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In patients with ischaemic cardiomyopathy and severely reduced left ventricular ejection fraction (LVEF), an arrhythmogenic milieu is created by a complex interplay between myocardial scarring (assessed by cardiac MRI) and multiple other factors (ventricular ectopy, ischaemia and autonomic imbalance), favouring the occurrence of arrhythmic sudden cardiac death (SCD). Currently, a dynamic and robust model of dichotomised SCD risk assessment after primary percutaneous coronary intervention (PCI) is lacking, underlining the urgent need for further refinement of the widely accepted and guidelines-based criteria (ischaemic cardiomyopathy, LVEF ≤35%) for primary prevention. This review addresses the potential additional value of the recently published Defibrillator After Primary Angioplasty (DAPA) trial results. The DAPA trial conveys important messages and provides novel perspectives regarding left ventricular function post-primary PCI as an (early) risk marker for SCD and the impact of prophylactic ICD implantation on survival in this cohort. In the context of other previous primary prevention trials, DAPA was the first trial including only ST-elevation MI patients all treated with acute PCI.

Post-infarct-related ventricular tachycardia (VT) occurs due to reentry over surviving fibres within ventricular scar tissue. The mapping and ablation of patients in VT remains a challenge when VT is poorly tolerated and in cases in which VT is non-sustained or not inducible. Conventional substrate mapping techniques are limited by the ambiguity of substrate characterisation methods and the variety of mapping tools, which may record signals differently based on their bipolar spacing and electrode size. Real world data suggest that outcomes from VT ablation remain poor in terms of freedom from recurrent therapy using conventional techniques. Functional substrate mapping techniques, such as single extrastimulus protocol mapping, identify regions of unmasked delayed potentials, which, by nature of their dynamic and functional components, may play a critical role in sustaining VT. These methods may improve substrate mapping of VT, potentially making ablation safer and more reproducible, and thereby improving the outcomes. Further large-scale studies are needed.

Thromboembolism is the most serious complication of AF, and oral anticoagulation is the mainstay therapy. Current guidelines place all AF types together in terms of anticoagulation with the major determinants being associated comorbidities translated into risk marker. Among patients in large clinical trials, those with non-paroxysmal AF appear to be at higher risk of stroke than those with paroxysmal AF. Higher complexity of the AF pattern is also associated with higher risk of mortality. Moreover, continuous monitoring of AF through cardiac implantable devices provided us with the concept of ‘AF burden’. Usually, the larger the AF burden, the higher the risk of stroke; however, the relationship is not well characterised with respect to the threshold value above which the risk increases. The picture is more complex than it appears: AF and underlying disorders must act synergically respecting the magnitude of its own characteristics, which are the amount of time a patient stays in AF and the severity of associated comorbidities.

AF contributes to increased stroke risk via various mechanisms, including deranged blood constituents, vessel wall abnormalities and abnormal blood flow. This excess risk is frequently managed with anticoagulation therapy, aimed at preventing thromboembolic complications. Yet, a significant proportion of patients with AF remain at high residual stroke risk despite receiving appropriate dose-adjusted anticoagulation. This article explores the residual stroke risk in AF and potential therapeutic options for these patients.

Sarcoidosis is an inflammatory granulomatous disease that can affect any organ. Up to one-quarter of patients with systemic sarcoidosis may have evidence of cardiac involvement. The clinical manifestations of cardiac sarcoidosis (CS) include heart block, atrial arrhythmias, ventricular arrhythmias and heart failure. The diagnosis of CS can be challenging given the patchy infiltration of the myocardium but, with the increased availability of advanced cardiac imaging, more cases of CS are being identified. Immunosuppression with corticosteroids remains the standard therapy for the acute inflammatory phase of CS, but there is an evolving role of steroid-sparing agents. In this article, the authors provide an update on the diagnosis of CS, including the role of imaging; review the clinical manifestations of CS, namely heart block, atrial and ventricular arrhythmias and heart failure; discuss updated management strategies, including immunosuppression, electrophysiological and heart failure therapies; and identify the current gaps in knowledge and future directions for cardiac sarcoidosis.

In this article, the authors discuss the differential diagnostic methods used in clinical practice to identify types of wide QRS tachycardias (QRS duration >120 ms). A correct diagnosis is critical to management, as misdiagnosis and the administration of drugs usually utilised for supraventricular tachycardia can be harmful for patients with ventricular tachycardia.

With catheter ablation becoming effective for non-pharmacological management of AF, many cases of atrial tachycardia (AT) after AF ablation have been reported in the past decade. These arrhythmias are often symptomatic and respond poorly to medical therapy. Post-AF-ablation ATs can be classified into the following three categories: focal, macroreentrant and microreentrant ATs. Mapping these ATs is challenging because of atrial remodelling and its complex mechanisms, such as double ATs and multiple-loop ATs. High-density mapping can achieve precise identification of the circuits and critical isthmuses of ATs and improve the efficacy of catheter ablation. The purpose of this article is to review the mechanisms, mapping and ablation strategy, and outcome of ATs after AF ablation.

