Prevention and treatment of complications of interventional treatment of giant atrial septal defect With the development of interventional technology, interventional treatment of atrial septal defect (ASD) has become a mature treatment method, but serious complications may still occur in the treatment of giant ASD. For this reason, this paper analyzes the causes of complications arising from the treatment of giant ASD and its prevention and control measures. The incidence of blocker dislodgement is one of the serious complications of ASD occlusion, which is reported in the literature as 0.24%-1.44%, mostly seen in giant ASD. It is often due to the small size of the blocker, special anatomical site of the lesion, improper operation or the quality of the device itself. Preventive and curative measures: In addition to the standardized operation, attention should be paid to the treatment of giant ASD mediators: ① Accurate measurement of the diameter of each surface of ASD: Generally speaking, the selection of ASD blocker mainly depends on the maximum diameter of ASD, but for giant ASD, in addition to the maximum diameter of ASD, the size of other diameters should be referred to. The possibility of successful blocking is small. In this way, it is best to measure the size of the defect on each side to form a spatial stereoscopic image. On the other hand, it is difficult to measure the extension diameter of a giant ASD balloon, and it is mainly dependent on echocardiography to measure its size. ② Pay attention to the marginal condition of ASD, especially it is easy to mistake mixed ASD or inferior chamber type ASD as central type and perform interposition treatment, and finally the blocker is dislodged. The authors have summarized 37 cases of giant ASD, 31 of which had deficient margins, 12 of which had deficient anterior marginal diameters, and 19 of which had deficient anterior marginal diameters, posterior marginal diameters, or both combined with deficient inferior vena cava margins. Insufficient anterior border diameter alone is not a contraindication to interposition therapy, but if combined with insufficient posterior border diameter, careful echocardiographic examination must be performed to prevent lateral inferior vena cava margins. The inferior vena cava side without a margin is bound to dislodge if the blocker is released during interposition therapy. On the other hand, if there is insufficient margin on the inferior vena cava side, even if it is partially borderless but occupies a small angle (less than 30 degrees), it can be successfully interposed if the blocker is selected appropriately. The maximum diameter of Amplatzer ASD blocker is 40mm, and the diameter of the blocker of domestic special blocker is 42~46mm, which is the largest blocker in the world for treating ASD through cardiac catheterization, and the left atrial diameter of the blocker is larger than 8mm of waist diameter. The huge blocker should have sufficient hardness and good resilience, otherwise the blocker will also fall off. We found that the same size blocker with too soft hardness cannot block the giant ASD, and the edge of ASD should be considered when choosing the blocker, if the edge of ASD is not enough, a slightly larger blocker should be chosen accordingly. Various types of foreign body clamps should be available for those who are able to do so. Once the blocker is dislodged, the choice of foreign body clamp grasping or surgical treatment is based on the dislodged site, type and size of blocker and patient condition. Generally, if the blocker is small or the embolization site has not yet caused significant abnormalities in vital signs, foreign body forceps can be attempted first. If unsuccessful or if the blockage is in an important organ, emergency surgery should be performed to avoid delaying the disease and causing serious adverse consequences or even death. In case of huge ASD blocker dislodgement, due to the thick sheath needed for foreign body clamp to grasp the blocker (especially for domestic blocker), sometimes more emergency surgery is performed. Second, the incidence of cardiac pressure blockage ASD blockage is 0.12% to 0.47%. Most of them occur in the early stage of interventional therapy, which is related to the lack of experience of the operator in interventional therapy, unfamiliarity with cardiac X-ray anatomy or improper operation. Cardiac tamponade is most often seen in the left auricle, which is so fragile that even the slightest touch of a cardiac catheter or guidewire can cause perforation of the auricle. The normal left auricle is adjacent to the left superior pulmonary vein, and under fluoroscopy, a catheter or guidewire located in the left auricle can easily be mistaken for being in the pulmonary vein, increasing the chance of perforating the left auricle (see Figure 1). If perforation occurs during catheter manipulation, the patient remains stable due to the sheath closure, and once the transfer sheath is removed, pericardial effusion and pericardial tamponade can occur. If not detected and treated in time, serious consequences will occur. The diameter of the left atrial umbrella of the oversized blocker is often larger than the transverse diameter of the left atrium, and the left atrial umbrella is easily positioned vertically with the atrial septum when the blocker is released. Preventive measures: The operation should be gentle, especially when the guidewire and catheter are trying to enter the left upper pulmonary vein, it must be judged accurately and must not injure the left auricle. To avoid perforation of the left auricle, it is best