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6.2.4.1.2. Patients without apparent structural heart disease. ‘Idiopathic VTs’ is the term for VTs that are not associated with SHD or a genetic arrhythmic syndrome. Most idiopathic VTs are mediated by triggered activity, but a re-entrant mechanism (involving the LV Purkinje network) explains verapamil-sensitive fascicular VTs.523 Three important key features distinguish idiopathic VTs from VTs associated with SHD. First, idiopathic VTs mostly originate from a single site and specific region of the heart (namely the right or left ventricular outflow tracts,524,525 along the valve annuli,526–528 papillary muscle,529 or the LV Purkinje network).523 Second, no detectable scar is found in idiopathic VTs.530 Finally, idiopathic VTs have a benign prognosis so that ICD implantation is generally not recommended.466 The earliest site of activation during VT is the ablation target for focal sources, while abnormal Purkinje tissue (with diastolic activity during VT) is the ablation target of left fascicular VTs.531,532 Catheter ablation is curative in most idiopathic VT patients and peri-procedural complications are rare.533–537

6.2.4.2 Autonomic modulation

The role of the autonomic nervous system in promoting arrhythmias has long been recognized, leading to the concept of Coumel’s triangle of arrhythmogenesis.538 Sympathetic activation has been demonstrated as playing a key role in inducing VAs in some entities, such as congenital LQTS and CPVT,539,540 and left cardiac sympathetic denervation was shown to be associated with a decrease in the frequency of arrhythmogenic syncope in congenital LQTS.541,542 The efficacy of cardiac sympathetic blockade by different approaches (thoracic epidural anaesthesia, percutaneous stellate ganglion anaesthesia, or surgical stellate ganglion resection) in reducing the arrhythmia burden in refractory VT/VF has been recognized in several small observational studies.326,328,340 Further studies are needed to assess which patients may benefit from a modulation of the autonomic nervous system to better control VT/VF.

7. Diagnostic evaluation, management, and risk stratification according to clinical presentation and known (likely) disease

7.1 Specific structural heart diseases

7.1.1. Coronary artery disease 7.1.1.1. Acute coronary syndromes and vasospasm 7.1.1.1.1. Acute coronary syndromes. SCD is a major cause of mortality in ACS, mostly caused by sustained VAs, in particular VF. The majority of studies have reported on patients with STEMI. Of patients with STEMI, 4–12% develop VA within the first 48 h after the onset of symptoms.69,543,544 Pre-reperfusion VAs are more common than reperfusion-induced or postreperfusion arrhythmias in STEMI.545 Haemodynamic instability, cardiogenic shock, LVEF , 40%, and the sum of ST-segment deviations in all leads are independent predictors of VA both in STEMI and non-STEMI.69,546 In addition, an early repolarization pattern has been associated with increased risk of VAs and SCD in ACS.547

Prevention of ventricular arrhythmias in ST elevation myocardial infarction Urgent reperfusion is the most important therapy,292,548 as acute ischaemia triggers arrhythmias. Beta-blocker treatment is also recommended to prevent VA.3,549 In a recent randomized trial of patients with STEMI, early intravenous metoprolol before percutaneous coronary intervention reduced the incidence of arrhythmias in the acute phase and was not associated with an increase in adverse events.550 Prophylactic treatment with AADs has not proven beneficial, and may even be harmful.322 Correction of electrolyte imbalances is strongly recommended.289

Management of sustained ventricular tachycardia and ventricular fibrillation in acute coronary syndrome Electrical cardioversion or defibrillation is the intervention of choice to acutely terminate VAs in ACS patients (Figure 14).205,339 Recurrent sustained VT, especially when polymorphic, or recurrent VF can indicate incomplete reperfusion or recurrence of acute ischaemia. In this case, immediate coronary angiography is indicated.3 For recurrent PVT degenerating into VF, beta-blockers are recommended.551,552 In addition, deep sedation may be helpful to reduce episodes of VT or VF.553 Intravenous amiodarone should be considered to acutely suppress recurrent haemodynamically relevant VAs, although there is a paucity of controlled studies for amiodarone during STEMI554 and the evidence in this setting is mainly extrapolated from studies of OHCA.555 If treatment with beta-blockers and amiodarone is not effective, lidocaine may be considered.322 The use of other AADs in ACS is not recommended.549,556 In haemodynamically unstable patients with refractory VA, mechanical circulatory support may be considered.336,557 For VA in the context of relative bradycardia or pause-related, pacing may be effective to prevent re-initiation.

The prognostic significance of early ventricular arrhythmias Early VAs are defined as VT/VF occurring within 48 h after a STEMI. In the contemporary percutaneous coronary intervention (PCI)-based revascularization era, almost all VA occur within the first 24 h.558 Early VA have been associated with an up to six-fold increase in in-hospital mortality, whereas long-term prognosis seems not to be significantly affected.543,559,560 In a prospective cohort study, patients with VF during the acute STEMI phase had low and very similar incidence of late SCD as compared with VF-free patients during 5-year observation.560 Of note, early monomorphic VT was associated with significantly higher incidence of adequate ICD interventions compared with early VF, and was an independent predictor of death during long-term follow-up.561 Thus, the prognostic significance of VT and VF occurring in the acute phase of MI may be different. The impact of VA occurring late after reperfusion (.48 h) on late SCD is less clear. Podolecki et al.559 recently demonstrated that long-term all-cause mortality after STEMI was predicted by VA occurring late after reperfusion (.48 h after reperfusion), while early reperfusion VAs did not affect 5-year outcome. Further studies are required to clarify Downloaded from academic.oup.com/eurheartj/article/43/40/3997/6675633 by guest on 07 October 2026