Item does not contain fulltext The exact frequency and clinical determinants of spontaneous conversion (SCV) in patients with symptomatic recent-onset AF are unclear. The aim of this systematic review is to provide an overview of the frequency and determinants of SCV of AF in patients presenting at the emergency department. A comprehensive literature search for studies about SCV in patients presenting to the emergency department with AF resulted in 25 articles - 12 randomised controlled trials and 13 observational studies. SCV rates range between 9-83% and determinants of SCV also varied between studies. The most important determinants of SCV included short duration of AF (

AF is the most common arrhythmia in clinical practice. In addition to the severe effect on quality of life, patients with AF are at higher risk of stroke and mortality. Recent studies have suggested that atrial and ventricular substrate play a major role in the development and maintenance of AF. Cardiac MRI has emerged as a viable tool for interrogating the underlying substrate in AF patients. Its advantage includes localisation and quantification of structural remodelling. Cardiac MRI of the atrial substrate is not only a tool for management and treatment of arrhythmia, but also to individualise the prevention of stroke and major cardiovascular events. This article provides an overview of atrial imaging using cardiac MRI and its clinical implications in the AF population.

Ventricular tachycardias originating from the Purkinje system are the most common type of idiopathic left ventricular tachycardia. The majority if not all of the reentrant circuit involved in this type of tachycardia is formed by the Purkinje fibres of the left bundle branch, particularly the left posterior fascicle. In general, slowly conducting Purkinje fibres (P1) form the antegrade limb, and normally conducting Purkinje fibres (P2) form the retrograde limb of the reentrant circuit of the ventricular tachycardia originating from the left posterior fascicle. Elimination of the critical Purkinje elements in the reentrant circuit is the route to successful ablation. While the reentrant circuit identified by activation mapping provides the roadmap to ablation targets, comparing the difference in the His-ventricular interval during sinus rhythm and tachycardia also helps to identify the critical site in the reentrant circuit.

Chagas disease is an important public health problem in Latin America. However, migration and globalisation have resulted in the increased presence of Chagas disease worldwide. Sudden cardiac death is the leading cause of death in people with Chagas disease, most often due to ventricular fibrillation. Although more common in patients with documented ventricular arrhythmias, sudden cardiac death can also be the first manifestation of Chagas disease in patients with no previous symptoms or known heart failure. Major predictors of sudden cardiac death include cardiac arrest, sustained and non-sustained ventricular tachycardia, left ventricular dysfunction, syncope and bradycardia. The authors review the predictors and risk stratification score developed by Rassi et al. for death in Chagas heart disease. They also discuss the evidence for anti-arrhythmic drugs, catheter ablation, ICDs and pacemakers for the prevention of sudden cardiac death in these patients. Given the widespread global burden, understanding the risk stratification and prevention of sudden cardiac death in Chagas disease is of timely concern.

Fibrosis plays a fundamental role in the initiation and maintenance of AF, mainly due to enhanced automaticity and anisotropy-related re-entry. The identification and quantification of atrial fibrosis is achieved either preprocedurally by late gadolinium enhancement MRI or intraprocedurally using electroanatomic voltage mapping. The presence and extent of left atrial fibrosis among AF patients may influence relevant decision making regarding the need for anticoagulation, the adoption of rate versus rhythm control and mainly the type of ablation strategy that will be followed during interventional treatment. Several types of individualised substrate modifications targeting atrial fibrotic areas have been proposed, although their impact on patient outcome needs to be further investigated in adequately powered prospective randomised controlled clinical trials.

Brugada syndrome (BrS) represents an inherited disorder associated with risk of sudden cardiac death due to VF in patients without structural heart disease. Currently, BrS is diagnosed by typical cove-shaped ST-segment elevation >2 mm in >1 RV precordial lead V1, V2 occurring spontaneously or after a sodium-channel blocker provocation test without any further evidence of malignant arrhythmias. An ICD should always be implanted in symptomatic BrS patients to prevent sudden death, despite high rates of complications with these devices. In asymptomatic people, an electrophysiological study should be performed to evaluate the need for an ICD. The recent discovery of a functional substrate has revolutionised our approach to the pathophysiology and management of BrS. Promising new therapeutic options have emerged in the last 3 years. Ajmaline is able to determine the extension of the substrate by prolonging the duration and fragmentation of abnormal epicardial electrograms. Substrate ablation results in the disappearance of both coved-type ECG and ventricular tachycardia/VF inducibility. These findings are clinically relevant, suggesting that epicardial ablation guided by ajmaline infusion may be an effective therapeutic option in BrS, potentially removing the need for ICD implantation.