to deliver the catheter or guidewire under fluoroscopy and withdraw it if resistance is encountered, even if a small resistance is encountered, and rotate the catheter clockwise when re-entering so that its tip points to the posterior pulmonary vein opening. If the catheter is found to beat with the atrial systole and diastolic cycle; and atrial premature beats, and the atrial premature beats disappear after withdrawing the catheter, it often suggests that the catheter is in the cardiac ear rather than in the pulmonary veins. This is because the pulmonary vein is a fairly fixed structure compared to the heart ear. If great care is taken during the procedure and attention is paid to these details, most complications will be avoided. Once atrial perforation has occurred, the most important thing is to stop the progression of the effusion before cardiac tamponade occurs and to monitor the condition closely. Atrioventricular conduction block is rare during or after ASD block. Hill et al. suggested that the mechanism of AVB in mediated block ASD is due to compression of the AV node by the umbrella disc of the blocker or friction of the AV node and its surrounding tissues, resulting in temporary edema of the tissue, leading to AV node dysfunction or hypofunction. A few patients were found to have varying degrees of AVB (including }I? AVB ) after blocking, while all patients who developed AVB had complete normalization of AVB after 1-6 months.Hill et al. reported one case of Ill? AVB after ASD blocking, which was later implanted with permanent AVB. AVB, which was later implanted with a permanent pacemaker. In the seven cases of AVB after ASD, the implanted blockers were all 38 mm or more. three cases of 4-8 year old children were implanted with blockers of 22-28 mm, which were obviously too large for the size of the heart chambers of young children. one case of a 15 year old adolescent was implanted with a 34 mm blocker, which was also too large for the size of the underdeveloped heart chambers. In one 7-year-old child, a 26 mm blocker was implanted and a type II AVB developed. Suda K et al. suggested that patients with a blocker size to height ratio greater than 0.18 are more likely to have AVB after blocker implantation. Preventive measures: The diameter of the blocker should not be too large, and once a third degree AV block occurs, in addition to the application of hormones, vitamin C and myocardial nutrients should be used, and a temporary pacemaker should be implanted as appropriate. If there is no recovery after the above treatment, special care should be taken to withdraw the blocker during the insurance period. Coronary artery air embolism is usually due to incomplete venting of the catheter and delivery sheath or the pushing of the blocker with gas, especially the domestic delivery sheath, the short sheath leak-proof cap is often not sealed well and easy to enter the gas; when the huge ASD is blocked, the 14F sheath is needed, and the domestic sheath is often mismatched. In some cases, it is difficult to push the sheath into the 14F delivery sheath, and some physicians use their hands to squeeze the blocker and send it directly into the 14F delivery sheath, which is impossible to ventilate. In addition, the patient is in the supine position during the operation, and the opening of the right coronary artery is facing upward. The clinical manifestations are sudden chest pain, chest tightness, slowed heart rate, marked ST-segment elevation in ECG II, III, aVF leads, and slowed heart rate. Echocardiography reveals bubble echoes in the left atrial chamber. In addition, air bubbles can embolize the cerebral vessels and cause altered consciousness, which can recover on its own if the amount of air is small. Preventive and curative measures:The key is to avoid the occurrence by strict operating procedures. The gas in the catheter and delivery sheath should be completely drained during the operation, and the blocker should be placed in saline containing heparin to fully soak and exhaust before being sent into the body. After pushing the blocker into the delivery sheath, open the valve on the side of the short sheath to let the blood flow back naturally and then push the blocker. After coronary air embolism has occurred, oxygen should be administered immediately. The patient can cough hard and use atropine and vasodilators as appropriate, and the symptoms can be relieved after 10 minutes or so. V. Valvular insufficiency Long-term left-to-right shunt, right ventricular dilatation and tricuspid annulus enlargement often lead to functional tricuspid insufficiency. Increased right heart load also causes mitral valve prolapse, the incidence of which increases with the age of the patient, generally about 10%-20%. The incidence of tricuspid valve incompetence can be gradually reduced or disappeared with the recovery of cardiac function after intervening treatment. After ASD closure, the left ventricular end-diastolic volume increases, the valve closure plane changes, and most mitral valve incompetence can be self-corrected or reduced to varying degrees. However, mitral valve insufficiency also occurs after ASD closure, especially after giant ASD closure. This is mainly because the edge of the septal defect is close to the mitral valve, and the edge of the left atrial side of the blocker affects the closure of the mitral valve or causes mitral valve perforation by mechanical abrasion. Preventive and curative measures: Before releasing the blocker, careful observation by echocardiography should be made to see if the edge of the blocker touches the mitral valve and