Ventricular septal perforation (VSR) is one of the serious complications after acute myocardial infarction (AMI), accounting for about 1% to 2% of patients with acute myocardial infarction. Conservative medical treatment is ineffective, and once perforation occurs, heart failure and cardiogenic shock often occur rapidly and lead to death. Surgical treatment is recognized as an effective treatment, but the risk of surgery is still high, early mortality is high, and the exploration of interventional treatment has recently emerged. Epidemiological data Ventricular septal perforation is a serious complication of myocardial infarction, often resulting in death due to rapid onset of acute heart failure. Acute myocardial infarction complicated by septal perforation is uncommon, and prior to the introduction of myocardial reperfusion therapy, septal perforation occurred in approximately 1% to 2% of patients with acute myocardial infarction within the first week after myocardial infarction. Timely myocardial reperfusion with thrombolytic therapy after acute myocardial infarction can reduce the extent of myocardial infarction and decrease the incidence of septal perforation to 0.2%.2 Yip et al. also reported that direct coronary intervention after acute myocardial infarction significantly reduced the incidence of septal perforation (0.24%).3 This suggests that effective coronary revascularization can reduce the incidence of septal perforation after acute myocardial infarction. Before myocardial reperfusion therapy, the average time to perforation was about 1 week after myocardial infarction, and after thrombolytic therapy the average time to septal perforation was advanced to about 1 day after myocardial infarction.Menon et al. reported that the average time to septal perforation after thrombolytic therapy was advanced to about 16 hours after myocardial infarction. Ventricular septal perforation after myocardial infarction is aggressive and has a poor natural prognosis, with mortality rates of 50% and 87% at 1 week and 2 months, respectively, with drug therapy alone.5 Gray et al. found that patients treated with conservative medical therapy alone had mortality rates of 24%, 46%, and 67% to 82% at 24 hours, 1 week, and 2 months, respectively, with a 1-year survival rate of 5 to 7%.5 Lemery et al. reported that When acute myocardial infarction was complicated by septal perforation, the survival rate within 1 month with medical therapy was only 24%. Although untreated survival for 14 years has been reported, it is rare.8 You Shijie et al. summarized 24 patients with septal perforation after myocardial infarction and concluded that echocardiography that showed a perforated site toward the mid-base of the posterior septum, a reduced left ventricular ejection index (≤40%), an increased left and right ventricular end-diastolic diameter, an increased pulmonary artery systolic pressure (≥50 mmHg), or a large ventricular wall tumor predicted that the patient was Deja et al. reported that septal perforation frequently occurred in patients with first myocardial infarction, most of whom were older than 65 years, and more than half had a single vessel lesion.10 Other reports suggested that risk factors for septal perforation after acute myocardial infarction included hypertension, advanced age, female sex, nonsmoking, absence of previous angina or myocardial infarction, complete occlusion of the infarct-related vessels, and a lack of complete occlusion of associated vessels, lack of collateral circulation, and anterior wall myocardial infarction.1,2,3,4,11 Xu Jianping of Fu Wai Cardiovascular Hospital reported 16 patients, including 5 cases of single vessel lesions, 4 cases of 2-vessel lesions, and 7 cases of 3-vessel lesions.12 Li Zhizhong et al. summarized 26 patients with septal rupture after acute myocardial infarction and concluded that elderly female hypertensive patients with initial acute myocardial infarction are at high risk for septal perforation.13 Prêtre et al. concluded that septal perforation occurs in myocardial tissue that lacks both collateral circulation and ischemic preadaptation protection, with previous angina pectoris or myocardial infarction, due to the stimulation of myocardial ischemia and the establishment of collateral circulation to improve myocardial ischemic tolerance, thereby reducing the occurrence of septal perforation.14 Pathophysiologic changes Coronary atherosclerosis leads to coronary artery stenosis, and if the lesion is limited and progresses slowly, an effective collateral circulation is established between the lesioned vessel and the adjacent coronary artery. The myocardium in the affected area can still receive adequate blood supply. If the lesion involves multiple vessels. Or the coronary blood supply is suddenly interrupted and the collateral