Catheter ablation of atrial fibrillation (AF) is one of the most complex electrophysiological interventions, requiring a higher level of skill and risk than other arrhythmias. As the indications for catheter ablation of atrial fibrillation continue to broaden and catheter ablation procedures become more widely performed, previously unrecognized complications are gradually being reported. This chapter focuses on the occurrence and management of these complications. I. Overall assessment of the risks of catheter ablation of atrial fibrillation There are risks associated with all methods of catheter ablation of atrial fibrillation, and although the overall complications are high, the incidence of serious complications (e.g., death, pericardial compression, stroke, etc.) is relatively low. Currently, the major complications include vascular complications at the puncture site, cardiac compression, stroke, esophago-atrial fistula, pulmonary vein stenosis, and rapid atrial arrhythmias after ablation. The mean incidence of cerebrovascular events was 1.0%, symptomatic pulmonary vein stenosis was 0.9%, and atrial major fibrillation arrhythmias was 29.0%. In another multicenter study enrolling 1,049 patients with atrial fibrillation, a pooled analysis of complications showed a significant sinus bradycardia of 0.5%, cardiac tamponade of 1.2%, stroke or transient ischemia of 1.0%, phrenic nerve injury of 1.0% to 2.0% (up to 5.0% with ultrasound balloon application), and pulmonary vein stenosis of >50% with a rate of 2.7%. Cappato summarized the complications of catheter ablation of atrial fibrillation in a total of 8,745 cases from 100 home physiology centers worldwide between 1995 and 2002, with an overall complication rate of 5.9%, including a serious complication rate of 2.2% and a mortality rate of 0.05% (4/8,745), including 2 deaths due to massive cerebral infarction, 1 death due to myocardial perforation, and 1 death of unknown cause. The cause of death was unknown. Packer et al. summarized the incidence of complications associated with ablation of circumferential pulmonary vein catheters in a total of 6,442 cases at a single center in Milan (1996-2004): 0% mortality, 0.37% cardiac compression or pericardial exudate, 0.37% esophageal-pericardial leakage, and 0.37% cardiac compression. 0.37%, esophago-atrial fistula 0.01%, stroke 0.02%, transient ischemic attack 0.12%, severe pulmonary vein stenosis 0%, and left atrial tachycardia 5.99%, for an overall complication rate of 6.5%. More recently, results of 1,011 atrial fibrillation catheter ablations from a registry of 10 Italian electrophysiology centers showed a complication rate of 3.9%, including 1.2% peripheral vascular complications, 0.8% pericardial exudates treated conservatively, 0.6% cardiac tamponade, 0.5% cerebral embolism, and 0.4% severe pulmonary vein stenosis. Recently, Spragg summarized 641 consecutive complications of catheter ablation of atrial fibrillation performed at Hopkins Hospital in the United States from January 2001 to June 2007, with an overall complication rate of 5%. Although the complication rate decreased with increasing number of procedures, patient age and female were still independent predictors of major complications. The main methods of atrial fibrillation catheter ablation include focal ablation within the pulmonary veins, segmental ablation of the pulmonary veins, linear ablation of the circumferential pulmonary veins, and ablation of the circumferential pulmonary veins with electrical isolation and complex fracture potential of the atria. The incidence of pulmonary vein stenosis is higher for intra-pulmonary vein focal ablation and pulmonary vein segmental ablation, while the incidence of pulmonary vein stenosis is relatively low, generally between 0 and 3%, because the ablation line diameter of circumferential pulmonary vein linear ablation or electrical isolation is biased toward the pulmonary vein vestibule and relatively far from the pulmonary vein opening. A small sample size (168 cases) study comparing the incidence of pulmonary vein stenosis among the three ablation methods showed that the incidence of pulmonary vein stenosis was 9.0% for focal ablation in the pulmonary veins, 2.0% for segmental ablation of the pulmonary veins, and 1.9% for circumferential pulmonary vein ablation, suggesting that the incidence of pulmonary vein stenosis is gradually decreasing with the improvement of catheter ablation methods. This suggests that the incidence of pulmonary vein stenosis is gradually decreasing as catheter ablation methods improve. At this stage, the most widely used circumferential pulmonary vein ablation guided by the 3D scaler system is characterized by a high incidence of atrial tachyarrhythmias after ablation and the possibility of fatal esophageal-atrial fistula. The incidence of other AF catheter ablation-related complications did not differ significantly among the above ablation methods. Complications related to