a mean age of 7.7 years and a mean weight of 25 Kg, the blocker was successfully inserted in 32 cases, and the ventricular shunt disappeared in 96% of the patients at 6 months. Preoperatively 26% of the patients had aortic regurgitation, and at 6 months postoperatively this value was 39%. There were three serious complications (one each of complete AV block, hepatic hemorrhage, and tricuspid tendon rupture.) In a European group of 54 patients with perimembranous ventricular defect in 2007, the Amplatzer blocker was used, and the blocker was successfully placed in 49 cases. One year after surgery, the ventricular shunt disappeared in 46 patients. Complications of the procedure included two cases of blocker embolism and one case of complete atrioventricular block. In a group of Italian patients, 104 patients with perimembranous ventricular defects were treated with the Amplatzer blocker from 1999 to 2006. The average age was 14 years, the average weight was 26.5 Kg, and the blocker was successfully placed in 100 cases. 6 patients (2 in early stage and 4 in late stage) were implanted with permanent pacemakers due to complete AV block, and the blocker was embolized in 2 cases. In China, there are also some reports, but the studies are not rigorous, and the credibility of the results is poor, so it is not a reference value. In conclusion, percutaneous interventional occlusion technique requires high anatomical conditions of ventricular defect, the incidence of serious complications is higher than that of surgical repair, and the cost is roughly comparable to that of surgery with small trauma. The current status of ventricular defect treatment in China is that surgical repair in large cardiac centers in first-tier cities is effective with few complications, and the age of patients is getting younger and younger, with children within one year of age accounting for a significant proportion. However, in some third-tier cities and underdeveloped areas, the majority of surgical patients are still over 3 years old and have more surgical complications. Many pediatricians and internists do not fully recognize the severity of the damage caused by unrestricted ventricular defects to the physical and mental development of children and the possibility that the onset and progression of pulmonary vascular disease may permanently deprive some children of the opportunity for ventricular defect repair at the age of 1-2 years, and still recommend that children be considered for surgery after the age of 3-4 years regardless of the size of the ventricular defect. There are no clear restrictions on the management of interventional sealing of ventricular defects by the domestic health care authorities, and many hospitals, including some with very low levels of cardiac surgery, are carrying out this practice, which can be described as blossoming. For patients, the obvious advantage of interventional occlusion is that it is less invasive, and the issue of indications and complications is avoided. This inevitably leads to some errors and mistakes in treatment indications or techniques, resulting in serious complications and poor outcomes.