circulation does not have time to be fully established. Then it can lead to severe myocardial ischemia and even myocardial infarction. A large number of neutrophils enter the necrotic area and release lytic enzymes after apoptosis, accelerating the destruction of the infarcted myocardium.15 Myocardial tissue in the lesion area is necrotic to the point of rupture, and myocardial contractile function is severely impaired, leading to cardiogenic shock and death.1,15 The size of septal perforation varies from a few millimeters to several centimeters, and is morphologically divided into simple and complex types. The simple type refers to the presence of a direct channel in the ventricular septum, with both sides of the perforation located at the same level of the ventricular septum. The composite type is an irregular tortuous channel in the septum, which often results in massive bleeding. In patients with anterior wall myocardial infarction resulting in septal rupture, it is often a simple type, located in the septum near the apex; in patients with inferior wall myocardial infarction, septal rupture is often a compound type, located in the posterior part of the septum, often accompanied by rupture of the papillary muscle1, 15. After acute myocardial infarction complicated by septal perforation occurs, the pressure step difference between the left and right ventricles causes blood to shunt from the left ventricle to the right ventricle, thus increasing the right ventricular volume load, which increases intrapulmonary blood flow and causes pulmonary stasis, and the left heart volume load can then be increased. With impaired ventricular systolic function, the antegrade flow of the body circulation is reduced, and compensatory constriction of the systemic small vessels occurs, increasing the resistance of the body circulation and contributing to a further increase in left-to-right shunt flow. When left heart failure occurs, due to the decrease in systolic pressure, the left-to-right shunt velocity can be decreased and the shunt flow is reduced accordingly.15 Diagnosis: The aura of septal perforation is mostly persistent or recurrent chest pain, nausea, and vomiting after myocardial infarction, and the electrocardiogram may show ST-segment elevation or depression, T-wave elevation or change from inverted to upright before rupture. Perforation of the ventricular septum may be followed by chest pain, dyspnea, right heart insufficiency, and cardiogenic shock. In the vast majority of patients, a rough and loud systolic murmur can be heard at the left border of the sternum, conduction to the fundus, apical and right border of the sternum, but it is difficult to distinguish from mitral valve insufficiency, for example. Due to heart failure, a gallop rhythm is often heard. Due to the increased pressure in the pulmonary circulation, it often causes an increased second heart sound in the pulmonary valve. In half of the patients, tremor may be palpable in the parasternal area. In cases of combined cardiogenic shock and low cardiac output, fibrillation is rarely palpable and murmurs are more difficult to detect due to reduced blood flow. In acute myocardial infarction combined with ventricular septal perforation, echocardiography not only shows results that are basically consistent with surgical or autopsy findings, but also provides a preliminary prognosis and is an important adjunct to the definitive diagnosis of ventricular septal perforation.9 Cardiac catheterization and ventriculography can be used to assist in the diagnosis and further clarify coronary lesions, but coronary angiography has the potential to further worsen the condition, so pre-surgical The use of coronary angiography before surgery is still controversial.5,16 Treatment: I. Conservative medical treatment: The main medical treatment is to maintain stable circulatory and respiratory function. Maintenance of circulatory stability includes the application of diuretics, vasodilators and positive inotropic drugs as well as adjuvant support such as intra-aortic balloon counterpulsation (IABP). Nitroprusside is recommended by the ACC/AHA because it not only reduces afterload but also allows precise intravenous drip delivery.17 Patients with hypotension often require positive inotropic drugs, yet the increased left ventricular pressure increases left-to-right fractional flow. Medications only temporarily stabilize the condition, and most patients will deteriorate and die soon. The maintenance of stable respiratory function includes: mask oxygenation, continuous positive airway pressure ventilation, bi-level positive airway pressure ventilation or intubation and other forms of mechanical ventilation therapy to improve the partial pressure of oxygen and oxygen saturation. Surgical treatment: Surgical method: In 1956, Cooley