atrial fibrillation catheter ablation and management 1. Vascular complications Puncture-related vascular complications are the most common complications of atrial fibrillation catheter ablation, and hematoma is the most common. According to the national registry data led by Huang Congxin in China, the complication rate of ablation of atrial tachycardia and other arrhythmias in addition to atrial flutter in 40 hospitals in China between l998 and 2005 was 7.48%, of which 3.04% were subcutaneous hematomas, accounting for nearly 50% of the total complications. The incidence of serious vascular complications among 454 patients undergoing catheter ablation of atrial fibrillation in 2006 was 1.10% (1 giant inguinal hematoma; 2 pseudoaneurysms; 1 femoral arteriovenous fistula; 1 giant left chest wall hematoma). , and aortic coarctation 0.3% to l%, but the incidence of subcutaneous hematoma was not mentioned in this registry study. Atrial fibrillation catheter ablation generally punctures the femoral vein and subclavian vein, and an experienced operator can avoid injury to large, medium, and small arteries, but injury to tiny subcutaneous arteries depends on patient anatomical features and is almost independent of operating experience and cannot be avoided. In addition, intensive anticoagulation with low-molecular heparin combined with warfarin after catheter ablation of atrial fibrillation is an important medical cause of the significantly increased incidence of postoperative hematoma compared with other interventional procedures. Prevention of hematoma complications should be based on improving the level of puncture and should also include the following aspects: (1) reasonable puncture access: if a hematoma develops after puncturing the subclavian vein, it may face the difficult problem of not being able to be compressed to stop the bleeding, and puncture of the internal jugular vein may cause tracheal collapse or cardiac arrest due to compression of the carotid sinus by the hematoma if it causes a neck hematoma. Therefore, subclavian and internal jugular vein access should be used cautiously for atrial fibrillation ablation, especially in older, significantly wasted individuals. Placement of coronary sinus electrodes through the left femoral vein can reduce the risk of hematoma caused by improper choice of puncture access, because the latter puncture site can be compressed; (2) reasonable braking and reasonable compression: our experience is that after removal of the femoral vein sheath after atrial fibrillation catheter ablation should be compressed for sufficient time according to the method of femoral artery compression, and the puncture site should be wrapped with compression by elastic tape or bandage until 24 h postoperatively, and the (3) early detection and early treatment: the occurrence and development of hematoma has a certain regularity, early bleeding because of blood infiltration into the muscle space, at this time, only deep pain and gradually increased, and ultrasound examination without hematoma formation, if continue to strengthen anticoagulation therapy, huge hematoma is almost inevitable if intensive anticoagulation therapy is continued. Therefore, our experience is that if the patient has pain at the puncture site, then immediate compression bandaging with elastic bandage and appropriate reduction of anticoagulation according to the risk of thrombosis/bleeding can avoid the formation of huge hematoma; (4) reasonable anticoagulation: Morady’s laboratory experience shows that the incidence of postoperative 1mg/kg enoxaparin hematoma is intolerable and 0.5mg/kg dose is more appropriate. Recently, Cleveland’s experience has shown that starting warfarin 2 months before surgery, continuing to take it until postoperative and maintaining INR at 2,0-3,5 is significantly less complication than starting combined warfarin and low molecular heparin bleeding after surgery. Pulmonary vein stenosis Pulmonary vein stenosis is a recognized complication of AF ablation and is caused by thermal injury to pulmonary vein muscle tissue. Although the definite pathophysiological mechanism is not known, it has been shown in canine animals that a progressive vascular response leads to the replacement of necrotic myocardial tissue by collagenous tissue, mainly due to mistaken ablation in the pulmonary veins, followed by excessive RF energy and prolonged ablation time. Pulmonary vein stenosis is currently classified as mild (≤50% stenosis), moderate (50%-70%) and severe (≥70%) according to the degree of stenosis revealed by pulmonary venography, CT or MRI. Pulmonary stenosis presents with chest pain, dyspnea, cough, hemoptysis, secondary infections and clinical manifestations associated with pulmonary hypertension, with symptoms correlating with severity. However, due to compensatory dilatation of the ipsilateral pulmonary veins, sometimes the pulmonary veins are extremely stenosed or even completely occluded, and