Currently, implantable cardioverter-defibrillators (ICDs) are the primary treatment for preventing sudden cardiac death (SCD) from ventricular tachycardia/ventricular fibrillation (VT/VF). However, ICD can only terminate VT/VF, but not prevent it from occurring. It has no effect on the cause of the arrhythmia and myocardial lesions, and may even continue to progress and cause VT events or an increase in new VT/VF. Currently, catheter ablation is an important treatment for VT. Catheter ablation can terminate or reduce recurrent VT episodes and prevent recurrent persistent VT events, as well as reduce ICD discharge, and is an effective method for controlling ventricular tachycardia. Studies in recent years have shown that catheter ablation for VT has achieved significant results and can significantly improve the early and mid-term prognosis of patients with VT. Catheter ablation is even more important in cases where other methods are ineffective or unfeasible. However, catheter ablation is not a cure for all VTs, and there are still many problems that need to be solved. The SMASH-VT study, published in 2007, evaluated infarcts with reduced ejection fraction (EF) and performed catheter ablation after secondary prevention ICD implantation in SCD. Catheter ablation was performed after implantation. Patients had hemodynamically unstable VT or VF, syncope, and electrophysiologically inducible VT. patients with an ICD who had their first electrical shock were also enrolled. No patients were treated with class I and class III antiarrhythmic drugs. In the control group, only the ICD was implanted; in the treatment group, the ICD was implanted + catheter ablation therapy. It is worth mentioning that only stromal-guided ablation was performed for VT, i.e., stromal labeling and ablation under sinus rhythm, but not ablation under VT induction. The primary endpoint of the study was the absence of recurrent VT episodes and the absence of ICD pacing for ventricular tachycardia and ventricular fibrillation. At (22.5 ± 5.5) months follow-up, ICD pacing for ventricular tachycardia and defibrillation was significantly reduced in the ablation group (12% vs. 33%, P = 0.007); appropriate ICD discharges were also reduced; and there was a tendency for fewer electrical storm episodes. The limitations of the SMASH-VT study are mainly the long duration of patients enrolled and the absence of standard ICD antiarrhythmic pacing parameters. In addition, this ablation study was done in large clinical centers. The multicenter VTACH study, published in 2010, evaluated radiofrequency ablation in VT patients with hemodynamically stable infarction with EF ≤50%. 110 patients were prospectively treated with ICD-only therapy or ablation prior to ICD implantation. VT ablation included agitation, pacing, and stromal markers and ablation. The primary endpoint of the study was first recurrent VT or VF, and the use of antiarrhythmic drugs during the study period was considered as appropriate. KaplanCMeier analysis showed a significantly higher rate of recurrent VT in the ablation group than in the ICD-implantation-only group (47% vs. 29%, hazard ratio = 0.61, P = 0.045), but there was no difference in mortality or quality of life between the two groups. For their subgroup analysis, the EF <30% group showed no significant benefit, while the ablation group of patients with EF >30% significantly reduced arrhythmia recurrence. Since patients with EF >30% can benefit from ablation, the mechanism needs to be investigated further. Apparently there was no significant effect in patients with EF ≤ 30%, but the results need to be further demonstrated in future studies. So far, catheter ablation still cannot be abandoned in patients with poor left ventricular function. Since more centers are involved in VTACH studies compared to SMASH-VT, and since VTACH is a multiple ablation modality, the results of VTACH studies with high VT recurrence are more reliable and more reflective of the real world. For post-infarction VT ablation, three non-randomized studies have evaluated it. Although all of these studies used antiarrhythmic drugs. At postoperative follow-up, VT recurrence rates were 47%, 56%, and 49%, respectively. In a Meta-analysis, VT recurrence rates decreased after catheter ablation of ventricular tachycardia in organic heart disease, but there was no significant effect on mortality. Because of the small number of cases, its effect on mortality needs to be studied on a large scale. Although this is only a single-center study report, and several studies, including our center, have shown approximately 70% to 80% success rates for catheter ablation, multicenter studies of patients with resistant and recurrent VT suggest that catheter ablation improves the disease, yet nearly half of patients have at least one or more recurrent VT events. Recurrent recurrent VT usually has severe heart disease. Data on the effectiveness and safety of ablation are only available from large research centers, so to date there are still no clear guidelines on what type of