Idiopathic ventricular arrhythmias are ventricular tachycardias or premature ventricular contractions presumably not related to myocardial scar or disorders of ion channels. Of the ventricular arrhythmias (VAs) without underlying structural heart disease, those arising from the ventricular outflow tracts (OTs) are the most common. The right ventricular outflow tract (RVOT) is the most common site of origin for OT-VAs, but these arrhythmias can, less frequently, originate from the left ventricular outflow tract (LVOT). OT-VAs are focal and have characteristic ECG features based on their anatomical origin. Radiofrequency catheter ablation (RFCA) is an effective and safe treatment strategy for OT-VAs. Prediction of the OT-VA origin according to ECG features is an essential part of the preprocedural planning for RFCA procedures. Several ECG criteria have been proposed for differentiating OT site of origin. Unfortunately, the ECG features of RVOT-VAs and LVOT-VAs are similar and could possibly lead to misdiagnosis. The authors review the ECG criteria used in clinical practice to differentiate RVOT-VAs from LVOT-VAs.

AF and heart failure (HF) commonly coexist. Left atrial ablation is an effective treatment to maintain sinus rhythm (SR) in patients with AF. Recent evidence suggests that the use of ablation for AF in patients with HF is associated with an improved left ventricular ejection fraction and lower death and HF hospitalisation rates. We performed a systematic search of world literature to analyse the association in more detail and to assess the utility of AF ablation as a non-pharmacological tool in the treatment of patients with concomitant HF.

While AF most often occurs in the setting of atrial disease, current assessment and treatment of patients with AF does not focus on the extent of the atrial myopathy that serves as the substrate for this arrhythmia. Atrial myopathy, in particular atrial fibrosis, may initiate a vicious cycle in which atrial myopathy leads to AF, which in turn leads to a worsening myopathy. Various techniques, including ECG, plasma biomarkers, electroanatomical voltage mapping, echocardiography, and cardiac MRI, can help to identify and quantify aspects of the atrial myopathy. Current therapies, such as catheter ablation, do not directly address the underlying atrial myopathy. There is emerging research showing that by targeting this myopathy we can help decrease the occurrence and burden of AF.

Low-level tragus stimulation (LLTS) is a non-invasive approach of transcutaneous vagus nerve stimulation. LLTS has applications in diseases of multiple systems, including epilepsy, depression, headache and potentially several cardiovascular diseases. LLTS has shown promising results in suppressing AF, alleviating post-MI ventricular arrhythmias and ischaemia-reperfusion injury along with improving diastolic parameters in heart failure with preserved left ventricular ejection fraction (HFpEF). Preliminary pilot clinical studies in patients with paroxysmal AF, HFpEF, heart failure with reduced ejection fraction and acute MI have demonstrated promising results. The beneficial effects are likely secondary to favourable alteration of the sympathovagal imbalance. On-going exploratory work focused on underlying mechanisms of LLTS in cardiovascular disease states and larger scale clinical trials will shed more light on the non-invasive modulation of the neuro-immune axis.

Ventricular arrhythmias are a therapeutic challenge, owing to their relatively unpredictable and deadly nature. Many patients are treated with an implantable cardioverter-defibrillator for either primary or secondary prevention of ventricular arrhythmias, meaning those who are at high risk of versus those who have experienced ventricular arrhythmias or sudden cardiac arrest, respectively. Despite the life-saving benefit, ICD comes with the risk of recurrent shocks for both appropriate and inappropriate rhythms. Patients with recurrent shocks have a poor quality of life and increased mortality rates. In this article, we review data for optimal device settings, medical management and radiofrequency ablation strategies to minimise the frequency of ICD shock, with a focus on treatment of ventricular arrhythmias, to reduce patient morbidity and mortality, and to maximise wellbeing and quality of life.

Ventricular remodelling can make the heart more susceptible to ventricular arrhythmias like torsades de pointes. Understanding the underlying mechanisms of initiation of ventricular arrhythmias and the determining factors for its severity has the potential to uncover new interventions. Beat-to-beat variation of repolarisation, quantified as short-term variability of repolarisation (STV), has been identified as an important factor contributing to arrhythmogenesis. This article provides an overview of experimental data about STV in relation to the initiation of torsades de pointes in a canine model of complete chronic atrioventricular block susceptible to torsades de pointes arrhythmias. Furthermore, it explores STV in relation to the severity of the arrhythmic outcome.

Over the past two decades, our understanding of inherited primary arrhythmia syndromes has been enriched by studies that have aimed to define the clinical characteristics and the genetic, cellular and molecular features predisposing patients to an enhanced risk of ventricular arrhythmias. In contrast, very little is known about the causative role of inherited cardiac channelopathies on atrial conduction abnormalities possibly leading to different atrial tachyarrhythmias. The diagnostic and therapeutic management of patients with an inherited cardiac channelopathy presenting with atrial arrhythmias remains highly challenging and is in urgent need of improvement. This review will assess the current knowledge on atrial electrical abnormalities affecting patients with different forms of inherited primary arrhythmia syndromes, including long and short QT syndromes, early repolarisation syndrome, catecholaminergic polymorphic ventricular tachycardia and Brugada syndrome.