patients can also be asymptomatic, with asymptomatic pulmonary vein stenosis accounting for 40% to 50% of cases clinically. leite et al. reported that the factors affecting the occurrence of pulmonary vein stenosis include (1) focal ablation within the pulmonary veins; (2) the distance of ablation from the pulmonary vein orifice; (3) the application of ICE; (4) ablation temperature and energy; and (5) operator experience. This report noted that 203 patients at the center underwent pulmonary vein ablation with a total pulmonary vein stenosis incidence of 6.0%, but only 1 pulmonary vein stenosis occurred in the latter 100 ablated patients, suggesting that the learning curve is quite important. In a clinical study aimed at elucidating the clinical presentation, diagnosis, and treatment of symptomatic pulmonary vein stenosis in a larger sample, Packer et al [4] reported 23 cases of severe pulmonary vein stenosis (34 pulmonary veins in total), 52% of whom underwent 2 ablations and 22% of whom underwent 3 ablations due to recurrent atrial fibrillation. Clinical symptoms of pulmonary vein stenosis appeared within 1 to 3 months after the last ablation. The most common clinical symptom was dyspnea after activity (83%), followed by dyspnea at rest (30%), recurrent cough (39%), chest pain (26%), flu-like symptoms (13%), and hemoptysis (13%).CT, transesophageal echocardiography (TEE), and pulmonary isotope ventilation and perfusion scans as noninvasive tests were effective in confirming pulmonary vein stenosis, but different CT is the most effective test to identify the site and degree of stenosis, whereas TEE detects only 47% of stenotic pulmonary veins and biases the evaluation of stenosis in the right and left lower pulmonary veins. Ventilation abnormalities were seen in only 26% of stenotic pulmonary veins on isotope scan, whereas perfusion abnormalities were seen in all stenotic pulmonary veins and behaved similarly to pulmonary embolism. In addition, it is worth noting that there are late findings of pulmonary vein stenosis and the time to symptom onset varies widely, from early onset during ablation to 2-3 months after the procedure, or as late as 6 months after the procedure in some patients. The diagnosis was confirmed during 6- to 12-month follow-up, so strict clinical follow-up is necessary after catheter ablation of atrial fibrillation. The treatment of pulmonary vein stenosis lacks effective drugs to dilate the pulmonary veins, so interventional treatment is preferred for symptomatic pulmonary vein stenosis, including simple balloon dilation and bare/drug-coated stent placement. packer et al [4] reported immediate stenosis relief of 9,0% to 80,0% and pressure reduction of 3-12 mmHg after interventional pulmonary vein stenosis. in addition, pulmonary isotope ventilation perfusion scans suggested a relative increase in pulmonary perfusion of 4.0% to 9.0%. However, four complications occurred during the intervention, including transient ST-segment elevation, bleeding from a peripheral pulmonary vein perforation caused by the guiding wire, hemothorax due to left upper pulmonary vein rupture, and iliac artery embolism. At postoperative follow-up, 57% of patients developed symptomatic recurrence at (3.2±2.8) months, and 14/23 patients (61%) developed restenosis, with no difference in the incidence of stenosis between stenting and dilatation alone. After (18±12) months of follow-up, a total of 15/23 patients (65%) were completely free of pulmonary vein stenosis symptoms, including multiple interventions. In another study, 17 patients with symptomatic pulmonary vein stenosis diagnosed by CT and pulmonary perfusion examination who underwent stent intervention had intraoperative hemoptysis in 1 patient, self-limiting pulmonary hemorrhage in 1 patient, pulmonary vein tear in 1 patient, and cerebrovascular accident in 1 patient. At a mean follow-up of 43 weeks, 8/17 (47%) patients underwent reintervention for in-stent restenosis, and a total of 15/17 (88%) patients, including those who underwent reintervention, had asymptomatic recurrences. In addition, Arentz et al. showed that in patients with a single pulmonary vein stenosis, there were no or only mild symptoms and pulmonary hypertension at rest or during exercise was rare, and that patients with symptoms of pulmonary vein stenosis within 1 month after ablation were mostly relieved by the formation of collateral circulation, and the degree of pulmonary vein stenosis remained relatively stable at 12-24 months follow-up. Given that there is not yet an ideal treatment for pulmonary vein stenosis, efforts at this stage should focus on prevention, and the operator must identify the pulmonary vein orifice at the time of surgery to avoid ablation within the pulmonary vein. For patients who present with respiratory manifestations after pulmonary vein ablation, special attention should be paid to the possibility of pulmonary vein stenosis, and appropriate investigations should