It has been shown that type I AADs have no obvious effect in the prevention of SCD after an MI based on the experimental results of the Cardiac Arrhythmia Suppression Trial (CAST), the second Cardiac Arrhythmia Suppression Trial (CAST II), and the Cardiac Arrest Study Hamburg (CASH) [20, 61, 62]. Type I AADs also increase all-cause mortality. Therefore, they are not recommended for use in the primary prevention of SCD.

Class II $\beta$-blockers are an important part of the treatment of an MI, but they should be used only after HF resolves [63]. In the METOCARD-CNIC clinical trials, intravenous administration of metoprolol early before reperfusion reduced the infarct size and increased LVEF. In the long-term therapy following an MI, metoprolol helps to normalize LVEF, reduces the incidence of severe LV systolic dysfunction and the need for ICDs, and reduces the rate of hospital admissions for HF [64]. In patients with an acute MI complicated with left ventricular systolic dysfunction, long-term treatment with carvedilol can reduce the frequency of all-cause and cardiovascular deaths and the recurrence of non-fatal MIs. In addition, in a retrospective study of 890 consecutive patients presenting with a NSTEMI, small doses of oral bisoprolol were protective against SCD in NSTEMI patients early after admission [65].

Amiodarone is an AAD with a class III effect and can be used for preventing SCD, especially in the first year after an MI. However, the EMIAT (European Myocardial Infarct Amiodarone Trial) failed to show any significant benefits of amiodarone on SCD [66]. A meta-analysis of 15 RCTs (8522 participants) showed that amiodarone could reduce the risk of SCD by 26% and that of all cardiovascular diseases by 18% in patients with cardiomyopathy, although it did not significantly reduce overall mortality. In addition, in another meta-analysis of 9997 participants with low-to-moderate quality evidence, amiodarone reduced SCD, cardiac, and all-cause mortality compared with placebo or interventions without primary prevention [67]. Therefore, amiodarone therapy may be reasonable for some patients who are at high risk for SCD.

In a multicentre, double-blind, randomized study enrolling 576 patients, diltiazem reduced the frequency of angina pectoris after a myocardial infarction by 49.7%. In addition, diltiazem can effectively prevent early re-infarction and severe angina after a non-Q wave infarction, and it is also safe and well-tolerated. However, the preventive effect against SCD after an MI remains to be seen.

Catheter ablation can eliminate abnormal electrical pathways from causing arrhythmias and reduce the risk of sudden cardiac death.

Catheter ablation is the most effective way to eradicate PVCs, which in addition to AADs is considered to be the first-line treatment in PVCs patients with decreased LVEF. However, there is still a need to conduct research to determine the best prevention and treatment methods for the underlying cause of PVCs to optimize treatment regimens while minimizing the risks [68].

In patients with recurrent VT, catheter ablation has become a recognized treatment option. In two prospective clinical trials, the Ventricular Tachycardia Ablation in Coronary Heart Disease (VTACH) and the Substrate Mapping and Ablation in Sinus Rhythm to Halt Ventricular Tachycardia (SMASH-VT) trials, the time and frequency of recurrent VT/VF were significantly longer and decreased in patients who received ablation treatment [69, 70]. In addition, the incidence of ICD shocks in these patients was also significantly reduced. However, the timing of ablation of ventricular tachycardia in patients has always been a controversial topic, and this was the basis for the Preventive Ablation of Ventricular Tachycardia in Patients with Myocardial Infarction (BERLIN VT) study [71]. In this trial, patients were randomly assigned (1 : 1) to either a prophylactic ablation strategy group or a delayed ablation strategy group, which received VT catheter ablation before ICD implantation or after the third appropriate ICD shock. Compared with the delayed ablation strategy, prophylactic VT ablation did not reduce the mortality or hospitalization rate of hospitalization due to worsening arrhythmia or HF within 1 year. Therefore, for secondary prophylaxis patients with ICD implantation indications, catheter ablation should be delayed until VT recurrence after ICD implantation is achieved to avoid the unnecessary risk of prophylactic ablation.