affects its function. Sixth, the blocker offload is mainly due to the quality of the device itself, individual improper operation can also cause this. In huge ASD, even if a 14F delivery sheath is selected, it often happens that the domestic blocker has difficulty in pushing from the short sheath to the long delivery sheath, and if the force or operation is improper, it may cause the blocker to be partially or completely offloaded. The authors had encountered a case of giant ASD with a 42 mm blocker that was too small, and difficulties occurred in retrieving the blocker to the delivery sheath of 14F, and only the right disc umbrella, lumbar and left disc were partially retrieved to the sheath, and finally the delivery sheath was retracted to the femoral vein. After successful placement of another 44 mm blocker from the contralateral femoral vein, the 42 mm blocker was surgically removed. Preventive measures:A larger delivery sheath should be selected, and intraoperative pushing of the blocker should be avoided to avoid rotational movements to avoid offloading. Once the blocker is offloaded, foreign body clamp can be used to remove it or surgical treatment as appropriate. Atrial arrhythmias are often combined with atrial arrhythmias in ASD, and anticoagulation therapy should be strengthened in the case of combined atrial fibrillation. In preoperative combined atrial fibrillation, it is necessary to know whether there is thrombus in the atrium. Interventional treatment itself does not make atrial fibrillation disappear, but after treatment, with the recovery of heart size, it is possible to make atrial fibrillation resume. Atrial arrhythmias often appear in the early postoperative period of giant ASD, which may be related to the blocker being too large, the blocker not being completely fixed and rubbing against the atrial septum during the heartbeat, and may disappear after about 1-2m postoperatively, and drug treatment is needed for frequent occurrences. Inadequate surface endothelialization after implantation of the blocker is a rare complication of distant residual shunt. After blocker implantation, the process of endothelial cells growing on the surface of blocker device and covering the device is called endothelialization. Evidence on endothelialization after blocker implantation comes from animal studies, and it is generally believed that the blocker surface is completely endothelialized by 3-6 months of blocker implantation. Thus, theoretically, it is not possible to have a late residual shunt in the blocker. The most direct evidence of this phenomenon is that in cases of late residual shunts in the blocker, when the blocker was removed to close the defect, the endocardium on the blocker surface was found to be distributed in an “island” pattern, indicating the presence of incomplete endothelialization on the blocker surface. Recently, Slesnick reported a case of late onset infective endocarditis combined with endothelial insufficiency of the blocker after atrial septal defect closure. The child, a 4-year-old girl, was implanted with a 22-mm-sized Amplatzer septal sealer for a secondary foramen ovale septal defect, mild mitral valve prolapse, and trace mitral regurgitation. After surgery for infective endocarditis in December, the septal sealer was found to be only partially endothelialized. The reason for the incomplete endothelial coverage on the surface of the blocker is unknown, but the selection of a large blocker was a major factor. In huge ASD, to prevent blocker dislodgement, some scholars choose blockers too large, which is more likely to have incomplete endothelialization of blocker surface, resulting in distant residual shunt and even infective endocarditis, etc. Prevention and treatment measures:The key is prevention and choosing the right size of blocker. If residual shunts occur, the blocker may be surgically removed and the ASD repaired;,ix. thromboembolism before the completion of endothelialization, the exposure of blocker metal and fibrous material to the atria may lead to activation of the coagulation system and platelets. Clinical studies have also confirmed the early postoperative activation of the coagulation system monitored after Amplatzer blocker implantation. It is generally accepted that the incidence of thrombosis after mediated occlusion of the atrial septum and patent foramen ovale is between 0% and 10.5%. If the blocker selection is large or endothelialization is incomplete during blocking of giant ASD, there is a risk of thrombus formation on the blocker surface, and thrombus formation on the blocker surface in the left atrium can cause systemic thromboembolism, such as peripheral artery embolism and retinal artery embolism. chessa et al. reported one case occurring 1. 5 years after surgery. If a thrombus forms at the disc of the right atrium, it can cause pulmonary embolism. Preventive measures:Intraoperative and postoperative application of heparin anticoagulation and application of antiplatelet drugs can reduce the complications of thromboembolism. Whether to routinely apply warfarin anticoagulation to prevent thrombosis after sealing of large diameter atrial septal defects is a topic worth studying. It has been suggested that:after giant ASD sealing, aspirin (81 to 325 mg/day, or 3 to 5 mg/kg/day) can be used in combination with clopidogrel (75 mg/day) for 6 to 8 weeks, followed by continued use of aspirin for 4 to 8 months. Warfarin was only used in combination if the patient was at high risk for coexisting thromboembolism such as atrial fibrillation, a history of thromboembolism, or already had thrombosis.