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Key Points A growing body of evidence suggests that both atrial fibrillation (AF) and right ventricular arrhythmia can be the result of intense exercise among highly trained athletes The risk of AF conferred by exercise progressively increases with the intensity of exercise Parasympathetic tone enhancement and atrial structural remodelling (that is, atrial dilatation and fibrosis) are progressively being recognized as contributors to increased exercise-induced proarrhythmogenic risk The most appropriate approach for treating exercise-induced AF remains unknown The evidence for a pure exercise-induced arrhythmogenic right ventricular cardiomyopathy (ARVC) is limited, but several studies have indicated that regular exercise is an important promoter of ARVC progression For athletes who fulfil ARVC criteria, guidelines published by scientific societies prohibit competitive sports and encourage avoidance of high-intensity dynamic sports in general The association between exercise and increased risk of atrial fibrillation among athletes is well established. In this Review, Guasch and Mont discuss the evidence supporting the existence of exercise-induced arrhythmias and describe the special considerations for management of these patients. The cardiovascular benefits of physical activity are indisputable. Nevertheless, growing evidence suggests that both atrial fibrillation and right ventricular arrhythmia can be caused by intense exercise in some individuals. Exercise-induced atrial fibrillation is most commonly diagnosed in middle-aged, otherwise healthy men who have been engaged in endurance training for >10 years, and is mediated by atrial dilatation, parasympathetic enhancement, and possibly atrial fibrosis. Cardiac ablation is evolving as a first-line tool for athletes with exercise-induced arrhythmia who are eager to remain active. The relationship between physical activity and right ventricular arrhythmia is complex and involves genetic and physical factors that, in a few athletes, eventually lead to right ventricular dilatation, followed by subsequent myocardial fibrosis and lethal ventricular arrhythmias. Sinus bradycardia and atrioventricular conduction blocks are common in athletes, most of whom remain asymptomatic, although incomplete reversibility has been shown after exercise cessation. In this Review, we summarize the evidence supporting the existence of exercise-induced arrhythmias and discuss the specific considerations for the clinical management of these patients.

Despite substantial technological and procedural advances that have improved the efficacy and safety of AF ablation in recent years, the long‐term durability of ablation lesions is still not satisfactory. There also remains concern regarding rare but potentially life‐threatening procedure‐related complications like cardiac tamponade and atrioesophageal fistulae. Current ablation strategies are aiming to optimize the trade‐off between efficacy and safety, where more extensive ablation appears to inevitably increase the risk of collateral injury. However, new forms of energy application may have the potential to resolve this quandary. The emerging concept of high power‐short duration radiofrequency ablation features a more favorable lesion geometry that appears ideally suited to create contiguous lesions in the thin‐walled atrium. Moreover, novel non‐thermal ablation methods based on electroporation appear to provide a unique selectivity for cardiomyocytes and to spare surrounding tissues composed of other cell types. Both, high power‐short duration and electroporation ablation might have the potential to break the trade‐off between effective lesions and collateral damage and to substantially improve risk‐benefit ratios in AF ablation. In addition, both approaches lead to considerable reductions in ablation times. However, their putative benefits regarding efficacy, efficiency, and safety remain to be proven in randomized controlled trials.

Late gadolinium enhancement (LGE) MRI is capable of detecting not only native cardiac fibrosis, but also ablation-induced scarring. Thus, it offers the unique opportunity to assess ablation lesions non-invasively. In the atrium, LGE-MRI has been shown to accurately detect and localise gaps in ablation lines. With a negative predictive value close to 100% it can reliably rule out pulmonary vein reconnection non-invasively and thus may avoid unnecessary invasive repeat procedures where a pulmonary vein isolation only approach is pursued. Even LGE-MRI-guided repeat pulmonary vein isolation has been demonstrated to be feasible as a standalone approach. LGE-MRI-based lesion assessment may also be of value to evaluate the efficacy of ventricular ablation. In this respect the elimination of LGE-MRI-detected arrhythmogenic substrate may serve as a potential endpoint, but validation in clinical studies is lacking. Despite holding great promise, the widespread use of LGE-MRI is still limited by the absence of standardised protocols for image acquisition and post-processing. In particular, reproducibility across different centres is impeded by inconsistent thresholds and internal references to define fibrosis. Thus, uniform methodological and analytical standards are warranted to foster a broader implementation in clinical practice.