be performed if necessary. This is an extremely serious complication unique to atrial fibrillation ablation, and Doll et al. reported that during surgical radiofrequency ablation for atrial fibrillation, atrioventricular-esophageal fistula occurred in 4 of 387 patients, 3 of whom survived via esophageal sutures and 1 died due to massive air embolism. Pappone was the first to report an atrioventricular-esophageal fistula during catheter ablation of atrial fibrillation. A recent national survey conducted by Ghia et al. in the United States showed that 6 of 20 425 patients who underwent left atrial ablation developed an esophageal-atrial fistula (0.03%), all of whom suffered a stroke, 5 of whom died and 1 survived with hemiparesis. In all cases, the ablation energy was higher than that of patients who did not have a fistula. The five deaths were due to ablation of the circumferential pulmonary vein and the one survivor was due to ablation of the pulmonary vein orifice. One case has also been reported in China (conference communication). Currently, the probability of atrio-esophageal fistula with circumpulmonary vein ablation is very low, but due to its fatal consequences, it should be avoided by all means possible. Atrioventricular-esophageal fistulas usually present with high fever, convulsions, multiple cardio-vascular infarctions, and may be accompanied by massive vomiting of blood, or even coma and death. Once patients become symptomatic, progression is extremely rapid. Therefore, patients with persistent hyperthermia, pericarditis-like chest pain, and multiple embolic symptoms after AF ablation must be on high alert for the possibility of atrioventricular-esophageal fistula. Unexplained fever within 2-4 weeks after the procedure should be suspected regardless of whether it is accompanied by neurological symptoms. Transesophageal echocardiography and gastroscopy are contraindicated in patients with suspected atrio-esophageal fistula, as they may cause air embolism and worsen the condition or even sudden death. Chest-enhanced CT scans can be used as a confirmatory method and help to observe the presence of mediastinal pneumothorax, and other noninvasive tests such as MRI can help to determine the diagnosis. Although successful treatment of AV-esophageal fistulas with esophageal stents has been reported, most scholars believe that surgical intervention should be performed immediately once the diagnosis of AV-esophageal fistula is confirmed, and that anti-infective therapy alone is not useful for the ever-present air and bacterial emboli. To prevent the development of AV-esophageal fistula, Pappone et al. suggested that the left posterior atrial wall ablation line should be shifted to the left atrial apex, and that the ablation temperature and energy should be controlled. However, recent reports have shown that the esophagus and the posterior wall of the left atrium are in close proximity and often coincide with the ablation site, and their relative positions are highly variable, making it difficult to design an ablation line that effectively avoids the esophagus. Another study enrolling 8l patients further pointed out that ablation at the posterior wall of the left atrium near the esophagus can significantly increase the intraluminal temperature of the esophagus, and the relative position of the esophagus and the left atrium is highly variable, which makes it difficult to design a uniform ablation pattern that avoids the esophagus and may cause a decrease in the ablation success rate. The level of RF energy is not an independent factor influencing the intraesophageal temperature. However, the local production of microbubbles suggests a significant increase in esophageal temperature. This author suggested that RF energy should be strictly controlled by continuous esophageal temperature monitoring during ablation and based on the observation of the presence or absence of microbubbles to effectively reduce the generation of atrio-esophageal fistula. Recently, Sherzer et al. reported the use of an opaque marker electrode placed in the esophagus as an esophageal marker, which could alert the ablation operator to avoid high-energy, prolonged ablation at the esophageal alignment site. Tsuchiya et al. used a cold water-filled esophageal balloon to effectively reduce esophageal temperature during ablation, which could theoretically reduce the probability of atrioventricular-esophageal fistula. Intra-cardiac ultrasound can help to locate the esophagus in real time during ablation, which can help to ablate the posterior wall of the left atrium and reduce the number of esophageal-atrial fistulas. In summary, to prevent damage caused by high esophageal temperature, it is recommended to: (1) control RF energy and temperature; (2) monitor microbubble formation by intracardiac ultrasound; (3) continuously monitor esophageal temperature; (4) clarify esophageal location by barium swallow and esophageal electrode positioning; (5) apply postoperative acid-suppressing and protective drugs for gastric and esophageal mucosa, and avoid hard food; (6) consider cryoablation if necessary, etc. (6) if necessary, cryoablation can be considered to effectively avoid the creation of atrioventricular-esophageal fistula. In addition, the recent analysis of atrial-tracheal anatomical relationship by Professor Chen Shih-an from Taiwan has theoretically reminded that attention should be paid to prevent the occurrence of atrial-tracheal fistula during the ablation of atrial fibrillation. 