In the latest systematic review and meta-analysis of existing RCTs, preventive catheter ablation in patients with ischemic cardiomyopathy has been shown to reduce ICD treatment, ICD shock, and VT storms without increasing complications, especially in LVEF $>$30%. Appropriate ablation therapy is also associated with a significant reduction in the incidence of ICD shock, VT storm, and cardiac hospitalization [72]. In a multicenter, randomized, controlled trial, The Vasopressin vs. Norepinephrine as Initial Therapy in Septic Shock (VANISH) trial, patients treated with AAD had more treatment-related adverse events than patients treated with ablation [73]. In order to explore whether catheter ablation is better than AADs in reducing mortality, the catheter ablation for VT in patients with an implantable cardioverter defibrillator (CALYPSO) pilot trial recruited 243 patients over 2 years. However, only 27 patients passed the screening because of prior AAD use, which resulted in the premature termination of the trial [74]. This trial highlights the difficulty in studying the current strategies that catheter ablation is used only after AAD fails. Recently, the VANISH2 trial (Ventricular Tachycardia Antiarrhythmics or Ablation in Structural Heart Disease 2, NCT02830360) enrolled 366 MI patients with a history of persistent uniform VT and randomized them to either catheter ablation or AAD, with the aim of determining the most appropriate first-line therapy for suppression of VT in persons with a prior MI by comparing the two strategies. And we look forward to encouraging results from this large clinical trial.

Another important aspect of ablation of ventricular tachycardia/sudden cardiac death is radiotherapy. Stereotactic arrhythmia radio ablation (STAR) is an emerging therapy for the treatment of VT. It has been shown to reduce the VT burden in patients who are difficult to treat with medication and/or catheter ablation or cannot tolerate catheter ablation [75]. However, there are significant differences in this emerging treatment between studies including a significant lack of consistency in the treatment protocols [76]. Therefore, more RCTs are still needed to establish a detailed treatment strategy.

According to the latest European Society of Cardiology/Heart Failure Association (ESC/HFA) consensus, the core treatment for HF contains beta-blockers, angiotensin-converting enzyme inhibitors (ACEI)/angiotensin receptor blockers (ARB)/angiotensin receptor neprilysin inhibitor (ARNI), mineralocorticoid receptor antagonists (MRAs) and sodium-glucose cotransporter-2 (SGLT2) inhibitors [78]. Moreover, with the rational use of evidence-based drugs, rates of SCD in patients with HF declined substantially over time [79].

The activation of the RAAS system and the sympathetic nervous system is the key neurohumoral mechanism that causes HF. Blocking the production of angiotensin II (Ang II) and the activation of its related receptors plays an important role in blocking the RAAS cascade [80].

Among 2231 patients who survived MI and had LVEF $\le$40%, captopril treatment reduced the risk of recurrent MI by 25% and the risk of death after MI recurrence by 32% [81]. In the Vasodilator-Heart Failure Trial II (V-HeFT II) trial, there was no significant difference between enalapril and isosorbide dinitrate/hydralazine in the treatment of patients with LVEF $\le$45% who survived an MI. This provides further evidence that treatment with captopril and enalapril are important agents to prevent SCD after an MI.

Representative drugs in the ARB class include valsartan and losartan. In two prospective studies, the Acute Myocardial Infarction (VALIANT) trial and the Optimal Trial in Myocardial Infarction with the Angiotensin II Antagonist Losartan (OPTIMAAL), valsartan, and losartan were effective in treating acute MI patients. In addition, in patients with HF after MI, valsartan can down-regulate the occurrence of arrhythmic events, for example, NSVT, through cardiac reverse remodeling [82].

In the consensus guidelines between the Canadian Cardiovascular Society (CCS) and the American College of Cardiology (ACC), ARNI (sacubitril/valsartan) is prescribed as the first-line therapy [83, 84]. In the PARADIGM-HF (Prospective Comparison of ARNI with ACEI to Determine Impact on Global Mortality and Morbidity in Heart Failure Trial) trial involving 8442 patients with LVEF $\le$40%, sacubitril/valsartan was shown to be superior to enalapril in reducing mortality and hospitalization rates in HFrEF patients [85]. In addition, sacubitril/valsartan also performed better than valsartan in reducing hospitalization rates in HFpEF patients [86]. However, whether ARNI prevents the development of HF after infarction and reduces SCD in patients with acute myocardial infarction (AMI) remains unknown. To address this issue, the PARADISE-MI (Prospective ARNI vs. ACE Inhibitor Trial to DetermIne Superiority in Reducing Heart Failure Events after MI) trial enrolled 5661 patients with an AMI randomized 1 : 1 to receive sacubitril/valsartan or ramipril therapy [87]. The results show that although sacubitril/valsartan failed to reduce the primary endpoint in the AMI population compared with ramipril, the incidence of sacubitril/valsartan was low and a composite endpoint that included all HF events shows the advantages with sacubitril/valsartan over ramipril.

Mineralocorticoid receptor antagonists (MRAs) are recognized to be effective in reducing the mortality of patients with HF after MI. In a meta-analysis involving 25 RCTs and 19,333 patients, MRAs effectively down-regulated all-cause and cardiovascular mortality [88]. In addition, in a meta-analysis of three placebo-controlled randomized trials; the Randomized Aldactone Evaluation Study (RALES), Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS), and the Eplerenone in Mild Patients Hospitalization and Survival Study in Heart Failure (EMPHASIS-HF), the risk of SCD in patients with HF treated with spironolactone or eplerenone was reduced by 23% [89].