patients VT ablation is indicated for. Do patients with ICD implants need prophylactic VT ablation? Is VT ablation widely available and does it reduce mortality? The mechanism of recurrence after VT ablation is still unclear, and it is difficult to judge the effect of VT ablation. In the future, larger and more prospective and randomized studies are needed and more methods should be applied to solve the above problems. Second, the mechanism of ventricular tachycardia and the technical problems of catheter ablation 1, the mechanism of ventricular tachycardia: In addition to common scar-related VT, VT occurring in patients with organic heart disease include bundle branch folding VT, Hitchcock bundle Pukenon fiber-related VT, papillary muscle-related VT, epicardial VT and other unexplained VT (about 5%), especially the first two types of VT can be ablated by means of catheter ablation The first two types of VT in particular can be cured by catheter ablation. Accurate identification of curable VT and timely ablation is one of the important objectives of electrophysiological examination and intracardiac markers, and should be the primary goal. Unfortunately, however, the reality is that the mechanism of VT remains unclear in a significant number of patients. Although we know that the main mechanism of VT in organic heart disease is folding, how folding is formed in a specific patient, how the folding loop operates, and the composition of the critical isthmus are not very clear. Two-dimensional and three-dimensional labeling techniques are helpful to clarify the mechanism of VT, and more accurate and practical labeling techniques are currently expected by clinicians. 2. Ablation target: The key to successful VT catheter ablation is to identify the different channels that can form the VT foldback loop, identify the VT narrow part, and then determine the best ablation line. Traditional methods include: sinus rhythm labeling, pacing labeling, excitation labeling and drag band labeling, which play an important role in two-dimensional labeling. However, these methods have many limitations: 1. The folding loop path of VT, including the isthmus, can be very wide, and point ablation is not sufficient to interrupt the folding loop. 2. Clinical experience shows that most organic heart disease VT episodes are hemodynamically unstable. 3. VT cannot be induced during electrophysiological examination and ablation. 7. The folding loops of VT are located in the deeper myocardial layer or in the epicardium, which limit the wide application of conventional ablation methods. In order to overcome these factors of VT ablation mentioned above, the use of 3D scaler (Carto and Ensite 3000) system for sinus rhythm or ventricular pacing downstream amplitude scaler and linear ablation has been carried out in clinical practice. Three-dimensional scaling techniques can clearly show areas of low voltage with slow conduction and can even determine the area and mechanism of operation of the foldback loop. Based on previous experience, pre-designed voltages above 1.5 mv are considered normal, below 0.5 mv are scarred areas, and between 0.5 and 1.5 mv is the junctional zone between normal and abnormal. Studies have shown that this technique correlates well with histology. It was found that scar areas with greater than 80% myocardial fibrosis had voltages mostly less than 0.5 mv; while myocardial fibers had voltages between 0.5 and 1.5 mv at 21% to 79%; and less than 20% myocardial fibrosis had voltages greater than 1.5 mv. Once voltage scaling was completed, the operator paced in and around the areas of fibrosis to verify areas of low voltage and slow conduction pathways that may be associated with VT episodes. These areas may in fact be the isthmus of the folding loop. The study showed that cardiac function was not affected before or after ablation by 3D electroanatomical markers, nor was it affected by ablation energy. Stromal markers include voltage, pacing and excitation markers. Ablation can be accomplished with only matrix markers, but often due to large myocardial scars and complex folding loops, a combination of excitation and drag band markers is required. In such cases, the likelihood of successful ablation is high even in unstable VT. However, in reality, 3D electroanatomical labeling with 1.5 mv defines scars with good validity and specificity, but has some limitations on sensitivity, and it is difficult to detect intramyocardial and epicardial scars. Three-dimensional electroanatomical labeling may be somewhat limited in non-ischemic cardiomyopathy because, unlike post-infarction VT, the fiber areas identified by voltage and slow conduction in non-ischemic cardiomyopathy may be fragmented and not necessarily the isthmus of VT. Therefore, the validity and feasibility of 3D electroanatomic labeling methods in patients with VT in nonischemic cardiomyopathy is compromised, often requiring epicardial labeling, or both endocardial and epicardial labeling. To date, it is still unknown which method is the best for VT ablation, as there are no randomized trials comparing different matrix ablations in VT, nor are there randomized trials comparing matrix-labeled ablations at the isthmus of the folding loop, linearly at the exit, or circumferentially. 