successfully repaired a case of ventricular septal perforation for 9 weeks after acute myocardial infarction for the first time.18 Since then, people have persistently explored surgical methods for the surgical treatment of ventricular septal perforation. The traditional surgical approach includes complete removal of necrotic tissue and reconstruction of the septum and right and left ventricles, a technique that has the disadvantage of increasing left and right ventricular insufficiency, which leads to a high operative mortality.19 Since 1987, a new classical technique of infarctexclusion has been applied, which does not remove the infarcted tissue, but rather uses a pericardial slice to connect the infarcted tissue to the left ventricle. Instead of removing the infarcted tissue, a pericardial slice is used to isolate the infarcted tissue from the left ventricular cavity. Since it does not damage the right ventricle and restores the geometry of the left ventricle, the operative mortality rate is reduced to 13.5%. Its surgical technique consists of incising the left ventricle parallel to and 1-50 px away from the anterior or posterior descending branches, suturing the allograft pericardial slice to the lower part of the septum of the noninfarcted myocardium and to the endocardium of the noninfarcted myocardium in the anterolateral wall of the left ventricle, thus isolating the infarcted myocardium from the left ventricle, and finally closing the left ventricular incision with 2 allograft pericardial slices or Teflon felt sheets. Applying this technique, they operated on 44 patients with postinfarction septal perforation, with 6 surgical deaths and a 6-year survival rate of 66% ± 7%, with only 1 residual shunt.20 Tabuchi et al. made a further reformation of the classic infarcted myocardial patent technique, the operative point of which was to close the septal perforation by suturing 1 smaller pericardial piece directly to the septum adjacent to the conventional pericardial piece The biologic adhesive was injected between the two slices to form a strong bond. They performed emergency repair procedures in a total of 9 patients within 24 hours of perforation, all of whom had no residual shunts, with 2 surgical deaths and the rest recovering well.21 Balkanay et al. began treating patients with posterior basal perforation with the double-patch technique, in which an incision is made in the left ventricle and 2 pericardial slices are placed on the right and left ventricular sides of the septum, respectively. They were fixed to the ventricular septum with the same suture. They reported a total of 4 patients within 1 week of perforation with no surgical death and no residual shunts.22 A doublepatchtechniqueandglue technique was tried, in which a double ventricular incision was made, the pericardial slices were placed in the right and left ventricles, and the pericardial slices were fixed with consecutive 4-0 sutures, and then biologic glue was applied between the pericardial slices to This technique was used to strengthen the necrotic septal tissue, reduce the incidence of septal reperforation, and thus reduce the operative mortality. Using this technique, they performed a total of 29 procedures with no recurrent perforations.23 However, any technique that applies bioadhesive has the theoretical potential for formaldehyde contamination of the circulatory system. Considering the technical difficulty of continuous suturing of the patch and the possibility of residual shunting with suture avulsion, HirotaniT et al. modified continuous suturing with 1 suture to interrupted suturing of the patch using multiple sutures and passing 1 or 2 sutures through the anterior papillary muscle at the posterior inferior edge of the patch. Using this method, they performed 9 procedures, and only 1 patient died of pneumonia postoperatively; the remaining patients were followed for an average of 4.8 years without cardiac events.24SiondalskiP et al. performed repairs for 5 patients with septal perforations located in the anterolateral apical region without the heart beating. With the support of IABP, they placed 2 Teflon felts on either side of the infarcted myocardium, passed interrupted spacer sutures through the Teflon felts sequentially, and knotted and tightened the sutures so that the infarcted myocardium, including the septal perforation, was left open. This procedure significantly shortened the operative time with no serious postoperative complications and a mean follow-up of 6 months, with 2 cases having moderate mitral valve insufficiency and no residual ventricular level shunts in all patients, achieving good results.25 Barker et al reported a case of anterolateral apical septal perforation in a 74-year-old woman 30 days post-infarction with uncontrollable cardiogenic shock, considering possible difficult to tolerate extracorporeal circulation, and with the support of IABP they closed the septal perforation by first passing the thread of 3 double-ended needles through the Teflon felt sheet, then entering the needle from below through the posterior aspect of the septum, then exiting the needle from the anterior aspect of the septum, and finally passing it through the other Teflon felt sheet and tying a knot to tighten and fold the left ventricular wall, the whole procedure being guided by esophageal ultrasound and cardiac surface ultrasound. 