Ventricular arrhythmias are challenging to manage in athletes with concern for an elevated risk of sudden cardiac death (SCD) during sports competition. Monomorphic ventricular arrhythmias (MMVA), while often benign in athletes with a structurally normal heart, are also associated with a unique subset of idiopathic and malignant substrates that must be clearly defined. A comprehensive evaluation for structural and/or electrical heart disease is required in order to exclude cardiac conditions that increase risk of SCD with exercise, such as hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. Unique issues for physicians who manage this population include navigating athletes through the decision of whether they can safely continue their chosen sport. In the absence of structural heart disease, therapies such as radiofrequency catheter ablation are very effective for certain arrhythmias and may allow for return to competitive sports participation. In this comprehensive review, we summarise the recommendations for evaluating and managing athletes with MMVA.

Atrial arrhythmias, including atrial fibrillation and atrial flutter, are common in patients with pulmonary hypertension and are closely associated with clinical decompensation and poor clinical outcomes. The mechanisms of arrhythmogenesis and subsequent clinical decompensation are reviewed. Practical implications and current evidence for the management of atrial arrhythmias in patients with pulmonary hypertension are summarised.

Contains fulltext : 171184.pdf (Publisher’s version ) (Open Access) Tachyarrhythmias are the most frequently observed cardiac complications during pregnancy. The majority of these maternal and foetal arrhythmias are supraventricular tachyarrhythmias; ventricular tachyarrhythmias are rare. The use of anti-arrhythmic drugs (AADs) during pregnancy is challenging due to potential foetal teratogenic effects. Maintaining stable and effective therapeutic maternal drug levels is difficult due to haemodynamic and metabolic alterations. Pharmacological treatment of tachyarrhythmias is indicated in case of maternal haemodynamic instability or hydrops fetalis. Evidenc e regarding the efficacy and safety of AAD therapy during pregnancy is scarce and the choice of AAD should be based on individual risk assessments for both mother and foetus. This review outlines the current knowledge on the development of tachyarrhythmias during pregnancy, the indications for and considerations of pharmacological treatment and its potential side-effects.

An increasing number of patients with congenital heart disease survive to adulthood; such prolonged survival is related to a rapid evolution of successful surgical repairs and modern diagnostic techniques. Despite these improvements, corrective atrial incisions performed at surgery still lead to subsequent myocardial scarring harbouring a potential substrate for macro-reentrant atrial tachycardia. Macroreentrant atrial tachycardias are the most common (75 %) type of supraventricular tachycardia (SVT) in patients with adult congenital heart disease (ACHD). Patients with ACHD, atrial tachycardias and impaired ventricular function – important risk factors for sudden cardiac death (SCD) – have a 2–9 % SCD risk per decade. Moreover, ACHD imposes certain considerations when choosing antiarrhythmic drugs from a safety aspect and also when considering catheter ablation procedures related to the inherent cardiac anatomical barriers and required expertise. Expert recommendations for physicians managing these patients are therefore mandatory. This review summarises current evidence-based developments in the field, focusing on advances in and general recommendations for the management of ACHD, including the recently published recommendations on management of SVT by the European Heart Rhythm Association.

There is evidence for a higher prevalence of atrial fibrillation (AF) in athletes engaged in long-term endurance sports training compared with the general population. Although atrial anatomic adaptations, alterations in autonomic nervous system, chronic systemic inflammation and fibrosis have been proposed as potential mechanisms, they remain speculative. Medical therapy with long-term antiarrhythmic agents or ‘pill in the pocket’ medications is hampered by limitations, such as sports eligibility and interference with exercise tolerance. AF ablation represents a valid therapeutic option with results similar to these achieved in other patients. Nevertheless, further clinical trials are needed to confirm whether endurance sport practice affects the maintenance of sinus rhythm following catheter ablation of AF.

Current guidelines recommend cardiac resynchronisation therapy (CRT) for patients with severe left ventricular dysfunction (left ventricular ejection fraction [LVEF] ≤35 %), QRS duration of ≥120–150 ms (Class IA and IB indications) on surface electrocardiogram (ECG) and New York Heart Association (NYHA) class III or IV heart failure (HF) symptoms. Ongoing studies aim to expand the use of CRT in patients with asymptomatic or minimal symptoms left ventricular dysfunction. There have been studies that have shown benefit of CRT extended to this group of patients. There have also been different implications of the role of CRT in patients with atrial fibrillation (AF), patients with narrow QRS duration or with right bundle branch block (RBBB) on surface ECG, as well as patients with end-stage renal failure on dialysis therapy. This article aims to review the current body of evidence of expanding use of CRT in these populations.