Background and Objectives: Left atrial (LA) remodelling and dilatation predicts atrial fibrillation (AF) recurrences after catheter ablation. However, whether right atrial (RA) remodelling and dilatation predicts AF recurrences after ablation has not been fully evaluated. Materials and Methods: This is an observational study of 85 consecutive patients (aged 57 ± 9 years; 70 [82%] men) who underwent cardiac magnetic resonance before first catheter ablation for AF (40 [47.1%] persistent AF). Four-chamber cine-sequence was selected to measure LA and RA area, and ventricular end-systolic image phase to obtain atrial 3D volumes. The effect of different variables on event-free survival was investigated using the Cox proportional hazards model. Results: In patients with persistent AF, combined LA and RA area indexed to body surface area (AILA + RA) predicted AF recurrences (HR = 1.08, 95% CI 1.00–1.17, p = 0.048). An AILA + RA cut-off value of 26.7 cm2/m2 had 72% sensitivity and 73% specificity for predicting recurrences in patients with persistent AF. In this group, 65% of patients with AILA + RA > 26.7 cm2/m2 experienced AF recurrence within 2 years of follow-up (median follow-up 11 months), compared to 25% of patients with AILA + RA ≤ 26.7 cm2/m2 (HR 4.28, 95% CI 1.50–12.22; p = 0.007). Indices of LA and RA dilatation did not predict AF recurrences in patients with paroxysmal AF. Atrial 3D volumes did not predict AF recurrences after ablation. Conclusions: In this pilot study, the simple measurement of AILA + RA may predict recurrences after ablation of persistent AF, and may outperform measurements of atrial volumes. In paroxysmal AF, atrial dilatation did not predict recurrences. Further studies on the role of RA and LA remodelling are needed.

To bridge the current gap between the known mechanisms of atrial fibrillation (AF) and the clinical management of patients with this arrhythmia, Fabritz and colleagues propose a roadmap to develop a set of clinical markers that reflect the major causes of AF in patients. A new, mechanism-based classification of AF can provide the basis for personalized prevention and management. Despite remarkable advances in antiarrhythmic drugs, ablation procedures, and stroke-prevention strategies, atrial fibrillation (AF) remains an important cause of death and disability in middle-aged and elderly individuals. Unstructured management of patients with AF sharply contrasts with our detailed, although incomplete, knowledge of the mechanisms that cause AF and its complications. Altered calcium homeostasis, atrial fibrosis and ageing, ion-channel dysfunction, autonomic imbalance, fat-cell infiltration, and oxidative stress, in addition to a susceptible genetic background, contribute to the promotion, maintenance, and progression of AF. However, clinical management of patients with AF is currently guided by stroke risk parameters, AF pattern, and symptoms. In response to this apparent disconnect between the known pathophysiology of AF and clinical management, we propose a roadmap to develop a set of clinical markers that reflect the major causes of AF in patients. Thereby, the insights into the mechanisms causing AF will be transformed into a format that can underpin future personalized strategies to prevent and treat AF, ultimately informing better patient care.

The original version of this article unfortunately contained a mistake. Francisco Alarcón, Susana Prat-Gonzalez, José Tomás Ortiz, Lluís Mont and Ivo Roca-Luque were not listed among the authors.

Although the benefits of moderate exercise in patients at high cardiovascular risk are well established, the effects of strenuous exercise remain unknown. We aimed to study the impact of strenuous exercise in a very high cardiovascular risk model. Nephrectomized aged Zucker obese rats were trained at a moderate (MOD) or high (INT) intensity or were kept sedentary (SED) for 10 weeks. Subsequently, echocardiography and ex vivo vascular reactivity assays were performed, and blood, aortas, perivascular adipose tissue (PVAT), and left ventricles (LVs) were harvested. An improved risk profile consisting of decreased body weight and improved response to a glucose tolerance test was noted in the trained groups. Vascular reactivity experiments in the descending thoracic aorta demonstrated increased endothelial NO release in the MOD group but not in the INT group, compared with SED; the free radical scavenger TEMPOL improved endothelial function in INT rats to a similar level as MOD. An imbalance in the expression of oxidative stress-related genes toward a pro-oxidant environment was observed in the PVAT of INT rats. In the heart, INT training promoted eccentric hypertrophy and a mild reduction in ejection fraction. Obesity was associated with LV fibrosis and a transition toward β-myosin heavy chain and the N2Ba titin isoform. Exercise reverted the myosin imbalance, but only MOD reduced the predominance of the N2Ba titin isoform. In conclusion, moderate exercise yields the most intense cardiovascular benefits in a high-cardiovascular-risk animal model, while intense training partially reverts them.