According to the guidelines, SGLT2 inhibitors, such as Dapagliflozin, are recommended for patients with mild to moderate HF with reduced LVEF ($\le$40%) or coronary heart disease to improve symptoms and quality of life and reduce the risk of hospitalization and cardiovascular mortality [90].

Other anti-heart failure drugs with different mechanisms of action have also been clinically effective, including vericiguat, omecamtiv mecarbil, and ivabradine. Vericiguat is an oral agonist for guanylate cyclase which improved outcomes in patients with an LVEF $\le$40% [91]. Omecamtiv mecarbil is a novel selective cardiac myosin activator, which has been shown to improve cardiac function and reduce ventricular volume, heart rhythm, and N-terminal pro-B-type natriuretic peptide in patients with chronic HF. The combined incidence of cardiovascular death or HF events decreased significantly after omecamtiv mecarbil treatment [92]. Of the drugs used clinically, only ivabradine directly reduces the heart rate of sinoatrial node cells in the absence of other known cardiovascular system effects, which significantly reduced cardiovascular mortality or HF hospitalization rates [93].

An ICD is designed to detect and treat life-threatening arrhythmias and then automatically discharge and defibrillate to significantly reduce malignant ventricular rhythms. Patients with an LVEF $\le$35% after an MI are the main beneficiaries of ICD management and prevention [94]. However, the majority of patients who die suddenly after an MI have LVEFs $>$35% and are ineligible for ICD treatment according to current guidelines [95]. The Risk Estimation Following Infarction Noninvasive Evaluation - ICD Efficacy trial (Refine-ICD; https://clinicaltrials.gov/ Identifier NCT 00673842), an ongoing study, is expected to randomly select 1400 survivors of an MI to evaluate whether ICD treatment reduces mortality in patients with an LVEF between 36% and 50%, abnormal cardiac depolarization (TWA) and autonomic tension impairment (HRT) after an MI, which will complement the ICD implant evidence in the current guidelines.

Some patients with HF have atrioventricular, interventricular, and/or intraventricular dyssynchrony, which leads to decreased myocardial contractility. Cardiac resynchronization therapy (CRT) improves HF symptoms, exercise tolerance, quality of life, hospitalization rate, and significantly lowers mortality by improving atrioventricular, interventricular, and/or inventricular systolic synchronization and increasing cardiac output [96].

In pursuit of physiologic inventricular, interventricular, and atrioventricular synchronization, the pacing sites, and modes have been continuously improved and developed from biventricular pacing (BVP), to His bundle pacing (HBP), and the current left bundle branch pacing (LBBP) [97]. LBBP is defined as the capture of the left bundle branch (LBB) via a transventricular septal approach. Zhang et al. [98] performed LBBP in 11 patients with HF, and the results showed that the LVEF of all patients improved. Wu et al. [99] analyzed a total of 137 CRT patients with LVEF $\le$40% who received BVP, HBP, or LBBP and found that patients treated with LBBP and HBP showed significantly better improvement in symptoms and left ventricular function than those treated with BVP. The R-wave amplitude and pacing threshold of LBBP were more satisfactory and stable than those of HBP [100]. However, many aspects of LBBP remain unknown and more RCTs are needed to explore its long-term safety and efficacy.

Further studies are necessary to determine whether using a more expensive defibrillator component such as (CRT-D) to CRT pacing (CRT-P) is needed. So far, no studies have provided clear evidence on the incremental survival advantage of CRT-D over CRT-P, in the ischaemic cardiomyopathy (ICM)/non-ischaemic cardiomyopathy (NICM) population [101]. The landmark COMPANION (Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure) trial demonstrated that the addition of a defibrillator to cardiac resynchronization therapy does not significantly affect the combined outcome of death or hospitalization from any cause. However, the addition of a defibrillator to cardiac resynchronization therapy gradually increased the survival benefit, resulting in a significant 36% reduction in the risk of death compared to optimal pharmacologic therapy, and patients with NICM had a greater survival benefit using CRT-D than CRT-P [102]. Recently, a European observational, multicenter cohort study involving 5307 patients compared CRT-D with CRT-P treatment and showed that there was no survival benefit from the addition of an ICD in NICM patients compared to ICM patients [103]. The most reasonable explanation for these results is that the proportional risk of SCD mainly determines the survival benefits of ICD implantation. This suggests that CRT-D has a greater benefit when the proportional risk of SCD is high while CRT-P has a greater benefit when the proportional risk of SCD is low [104]. However, more evidence is needed to identify the incremental survival advantage of CRT-D and the specific population that may benefit from it, so that patients can select the most appropriate device for treatment.