Clinical electrophysiology has made the traditional classification of rapid atrial rhythms into flutter and tachycardia of little clinical use. Electrophysiological studies have defined multiple mechanisms of tachycardia, both re-entrant and focal, with varying ECG morphologies and rates, authenticated by the results of catheter ablation of the focal triggers or critical isthmuses of re-entry circuits. In patients without a history of heart disease, cardiac surgery or catheter ablation, typical flutter ECG remains predictive of a right atrial re-entry circuit dependent on the inferior vena cava-tricuspid isthmus that can be very effectively treated by ablation, although late incidence of atrial fibrillation remains a problem. Secondary prevention, based on the treatment of associated atrial fibrillation risk factors, is emerging as a therapeutic option. In patients subjected to cardiac surgery or catheter ablation for the treatment of atrial fibrillation or showing atypical ECG patterns, macro-re-entrant and focal tachycardia mechanisms can be very complex and electrophysiological studies are necessary to guide ablation treatment in poorly tolerated cases. Sin financiación 0.760 SJR (2017) Q2, 133/362 Cardiology and Cardiovascular Medicine, 52/102 Physiology (medical) UEM

Atrioventricular nodal reentrant tachycardia (AVNRT) should be classified as typical or atypical. The term ‘fast-slow AVNRT’ is rather misleading. Retrograde atrial activation during tachycardia should not be relied upon as a diagnostic criterion. Both typical and atypical atrioventricular nodal reentrant tachycardia are compatible with varying retrograde atrial activation patterns. Attempts at establishing the presence of a ‘lower common pathway’ are probably of no practical significance. When the diagnosis of AVNRT is established, ablation should be only directed towards the anatomic position of the slow pathway. If right septal attempts are unsuccessful, the left septal side should be tried. Ablation targeting earliest atrial activation sites during typical atrioventricular nodal reentrant tachycardia or the fast pathway in general for any kind of typical or atypical atrioventricular nodal reentrant tachycardia, are not justified. In this review we discuss current concepts about the tachycardia circuit, electrophysiologic diagnosis, and ablation of this arrhythmia.

The authors describe a novel three-dimensional, 252-lead electrocardiography (ECG) and computed tomography (CT)-based non-invasive cardiac imaging and mapping modality. This technique images potentials, electrograms and activation sequences (isochrones) on the epicardial surface of the heart. This tool has been investigated in the normal cardiac electrophysiology and various tachyarrhythmic, conduction and anomalous depo-repolarisation disorders. The clinical application of this system includes a wide range of electrical disorders like atrial arrhythmias (premature atrial beat, atrial tachycardia, atrial fibrillation), ventricular arrhythmias (premature ventricular beat, ventricular tachycardia) and ventricular pre-excitation (Wolff-Parkinson-White syndrome). In addition, the system has been used in exploring abnormalities of the His-Purkinje conduction like the bundle branch block and intraventricular conduction disturbance and thereby useful in electrically treating the associated heart failure (cardiac resynchronisation). It has a potential role in furthering our understanding of abnormalities of ventricular action potential (depolarisation [Brugada syndrome and repolarisation], long QT and early repolarisation syndromes) and in evaluating the impact of drugs on His-Purkinje conduction and cardiac action potential.

The early repolarisation (ER) pattern is a common ECG finding. Most individuals with the ER pattern are at minimal risk for arrhythmic events. In others, ER increases the arrhythmic risk of underlying cardiac pathology. Rarely ER syndrome will manifest as a primary arrhythmogenic disorder causing ventricular fibrillation (VF). ER syndrome is defined as syncope attributed to ventricular arrhythmias or cardiac arrest attributed to ER following systematic exclusion of other etiologies. Some ECG features associated with ER portend a higher risk. However, clinically useful risk-stratifying tools to identify the asymptomatic patient at high risk are lacking. Patients with asymptomatic ER and no family history of malignant ER should be reassured. All patients with ER should continue to have modifiable cardiac risk factors addressed. Symptomatic patients should be systematically investigated, directed by symptoms.

Arrhythmogenic right ventricular cardiomyopathy is an inherited disorder characterised by progressive replacement of ventricular myocardium by fibrofatty tissue that predisposes patients to ventricular arrhythmias, heart failure and sudden death. Treatment focuses on slowing disease progression, decreasing the burden of arrhythmias and preventing sudden cardiac death through placement of implantable cardioverter-defibrillators (ICDs), catheter ablation and the use of antiarrhythmic medication. Although only ICDs have been demonstrated to affect patient mortality, antiarrhythmic medications are important adjuncts in reducing patient morbidity and inappropriate ICD therapy. Of the individual antiarrhythmic agents available, sotalol, beta-blockers and amiodarone appear to be most effective in arrhythmia suppression. Calcium-channel blockers may be effective in selected patients. For patients who are refractory to single agent therapy, combination therapy may be considered with the most effective combinations being sotalol + flecainide and amiodarone + beta-blockers.