4. Atrial tachycardia after ablation The incidence of atrial tachycardia (AT) after the first AF ablation has been reported differently in the literature, ranging from 5% to 25%, with some AT recovering on its own 3 to 6 months after the procedure. Studies on the mechanism of early recurrence after atrial fibrillation ablation are rare, and the current literature speculates that the mechanism is mainly related to atrial myocyte edema, inflammatory response, inhomogeneous atrial myocyte nonphase, and imbalance of cardiac autonomic function in the early post-ablation period. In addition, atrial reverse remodeling after atrial fibrillation ablation requires a process, so the early recurrence may be transient and may gradually decrease and disappear with longer follow-up time. However, this is only a theoretical inference and lacks the basis of objective electrophysiological studies. Although some scholars have suggested otherwise, most of them and our center also believe that the recurrence of atrial arrhythmia after ablation is related to the recovery of electrical conduction in the pulmonary veins. jais et al. reported 12/74 patients (16%) with regular atrial tachycardia after linear ablation of pulmonary veins, and AT was found to be related to the ablation line or the recovery of local potentials in the pulmonary veins during reablation. ouyang et al. reported also supported the above The view that ATa occurred in 29 patients (29,0%) after circumferential pulmonary vein ablation, 26 of whom underwent reablation, of whom 2l (81,0%) had pulmonary vein conduction recovery (9 in the right pulmonary vein and l6 in the left pulmonary vein), and another 7 volunteers without recurrence after circumferential pulmonary vein ablation underwent re-electrophysiological examination, the results of which suggested that none of them had pulmonary vein conduction recovery, so Pappone et al. reported that the incidence of postoperative rapid atrial arrhythmias ranged from 3.9% to 10.0%, and 82% of AT was related to the “Gap” on the ablation line, and its distribution was most frequent in the right pulmonary vein septum and between the left superior pulmonary vein and the left auricle. The authors also pointed out that the postoperative atrial tachycardia could be effectively terminated by increasing the line between the pulmonary veins of the posterior wall of the left atrium and the ablation line of the mitral isthmus, and later added in the report that the ablation line of the mitral isthmus only needs to achieve a conduction delay of 120 ms to prevent the occurrence of left atrial tachycardia without achieving complete conduction block. 5. Embolism The complication of atrial fibrillation ablation-related embolism is one of the serious complications of atrial fibrillation catheter ablation. The causes of embolism can be classified as intrathecal thrombus, ablation catheter-attached thrombus, ablation-induced crust, original atrial appendage thrombus, and air embolism, with an incidence of approximately 0% to 7%. In almost all clinical studies, ablation-related embolism is reported to occur 24 hours after ablation, but 2 weeks after the procedure is also a high-risk period for embolism. The incidence of embolism in our center in 2006 was 0.09% (4/454) (1 embolism in the left thalamus due to crust detachment, 1 embolism in the mesenteric artery, 1 transient ischemic attack, and 1 embolism in the left internal capsule). Intra-cardiac ultrasound monitoring revealed that in the anticoagulated state with activated clotting time (ACT) >250s, wall-attached thrombus formation was still seen in 24/232 cases (10,3%) on the ablation catheter and sheath, suggesting that we should not take the risk of thromboembolism lightly. Several studies have shown that intravenous application of heparin to maintain ACT above 300-400s and maintaining a high flow of heparin (180 ml/h) drip through the septal sheath can significantly reduce the occurrence of left atrial thrombosis and embolic events. To reduce this complication, anticoagulation therapy should be administered preoperatively, intraoperatively, and postoperatively. For patients with persistent AF, preoperative oral warfarin for 1 month to keep INR at 2,0 to 3,0 and subcutaneous injection of low molecular heparin for 1 week after admission; for patients with paroxysmal AF with episode duration less than 48h, only subcutaneous injection of low molecular heparin for 1 week after admission; if duration is greater than 48h, treatment is the same as for persistent AF, 1 to 2 days before surgery for all patients (not more than 3 days earlier) Transesophageal echocardiography is performed to exclude atrial and left ear thrombus. Intraoperative heparinization should be adequate. 