26 Massetti et al performed transventricular right atrial repair early (mean time from infarction to surgery 7.3 days) in 12 patients with inferior basal septal perforation; 3 died early and 1 late after the procedure, and the rest were followed up for a mean of 59 months, with only 1 patient presenting with a small residual shunt. They concluded that the transventricular approach may have complications such as bleeding and low cardiac output when the myocardial infarction is large, and that the transventricular approach may also be chosen when the infarction is mainly confined to the septum without ventricular wall tumor formation.27TokuiT also emphasized the importance of intraoperative use of esophageal ultrasound, which confirmed the high and posterior location of the septal perforation, thereby repairing the septal perforation via a right atrial incision with good results.28 Pitsis et al. performed surgery on a patient with a large hematoma in the anterior left ventricular wall and free right ventricular wall, and considering the high possibility of tearing the edematous tissue for direct repair of the perforation, they withheld surgical repair and installed a left ventricular assist device as a transition: it was led from the left atrium and drained through the descending aorta while evacuating the IABP, and 4 The perforation was repaired 4 days later, the left ventricular assist device was removed, the IABP was installed, and the IABP was withdrawn 3 days later; the patient was discharged 10 days after surgery and survived without residual shunts at 1 year follow-up.29Costache et al. performed a sealing procedure for a patient with an apical septal perforation, which failed to completely seal the perforation but significantly improved the patient’s clinical condition, and 10 days after sealing the perforation the patient The patient was reoperated and repaired successfully 10 days after the occlusion. This strategy of combined interventional occlusion and surgical repair may be an option: for patients with more severe disease, it may be possible to perform interventional occlusion first as a transition to delay surgery and reduce surgical mortality.30 Some patients may have residual shunts or new perforations after surgery. If the patient is asymptomatic and has a small shunt volume, conservative treatment can be considered, and if the patient develops heart failure, reoperation can be considered to improve the prognosis.5 Timing of surgery: It was previously believed that once a patient has an acute ventricular septal perforation with pulmonary edema and cardiogenic shock, and is still hemodynamically unstable after medical treatment and intra-aortic balloon counterpulsation, emergency surgery can be considered, but the surgical risk is high. The outcome of elective surgery for ventricular septal perforation is significantly improved compared to emergency surgery because the necrotic tissue around the ventricular septal perforation is already fibrotic at the time of elective surgery, while the patient’s hemodynamics are generally stable. However, the vast majority of patients are difficult to maintain to this stage by relying on drug therapy alone. Emergency surgery is now considered equally important even in hemodynamically stable patients. The ACC/AHA guidelines for the management of acute myocardial infarction are: unless the patient is unwilling to undergo surgery or surgery is contraindicated, patients with septal perforation should be treated with surgery. Patients with septal perforation should undergo emergency surgery unless they are unwilling to undergo surgery or are contraindicated.17 Preoperative coronary angiography: Because septal perforation in myocardial infarction quickly leads to right heart system failure and cardiogenic shock, surgery is required as soon as possible to save life, and preoperative coronary angiography may further worsen the condition, However, most scholars believe that for early recovery of cardiac function and reduction of late angina and infarction, preoperative coronary angiography should be performed to identify the location of the lesion, and coronary artery bypass grafting should be performed if the stenosis of the main coronary artery and its large