Atrial fibrillation (AF) is associated with increased mortality that is largely due to the severe co-morbidities of patients with this rhythm disturbance rather than to its electrocardiographic features. Available evidence indicated that ageing, heart failure and stroke are the most important predictors of all-cause mortality. Additional clinical parameters such as smoking, renal impairment, chronic obstructive pulmonary disease may also identify patients at risk. The prevention of thromboembolic events is based on oral anticoagulant therapy, which reduces the severity and mortality of ischaemic strokes but slightly increase the rate of haemorrhagic events. Most of the traditional risk stratifiers commonly used in patients in sinus rhythm such as New York Heart Association (NYHA) functional class, left ventricular ejection fraction (LVEF) and resting heart rate seem to be less effective in AF patients thus leaving to the physician judgment the main responsibility of identifying patients with an increased mortality risk.

Long-standing tachycardia is a well-recognised cause of heart failure and left ventricular dysfunction, and has led to the nomenclature, tachycardia-induced cardiomyopathy (TIC). TIC is generally a reversible cardiomyopathy if the causative tachycardia can be treated effectively, either with medications, surgery or catheter ablation. The diagnosis is usually made after demonstrating recovery of left ventricular function with normalisation of heart rate in the absence of other identifiable aetiologies. One hundred years after the first reported case of TIC, our understanding of the pathophysiology of TIC in humans remains limited despite extensive work in animal models of TIC. In this review we will discuss the proposed mechanisms of TIC, the causative tachyarrhythmias and their treatment, outcomes for patients diagnosed with TIC, and future directions for research and clinical care.

Since the first description of the Brugada syndrome (BS) in 1992, scientific progress in the understanding of this disease has been enormous; at the same time more and more individuals with the disease have been diagnosed. The profile of patients with BS has changed with more asymptomatic individuals and less expressive clinical features. Asymptomatic BS individuals are at lower arrhythmic risk than those presenting with syncope or sudden cardiac death (SCD). The event incidence rate is around 0.5 % per year; this figure is relevant due to the fact that individuals have a long life expectancy and are otherwise healthy. As a result of the risk of SCD, risk stratification is of utmost importance. As the implantation of a cardioverter defibrillator is the main treatment for those patients at higher risk, benefits and long-term potential risks have to be adequately considered. Some risk factors, such as spontaneous type 1 electrocardiogram (ECG) pattern, are widely accepted, whilst for others contradictory data are present. Furthermore, novel risk factors are now available that might help in the management of BS. The presence of a spontaneous type 1 ECG pattern, history of sinus node dysfunction and inducible ventricular arrhythmias during programmed electrical stimulation of the heart allow us to risk stratify these patients.

Atrial septal defects (ASDs) are among the most common of congenital heart defects and are frequently associated with atrial arrhythmias. Atrial and ventricular geometrical remodelling secondary to the intracardiac shunt promotes evolution of the electrical substrate, predisposing the patient to atrial fibrillation and other arrhythmias. Closure of an ASD reduces the immediate and long-term prevalence of atrial arrhythmias, but the evidence suggests that patients remain at an increased long-term risk in comparison with the normal population. The closure technique itself and its timing impacts future arrhythmia risk profile while subsequent transseptal access following surgical or device closure is complicated. Newer techniques combined with increased experience will help to alleviate some of the difficulties associated with optimal management of arrhythmias in these patients.

Cardiovascular-related sudden death is the leading cause of mortality in athletes during sport. Thus, it is of clinical importance to identify ECG changes that represent normal adaptation in athletes, and differentiate them from truly pathological findings. However, a distinction between adaptive and pathological ECG changes in athletes is not always easy. This article discusses exercise-induced ECG changes and the differential diagnosis of conditions that present with similar ECG patterns.

Lightning strikes are a common and leading cause of morbidity and mortality. Multiple organ systems can be involved, though the effects of the electrical current on the cardiovascular system are one of the main modes leading to cardiorespiratory arrest in these patients. Cardiac effects of lightning strikes can be transient or persistent, and include benign or life-threatening arrhythmias, inappropriate therapies from cardiac implantable electronic devices, cardiac ischaemia, myocardial contusion, pericardial disease, aortic injury, as well as cardiomyopathy with associated ventricular failure. Prolonged resuscitation can lead to favourable outcomes especially in young and previously healthy victims.

Hypertrophic cardiomyopathy (HCM) represents a common inherited cardiac disorder with well-known complications including stroke and sudden cardiac death. There is a recognised association between HCM and the development of AF. This review describes the epidemiology of AF within the HCM population and analyses the risk factors for the development of AF. It further discusses the outcomes associated with AF in this population, including the evidence in support of higher stroke risk in patients with HCM with AF compared with the general AF population. Finally, the evidence and recommendations for anticoagulation in this patient group are addressed.