75-100 U/Kg of heparin should be applied at the beginning of surgery according to body weight, and additional 1 O00 U every hour thereafter (when ACT is not measured), and intraoperative ACT testing is desirable to determine the intraoperative heparin application according to ACT. Intraoperative ablation catheter or marker electrode withdrawal from the sheath should pay attention to the aspiration of at least 5 ml of blood from the valve on the outside of the sheath and observe whether there is thrombus in the aspirated fluid. Subcutaneous injection of low-molecular heparin for 3-5 days after the operation, and oral warfarin at the same time, and follow up the INR until it reaches the standard. Air embolism can occur during catheter ablation of atrial fibrillation, mostly related to careless intraoperative handling, but may also be caused by negative aspiration due to rapid catheter withdrawal. Air embolism can obstruct the coronary arteries (mostly the right coronary artery) and intracranial vessels, causing acute coronary ischemia and/or atrioventricular block and neurological related symptoms. Since the complication of air embolism is obviously related to the operator’s operation, the operator should be aware of this complication. During pulmonary venography, care should be taken not to inject air bubbles into the sheath, not to remove the catheter from the sheath too fast, and to suction the blood sufficiently. If the patient has cerebral embolism caused by air embolism, the patient should be put in head-down position, high-flow oxygenation, and if necessary, hyperbaric oxygen therapy. If coronary artery air embolism occurs, if it is transient, no treatment is needed, but if the symptoms persist or progressively worsen, the femoral artery should be punctured urgently, and a coronary angiographic catheter should be sent to the coronary artery with air embolism, and blood should be repeatedly pumped and pushed to flush the air embolism to the distal coronary artery as far as possible. 6, phrenic nerve palsy Phrenic nerve injury is a reversible complication of ablation of atrial fibrillation, with an incidence of about 0% to 0, 48%, and right phrenic nerve injury is more common during ultrasound balloon ablation. Currently, thermal injury is the most widely accepted mechanism for phrenic nerve palsy. For example, the right phrenic nerve is close to the superior vena cava and right superior pulmonary vein and passes through the posterior free wall of the right atrium, which makes it vulnerable to right phrenic nerve injury; the left phrenic nerve is close to the great cardiac vein, the left auricle, and the free wall of the left ventricle, all of which can be injured by ablation. In addition, ablation energy is also closely related to phrenic nerve injury. Compared with radiofrequency energy, microwaves have a theoretical higher risk of phrenic nerve injury, whereas cryo- and ultrasound seem to reduce the potential risk of phrenic nerve injury, but in practice, both cryo- and ultrasound have been reported to cause phrenic nerve injury when performing pulmonary vein isolation. Although the incidence of phrenic nerve palsy is low, it should still be of high concern to the operator because permanent phrenic nerve palsy can lead to persistent shortness of breath, cough, eruption, pulmonary atelectasis, pleural effusion, and chest pain. Intraoperatively, especially when ablating the anterior wall of the two upper pulmonary veins, attention should be paid to X-ray fluoroscopy to check the condition of the diaphragm, and the diaphragm movement should be observed under X-ray during discharge, and the discharge should be stopped as soon as the diaphragm movement disappears. Some foreign scholars, before ablation of the relevant parts, identify the position of the phrenic nerve by pacing stimulation with or without diaphragm contraction, thus reducing the occurrence of complications of phrenic nerve paralysis. In general, phrenic nerve function is restored within 1 day to 1 year, and a few patients are left with permanent phrenic nerve injury for which there is no effective treatment. In terms of clinical presentation, phrenic nerve injury can be missed without any symptoms, can be completely or partially healed, or can manifest as severe pulmonary insufficiency that necessitates dependence on a ventilator; therefore, phrenic nerve injury should be considered as one of the differential diagnoses when encountering patients with postoperative respiratory distress. At the same time, clinical healing (asymptomatic) does not mean complete recovery of the phrenic nerve, especially since