branches is greater than 50% and the blood supply area is not the infarct area.12,16,17,23 According to Barker et al. Barker et al. concluded that simultaneous coronary artery bypass grafting improves midterm mortality in patients with ventricular septum.31 Prognosis: Skillington et al. reported survival rates of 80%, 76%, 71.1%, and 40% at 1 month, 1 year, 5 years, and 10 years, respectively, after surgical repair of ventricular septal perforation, and the main factors affecting early surgical mortality were related to inferior wall myocardial infarction, time from infarction to surgery of less than 1 week, cardiogenic shock, and age (>65 years).5 Daja et al. concluded that patients with preoperative combined cardiogenic shock and early onset of septal perforation after infarction had a poor prognosis.10 Lemery et al. reported that patients with preoperative combined cardiogenic shock had a poor prognosis.7 ParryG et al. concluded that particularly early surgical procedures had a higher mortality rate than procedures performed 48 hours after the onset of perforation, especially in patients with combined cardiogenic shock.32 David concluded that although there was no evidence of cardiogenic shock in patients with preoperative combined cardiogenic shock, there was no evidence of cardiogenic shock. David concluded that although cardiogenic shock is an important influence on operative mortality, it does not affect the long-term survival of operated patients.20 There are conflicting reports on whether the site of infarction or perforation is associated with operative mortality.10,32,33,34 Patients with high body circulating blood pressure have the best prognosis, and those with high right atrial pressure and low body circulating blood pressure have a poorer prognosis.35 Blanche et al. concluded that high right atrial pressure and preoperative application of IABP affect early mortality.36 However, preoperative use of IABP only reduces early surgical mortality but does not improve long-term prognosis.34 MantovaniV. et al. reviewed 50 patients with ventricular septal perforation who underwent surgery between 1983 and 2002 and concluded that emergency surgery and an interval of less than 3 days between septal perforation and surgery as univariate predictors of early death, with a 5-year survival rate of 76% excluding surgical death. The results were similar for different surgical techniques, with a poor short-term prognosis for emergency surgery but a fair long-term survival rate.37 Interventional occlusion: Interventional occlusion for ventricular septal perforation has been used in the past mainly for surgical repair of residual shunts or chronic ventricular septal perforation, and the procedure is essentially the same as that used for occlusion of membrane or muscle septal defects in congenital heart disease, but it has been reported in a small number of cases and lacks a large sample of prospective or retrospective studies. ThieleH et al. performed immediate occlusion in the acute phase in 29 patients with ventricular septal perforation, with a mean time from perforation to occlusion of 1 day, a 30-day survival rate of 35%, and a mean follow-up of 730 days, with a survival rate of 31%. As with surgical repair, the main factor influencing mortality is cardiogenic shock.38 Maltais et al. suggested that even incomplete occlusion may temporarily improve the patient’s circulatory status, providing time for fibrosis of the tissue surrounding the necrotic myocardium, leading to surgical repair.39 Problems: If the septal perforation is too large in diameter, more than 15 mm, surgical repair is preferable because the perforation is too large in diameter The diameter of the blocker should preferably be twice the size of the perforation or at least 10 mm larger than the diameter of the perforation.39 The location of the perforation is close to important structures such as the mitral and tricuspid valves, which may lead to mitral and/or tricuspid regurgitation; the blocker umbrella is not easily opened in the apical region or in the free wall of the left and right ventricles, which may even cause distortion of the ventricular wall structure; the tissue surrounding the perforation in the acute phase of the infarction Therefore, careful echocardiographic examination should be performed before blocking to clarify the location of the perforation and its relationship with the surrounding tissues, and it is best to perform it 2-6 weeks after myocardial infarction. In summary, the treatment of acute myocardial infarction combined with septal perforation mainly relies on surgery based on active medical comprehensive treatment. Transcatheter occlusion therapy, which has been gradually applied in clinical practice in recent years, is a new attempt, but further research is still needed.