Anticoagulation is routinely prescribed to patients with persistent AF before cardioversion to reduce the risk of thromboembolic events. As direct oral anticoagulants (DOACs) have a rapid onset of action, a consistent anticoagulant effect, if taken correctly, and do not need monitoring or dose adjustments, there is considerable interest in their use for patients with AF undergoing cardioversion. Post-hoc analyses show that DOACs are safe to use prior to and following cardioversion. In addition, two randomised controlled trials, X-VeRT and ENSURE-AF, have demonstrated the efficacy and safety of the DOACs rivaroxaban and edoxaban, respectively, in this setting. The use of DOACs allows cardioversions to be performed promptly and reduces the number of cancelled procedures compared with the use of warfarin.

Recurrent episodes of ventricular tachycardia in patients with structural heart disease are associated with increased mortality and morbidity, despite the life-saving benefits of implantable cardiac defibrillators. Reducing implantable cardiac defibrillator therapies is important, as recurrent shocks can cause increased myocardial damage and stunning, despite the conversion of ventricular tachycardia/ventricular fibrillation. Catheter ablation has emerged as a potential therapeutic option either for primary or secondary prevention of these arrhythmias, particularly in post-myocardial infarction cases where the substrate is well defined. However, the outcomes of catheter ablation of ventricular tachycardia in structural heart disease remain unsatisfactory in comparison with other electrophysiological procedures. The disappointing efficacy of ventricular tachycardia ablation in structural heart disease is multifactorial. In this review, we discuss the issues surrounding this and examine the limitations of current mapping approaches, as well as newer technologies that might help address them.

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare but severe genetic cardiac arrhythmia disorder, with symptoms including syncope and sudden cardiac death due to polymorphic VT or ventricular fibrillation typically triggered by exercise or emotions in the absence of structural heart disease. The cornerstone of medical therapy for CPVT is β -blockers. However, recently flecainide has been added to the therapeutic arsenal for CPVT. In this review we summarise current data on the efficacy and role of flecainide in the treatment of CPVT.

The invasive management of atrial fibrillation (AF) has been considerably changed by the identification of major sites of AF initiation and/or maintenance within the pulmonary vein antra. Percutaneous catheter ablation of these targets has become the standard of care for sustained maintenance of sinus rhythm. Long-term failure of ablation is related to an inability to create a durable transmural lesion or to identify all of the non-pulmonary vein arrhythmia triggers. Pharmacological challenges during catheter ablation have been suggested to improve outcomes in both paroxysmal and persistent AF. Herein we review the mechanism and evidence for the use of pharmacological adjuncts during the catheter ablation of AF.

Large-scale implantable cardioverter defibrillator (ICD) trials have unequivocally shown a reduction in mortality in appropriately selected patients with heart failure and depressed left ventricular function. However, there is a strong association between shocks and increased mortality in ICD recipients. It is unclear if shocks are merely a marker of a more severe cardiovascular disease or directly contribute to the increase in mortality. The aim of this review is to examine the relationship between ICD shocks and mortality, and explore possible mechanisms. Data examining the effect of shocks in the absence of spontaneous arrhythmias as well as studies of non-shock therapy and strategies to reduce shocks are analysed to try and disentangle the shocks versus substrate debate.

This overview gives an update on the molecular mechanisms, clinical manifestations, diagnosis and therapy of arrhythmogenic cardiomyopathy (ACM). ACM is mostly hereditary and associated with mutations in genes encoding proteins of the intercalated disc. Three subtypes have been proposed: the classical right-dominant subtype generally referred to as ARVC/D, biventricular forms with early biventricular involvement and left-dominant subtypes with predominant LV involvement. Typical symptoms include palpitations, arrhythmic (pre)syncope and sudden cardiac arrest due to ventricular arrhythmias, which typically occur in athletes. At later stages, heart failure may occur. Diagnosis is established with the 2010 Task Force Criteria (TFC). Modern imaging tools are crucial for ACM diagnosis, including both echocardiography and cardiac magnetic resonance imaging for detecting functional and structural alternations. Of note, structural findings often become visible after electrical alterations, such as premature ventricular beats, ventricular fibrillation (VF) and ventricular tachycardia (VT). 12-lead ECG is important to assess for depolarisation and repolarisation abnormalities, including T-wave inversions as the most common ECG abnormality. Family history and the detection of causative mutations, mostly affecting the desmosome, have been incorporated in the TFC, and stress the importance of cascade family screening. Differential diagnoses include idiopathic right ventricular outflow tract (RVOT) VT, sarcoidosis, congenital heart disease, myocarditis, dilated cardiomyopathy, athlete’s heart, Brugada syndrome and RV infarction. Therapeutic strategies include restriction from endurance and competitive sports, β-blockers, antiarrhythmic drugs, heart failure medication, implantable cardioverter-defibrillators and endocardial/epicardial catheter ablation.

Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is an inherited cardiomyopathy characterised by frequent ventricular arrhythmias and slowly progressive predominant RV dysfunction. Up to two-thirds of ARVD/C patients have mutations in genes encoding the cardiac desmosome. Mutations in other genes are increasingly recognised. Inheritance of ARVD/C is generally autosomal dominant with reduced age-related penetrance and significant variable expressivity. While the full explanation for this phenotypic heterogeneity remains unclear, there is increasing evidence that exercise plays a major role in disease penetrance and arrhythmic risk. The disproportionate representation of athletes among ARVD/C patients has long been noted. Recently, the association of exercise with earlier onset and more severe arrhythmic and structural disease has been documented. This article reviews current evidence regarding the association of genotype, exercise and clinical outcomes and discusses the emerging paradigm in which genetic predisposition and environmental factors (exercise) interact around a threshold for phenotypic expression of ARVD/C.

International audience; Atrial fibrillation (AF) is the most common rhythm disorder, and is strongly associated with thromboembolic events and heart failure. Over the past decade, catheter ablation of AF has advanced considerably with progressive improvement in success rates. However, interventional treatment is still challenging, especially for persistent and long-standing persistent AF. Recently, AF analysis using a non-invasive body surface mapping technique has been shown to identify localised reentrant and focal sources, which play an important role in driving and perpetuating AF. Non-invasive mapping-guided ablation has also been reported to be effective for persistent AF. In this review, we describe new clinical insights obtained from non-invasive mapping of persistent AF to guide catheter ablation.

Orthotopic heart transplantation (OHT) is currently the most effective long-term therapy for patients with end-stage cardiac disease, even as left ventricular devices show markedly improved outcomes. As surgical techniques and immunosuppressive regimens have been refined, short-term mortality caused by sepsis has decreased, while morbidity caused by repeated rejection episodes and vasculopathy has increased, and is often manifested by arrhythmias. These chronic transplant complications require early and aggressive multidisciplinary treatment. Understanding the relationship between arrhythmias and these complications in the acute and chronic stages following OHT is critical in improving patient prognosis, as arrhythmias may be the earliest or sole presentation. Finally, decentralised/denervated hearts represent a unique opportunity to investigate the underlying mechanisms of arrhythmias.

Atrial fibrillation (AF) is the most common sustained arrhythmia encountered in clinical practice, yet our understanding of the mechanisms that initiate and sustain this arrhythmia remains quite poor. Over the last 50 years, various mechanisms of AF have been proposed, yet none has been consistently observed in both experimental studies and in humans. Recently, there has been increasing interest in understanding how spiral waves or rotors – which are specific, organised forms of functional reentry – sustain human AF and how they might be therapeutic targets for catheter-based ablation. The following review describes the historical understanding of reentry and AF mechanisms from earlier in the 20th century, advances in our understanding of mechanisms that are able to sustain AF with a focus on rotors and complex fractionated atrial electrograms (CFAEs), and how the study of AF mechanisms has resulted in new strategies for treating AF with novel forms of catheter ablation.

The incidence of atrial fibrillation (AF) was around 1.5 per 1000 person-years in Taiwan. Systemic thromboembolism is the most severe complication of AF. Risk stratification and adequate thromboembolism prophylaxis is the cornerstone of treatment in AF patients. The CHA2DS2-VASc score is powerful in selecting “truly low-risk” patients who are not necessary to receive anticoagulation therapies. It is also useful in predicting thromboembolic events and mortality for patients undergoing AF ablation. Recently, more and more biomarkers and imaging parameters were reported to be associated with adverse events in AF patients. How could these biomarkers and imaging tools change the current strategy of stroke prevention in AF deserves further investigations.

Cardiac resynchronisation therapy (CRT) is a well-established non-pharmacological treatment option for patients with refractory symptomatic heart failure (HF) already under optimal medical therapy. CRT is founded on the principle that interventricular conduction disturbances and more in particular left bundle branch block (LBBB) are deleterious to cardiac performance, and may contribute to the systolic and diastolic incompetency typical of patients with HF. Although CRT is associated with a not negligible percentage of non-response, all the international guidelines on chronic HF have extended their indications to CRT, also to patients with less symptomatic HF who are already showing signs of systolic dysfunction and interventricular dyssynchrony, without giving any substantial advice to reduce the number of failures of this therapy. This review seeks to point out the potential issues linked to CRT, with the aim of making a reappraisal of the clinical evidences supporting the current indications to CRT, and to figure out which type of research should be warranted in the field for the future to reduce the percentage of non-responders to this therapy.