There is growing appreciation of oligogenic disorders, 2,3 the role of modifier genes, 2 and the use of genetic testing for risk stratification, even in common cardiac diseases such as coronary artery disease or atrial fibrillation (AFib), including a proposal for a score awaiting validation. 4 This document reviews the state of genetic testing at the present time, and addresses the questions of what tests to perform and when to perform them. Additionally, the document presents the state of genetic testing for inherited arrhythmia syndromes, cardiomyopathies, sudden cardiac death (SCD), congenital heart disease (CHD), coronary artery disease, and heart failure. The writing committee recognizes that the feasibility of genomic testing by gene panel testing or by WES or WGS depends on the availability of genomic technology and on regional reimbursement policy. [...]the recommendation ‘should do this’ can be read as ‘should do this when available’. Table 2 Relevant clinical practice documents or guidelines Title Publication year Consensus documents/guidelines of scientific societies APHRS/HRS expert consensus statement on the investigation of decedents with sudden unexplained death and patients with sudden cardiac arrest, and of their families 6 2021 HRS/EHRA/APHRS/LAHRS Expert Consensus Statement on Catheter Ablation of Ventricular Arrhythmias 7 2020 Genetic Testing for Inherited Cardiovascular

Sustained re‐entrant tachyarrhythmias treatment has become pivotal in the grown‐up congenital heart patients clinical management. Cardiac LGE‐MRI tissue characterization integrated with high definition electroanatomic map could allow fast recognition and effective treatment of substrate of tachyarrhythmias. Cardiac LGE‐MRI areas were suggestive of post‐surgical changes both in atrium and ventricle. High‐density electro‐anatomical map localized areas of slow conduction identifying conducting isthmuses of re‐entrant arrhythmias.

ObjectiveTo investigate the association of corrected QT (QTc) interval duration and short-term outcomes in patients with acute heart failure (AHF).MethodsWe analyzed AHF patients enrolled in 11 Spanish emergency departments (ED) for whom an ECG with QTc measurement was available. Patients with pace-maker rhythm were excluded. Primary outcome was 30-day all-cause mortality and secondary outcomes were need of hospitalization, in-hospital mortality and prolonged hospitalization (> 7 days). Association between QTc and outcomes was explored by restricted cubic spline (RCS) curves. Results were expressed as odds ratios (OR) and 95%CI adjusted by patients baseline and decompensation characteristics, using a QTc = 450 ms as reference.ResultsOf 1800 patients meeting entry criteria (median age 84 years (IQR = 77–89), 56% female), their median QTc was 453 ms (IQR = 422–483). The 30-day mortality was 9.7%, while need of hospitalization, in-hospital mortality and prolonged hospitalization were 77.8%, 9.0% and 50.0%, respectively. RCS curves found longer QTc was associated with 30-day mortality if > 561 ms, OR = 1.86 (1.00–3.45), and increased up to OR = 10.5 (2.25–49.1), for QTc = 674 ms. A similar pattern was observed for in-hospital mortality; OR = 2.64 (1.04–6.69), for QTc = 588 ms, and increasing up to OR = 8.02 (1.30–49.3), for QTc = 674 ms. Conversely, the need of hospitalization had a U-shaped relationship: being increased in patients with shorter QTc [OR = 1.45 (1.00–2.09) for QTc = 381 ms, OR = 5.88 (1.25–27.6) for the shortest QTc of 200 ms], and also increasing for prolonged QTc [OR = 1.06 (1.00–1.13), for QTc = 459 ms, and reaching OR = 2.15 (1.00–4.62) for QTc = 588 ms]. QTc was not associated with prolonged hospitalization.ConclusionIn ED AHF patients, initial QTc provides independent short-term prognostic information, with increasing QTc associated with increasing mortality, while both, shortened and prolonged QTc are associated with need of hospitalization.