diaphragmatic activity directly affects pulmonary ventilation, with unpredictable effects on physical activity and quality of life years later. Therefore, it is necessary to follow up patients with suspected phrenic nerve injury with postoperative x-ray examinations. Cardiac compression is a serious complication of atrial fibrillation ablation. A report by Mayo Clinic showed that cardiac compression occurred in 15 cases (2 or 4%) of 632 cases of atrial fibrillation ablation, and 2 cases required open-heart repair. The management of cardiac tamponade is based on timely detection, and it is not life-threatening to repair the tamponade by puncture and drainage or open-chest repair if necessary. The occurrence of cardiac tamponade is usually associated with excessive intracardiac catheterization, ablation, two or more punctures of the atrial septum, and heparin anticoagulation. Pericardial tamponade due to cardiac rupture is associated with high local temperature and a bursting sound (“pop” sound) during ablation or is the result of direct mechanical injury, particularly if the atrial septum is punctured too far anteriorly (aortic root) or too far posteriorly (posterior wall of the right atrium). A typical pericardial tamponade may manifest as the Beck’s triad of decreased blood pressure, jugular venous anger, and distant heart sounds, with dyspnea, irritability, confusion, or loss of consciousness. However, sometimes the presentation is insidious, with a slow or even no drop in blood pressure (organism compensation or rehydration), which is easily missed, followed by a sudden drop. loss of cardiac shadow pulsation and appearance of translucent bands on X-ray, and echocardiography can confirm the diagnosis. The operator needs to be highly vigilant and record the cardiac shadow beats before puncturing the atrial septum. After the puncture needle breaks through, the contrast agent should be gently pushed to confirm the entry into the left atrium before pushing the outer sheath tube. After the catheter enters the left atrium via the interatrial septum, care should be taken to identify the left auricle according to the potential and image position of the ablation catheter to prevent perforation of the left auricle. The blood pressure and heart rate should be closely monitored during the procedure and for 24 hours after the procedure, and once a decrease in blood pressure or an increase in heart rate is detected, a fluoroscopic cardiac image or an echocardiogram should be performed immediately, and if acute cardiac compression is identified, pericardial puncture and drainage should be performed immediately under fluoroscopic or ultrasound guidance, and the pigtail catheter should be retained for 24 h after drainage is completed and stabilized. Although open-heart surgery can be avoided in most cases with this measure, close coordination with cardiac surgery is essential because of the lack of contractility of the left auricle, the difficulty of self-closing the perforation, and the fact that a few atrial perforations bleed more than once for anticoagulation reasons. It is worth noting that some patients have postoperative pericardial reactive exudate, which may be accompanied by chest pain, dyspnea, fever and elevated leukocytes, which is related to the inflammation of pericardium caused by radiofrequency energy through myocardium during ablation. If the blood pressure is stable and there is no acute blood loss, it is not necessary to perform pericardiocentesis and drainage urgently, apply corticosteroids for a short time, observe the vital signs closely, follow up the amount of pericardial fluid with echocardiography, and perform pericardiocentesis and drainage again if necessary. 8. Acute coronary artery injury Because some ablation strategies for chronic atrial fibrillation require linear ablation of the mitral isthmus, or even ablation in the coronary sinus, this increases the risk of injury to the gyral branch of the coronary artery. Haissaguerre recommends reducing the ablation energy if ablation is performed in the coronary sinus and performing percutaneous transluminal coronary angioplasty if the coronary artery is severely stenosed or occluded. 9.Post myocardial injury syndrome Catheter ablation for supraventricular arrhythmias has long been reported to cause “post cardiac injury syndrome”. Clinical symptoms may include fever, dyspnea, hypoxemia, hypotension, pericardial exudate, pleural exudate, increased hematocrit, and elevated white blood cells, etc. The diagnosis requires exclusion of pulmonary embolism, pneumonia, heart failure, and pulmonary vein stenosis. The etiology may be related to the expression of anti-myocardial antibodies caused by autoimmune reactions, so non-steroidal anti-inflammatory drugs as well as glucocorticoid therapy are effective. Early reported symptoms occur mostly within 1 week to several weeks after intervention, and later case reports are also seen in the immediate and early postoperative stages. 