3. Ablation depth: Due to the thick ventricular muscle, even if an ablation target is found, it may not be successfully ablated because the foldback loop is deep in the ventricular wall and the catheter ablation depth is insufficient. For these patients, many research centers apply ice saline perfusion technique for ablation to increase the effectiveness of ablation, but still some of them have difficulty in achieving efficacy. New studies of bipolar ablation catheters have recently reported that they are more effective than traditional monopolar techniques, offering new hope for these patients. New ablation techniques such as ablation catheters with retrievable needles may also be used in the clinic to increase the depth and area of ablation, thus increasing the likelihood of successful VT ablation. Simultaneous ablation of endocardium and epicardium can also increase the depth of ablation, but so far there is no uniform ablation procedure. Although it is generally believed that the prognosis is better when VT is not induced in ablation, the Calkins study concluded that successful ablation of all measured VTs may not be the best outcome. The definition of successful ablation in the VTACH study was that none of the VTs could be induced. In some patients, a monomorphic VT event may induce another monomorphic VT with another distinctly different QRS waveform. Spontaneous VT is often called “clinical VT,” and procedural stimuli may induce other shapes of VT that are not associated with clinical VT and do not necessarily occur spontaneously in the clinic. Therefore, there is still a need for larger prospective and randomized studies to address the above-mentioned issues in determining the endpoints and success criteria for VT ablation in the clinical setting. Evaluating VT ablation in organic heart disease is more complicated for a number of reasons: 1. Because current case reports and studies of VT ablation are still relatively limited in terms of published data, there are even fewer randomized controlled studies specifically on VT in organic heart disease, and there is also a lack of medium- and long-term follow-up data. 2. Successful treatment cases utilize different methods; for recent success most are based on the criterion of non-inducible VT, while For long-term results it may be determined by the disease itself.3. The application of new techniques for ablation of VT in organic heart disease with three-dimensional markers has only been available for more than 10 years because of the limited follow-up time. Early studies may have underestimated the effect of catheter ablation of VT, while more recent studies may have overestimated its effect.4. A technique may be effective in some patients and less effective in others.5. For some very experienced single centers may report showing good results, but this may not be the case for multicenter results due to their limited case numbers.6. Current Meta-analyses including data studies for hemodynamic instability, have limited data for the study of mortality endpoints for different ablation techniques. In the future, large multicenter, prospective, randomized studies will be published that may also include detailed coverage of different VT ablations for organic heart disease. The data from these studies will likely help us to develop a consensus. IV. Outlook VT ablation for organic heart disease has made many substantial advances in the last 20 years or so. In this time, ICD is still regarded as the main method to prevent VT/VF and cause SCD, but it also brings a series of problems such as affecting quality of life and increasing morbidity. The efficacy of antiarrhythmic drugs in patients with recurrent VT remains unsatisfactory. Therefore, in experienced medical centers, early catheter ablation should be considered for recurrent monomorphic symptomatic VT. The choice of catheterization for VT must be made with due consideration of the risks and benefits, and its prognosis depends largely on the type and severity of the heart disease. There is no single treatment currently available to control VT, and a significant proportion of patients require a combination of treatments to improve survival and quality of life. Although there are still no uniform standards for VT ablation in terms of clinical case selection, ablation techniques and ablation endpoints, VT catheter ablation will be used for more patients as VT research continues to progress and new technologies are applied, such as routine myocardial evaluation with MRI and other imaging before ablation, robotic catheter ablation, catheter ablation energy and more and better clinical studies. In addition, the development and maturation of other ablation techniques, such as denervation ablation, transcoronary alcohol ablation and even molecular ablation, all provide more means for VT ablation.