10, Acute pulmonary edema Catheter ablation for atrial fibrillation can cause myocardial damage and myocardial edema, most of the cases reported by Okada had left atrial edema until about 1 month, and Steel et al. reported a case of severe left atrial edema until 2 months after the procedure, and the mechanical depression of the left atrium caused by left atrial edema led to congestive heart failure. 2008 Weber reported 4 cases of atrial fibrillation after circumferential pulmonary vein ablation Acute pulmonary edema occurred 18 to 48 hours after atrial fibrillation circumferential pulmonary vein ablation, manifesting as dyspnea, bilateral pulmonary edema, and systemic inflammatory response (fever, elevated leukocytes and C-reactive protein). All patients were excluded from pulmonary vein stenosis, acute lung injury, left ventricular dysfunction, circulatory failure, and infection, and all symptoms resolved 3 to 4 days after symptomatic supportive therapy was given, and the authors concluded that the mechanism was “non-infectious systemic inflammatory response syndrome” (SIRS). Among more than 1,000 cases of catheter ablation of atrial fibrillation with normal preoperative cardiac function in our center in the past 2 years, we also found 12 cases of acute heart failure episodes within 48 hours after ablation, 9 cases in men and 3 cases in women, 11 cases of chronic atrial fibrillation and 1 case of paroxysmal atrial fibrillation. The clinical manifestations were shortness of breath in 12 cases (100%), seated breathing in 8 cases (67%), severe chest pain in 2 cases (17%), fever in 6 cases (37,5°C-38,5°C) (50%), wet rales in the lungs in 12 cases (100%), increased ventricular rate in 12 cases (100%), hypotension in 1 case (8%), pleural effusion in 3 cases (25%), pulmonary edema changes in 4 cases (33%), and a small amount of pericardium. （The left ventricular ejection fraction was 59.6±3.2%, and the white blood cell count was greater than 10.0×109/L in 7 cases (58%). All patients disappeared clinically within 2-7 d after treatment with diuresis, oxygen, and glucocorticoids. Unlike PCIS, Weber and all cases in this group had obvious symptoms of acute pulmonary edema as well as chest radiograph features. Although the left atrial edema caused by extensive ablative destruction of left atrial tissue may be one of the reasons for the occurrence of pulmonary edema in this group of cases, the exact mechanism is not clear. The authors speculate that this may be related to peri-esophageal vagal nerve injury caused by ablation of the posterior wall of the left atrium, and the treatment of this complication includes pyloric dilation and local injection of botulinum toxin. More recently, Schmidt et al. performed esophageal endoscopy in 28 patients undergoing catheter ablation of atrial fibrillation within 24 hours of performing the ablation. 47% of the patients showed changes in the esophageal wall, 29% showed erythema, and 18% showed necrosis and ulcer-like changes. Patients showed reflux-like symptoms coinciding with changes in the esophageal wall, and this injury was usually fully recovered with the application of proton pump inhibitors for 2 to 4 weeks after ablation. The indications for atrial fibrillation catheter ablation have also been broadened to include patients with atrial fibrillation after valve replacement, and because atrial fibrillation catheter ablation requires calibration and ablation in the left atrium, there is a possibility of calibration electrodes or ablation catheter jamming. Although the authors were lucky to free the electrode, they must be prepared for emergency chest opening if they encounter such complications. In 2005, Ong reported a patient with intermittent sinus arrest during superior vena cava isolation, suggesting a transient impairment of sinus node function. 2006, Risius reported 4 patients with transient ST-segment elevation during atrial fibrillation ablation. In 2007, Zoppo reported a case of third-degree atrioventricular block during further ablation of left atrial flutter during ablation of atrial fibrillation. In 2008, Hoestje reported a case of right ureteral injury caused by catheter sheathing of atrial fibrillation, which resulted in the implantation of a ureteral stent. 2008, Ahsan reported a case of restrictive pericarditis caused by catheter ablation of atrial fibrillation, which was relieved by pericardial dissection. In conclusion, the technique of atrial fibrillation catheter ablation is relatively complex and requires a high level of operator experience. Understanding the various potential complications and risk factors of atrial fibrillation ablation and formulating reasonable preventive measures can improve the safety of ablation. It is believed that the safety of atrial fibrillation catheter ablation will be improved with the gradual accumulation of operator experience and the continuous updating of technology and equipment in the future.