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Aims To study the impact of genotype on the performance of the 2019 risk model for arrhythmogenic right ventricular cardiomyopathy (ARVC). Methods and results The study cohort comprised 554 patients with a definite diagnosis of ARVC and no history of sustained ventricular arrhythmia (VA). During a median follow-up of 6.0 (3.1,12.5) years, 100 patients (18%) experienced the primary VA outcome (sustained ventricular tachycardia, appropriate implantable cardioverter defibrillator intervention, aborted sudden cardiac arrest, or sudden cardiac death) corresponding to an annual event rate of 2.6% [95% confidence interval (CI) 1.9–3.3]. Risk estimates for VA using the 2019 ARVC risk model showed reasonable discriminative ability but with overestimation of risk. The ARVC risk model was compared in four gene groups: PKP2 (n = 118, 21%); desmoplakin (DSP) (n = 79, 14%); other desmosomal (n = 59, 11%); and gene elusive (n = 160, 29%). Discrimination and calibration were highest for PKP2 and lowest for the gene-elusive group. Univariable analyses revealed the variable performance of individual clinical risk markers in the different gene groups, e.g. right ventricular dimensions and systolic function are significant risk markers in PKP2 but not in DSP patients and the opposite is true for left ventricular systolic function. Conclusion The 2019 ARVC risk model performs reasonably well in gene-positive ARVC (particularly for PKP2) but is more limited in gene-elusive patients. Genotype should be included in future risk models for ARVC.

Background Ostensibly healthy male master endurance athletes have a greater prevalence of high coronary calcium (CAC) scores and coronary artery plaque burden, compared to similar aged, healthy sedentary counterparts. A number of theories have been postulated but reasons remain unclear. Hypertension is the leading cardiovascular risk factor in the general population. The role of subclinical hypertension and the hypertensive response to exercise (HRE) in the pathophysiology of high CAC scores and other CT markers of high-risk coronary artery disease, has not previously been reported in the healthy master endurance athlete population. Methods A cohort of 214 low Q-risk, male master (40-65 years) endurance athletes were prospectively evaluated between February 2018 and September 2019. All athletes were free from any cardiovascular risk factors, symptoms and any relevant health conditions. Clinical evaluation included cycle ergometer cardiopulmonary exercise test, ambulatory BP monitoring and coronary computed tomogram angiography (CCTA). The CCTA assessed CAC score, coronary stenosis, defined as >50%, plaque morphology (i.e. calcified, soft or mixed), and markers of plaque vulnerability including spotty calcification, ruptured plaque, positive remodelling, low attenuation plaque and napkin ring sign. Resting BP, HRE and ambulatory hypertension were defined in accordance with the latest European Society of Cardiology (ESC) guidelines and are detailed in table 1. Results All athletes (mean age 51, SD 70.1) exercised for at least 6 hours per week (median 8.5 hours) for a median of 15 years of either cycling, running or swimming or any combination of the three. The median Q risk score was 3.5%. A quarter (26%) of athletes were hypertensive at rest. A significant proportion of athletes exhibited exercise (12%) and ambulatory hypertension (41%). A CAC score >100 Agatston units (AU) was present in (16%) of athletes, with 5% exhibiting significant coronary stenosis. A third (32%) of all plaque morphologies were non-calcified (27% mixed and 5% soft) and 13% had additional plaque vulnerability markers. The most prevalent marker was spotty calcification (11.3%), followed by positive remodelling (8.9%). Logistic regression identified the BP parameters predictive for a CAC score >100 AU, significant stenosis and plaque vulnerability markers. A 5 mmHg increase in resting systolic BP, maximal systolic exercise BP and 24 hour and nocturnal ambulatory systolic were associated with both significant stenosis and plaque vulnerability markers and a 5 mmHg increase in resting systolic BP (SBP) and 24 hour and nocturnal ambulatory SBP were associated with a CAC score >100 AU. The p values, odds ratios (OR) and respective 95% confidence intervals are detailed in table 3. BP parameters were not associated with calcified plaque by multinomial logistic regression, however for every 5mmHg increase in maximal exercise SBP, resting SBP and 24-hour and nocturnal ambulatory SBP, the relative risk (RR) of mixed morphology plaque was increased by 19.27% (p=0.001, CI 1.07-1.33), 18.49% (p=0.024, CI 1.02-1.37), 46.45% (p=0.001, CI 1.12-1.91) and 50.54% (p=0.001, CI 1.18-1.93) respectively. Conclusions Hypertension is prevalent, under diagnosed, and contributes to the development of potentially unstable coronary artery disease in healthy male endurance athletes. Recommendations for cardiovascular evaluation of master athletes should consider a low threshold for non-invasive exercise testing and ambulatory BP monitoring for for athletes with hypertension and even high-normal BP. Table 1. ESC definitions of hypertension. Table 2. Prevalence of hypertension according to ESC guideline classifications. Table 3. Logistic regression P values, odds ratios and confidence intervals for a 5mmHg increase in BP parameters. Conflict of Interest Nil

Prominent J-waves are observed in several clinical conditions many of which are highly arrhythmogenic and may lead to ventricular fibrillation (VF) and/or sudden cardiac death. We present the case of a 34-year-old male patient with hypothermia. Prominent J-waves (Osborn waves) and prolonged QT interval was evident in nearly every lead. Early recognition of these arrhythmogenic electrocardiogram (ECG) findings and treatment of hypothermia is important to minimize the risk of arrhythmic events.

Key Clinical Message Fluoroscopy permits rapid and straightforward assessment of mechanical valve function and allows a distinction between normal and malfunctional prostheses, acting as a complementary diagnostic step.

Atrial fibrillation (AF) is the most common arrhythmia affecting elderly patients. Management and treatment of AF in this rapidly growing population of older patients involve a comprehensive assessment that includes comorbidities, functional, and social status. The cornerstone in therapy of AF is thromboembolic protection. Anticoagulation therapy has evolved, using conventional or newer medications. Percutaneous left atrial appendage closure is a new invasive procedure evolving as an alternative to systematic anticoagulation therapy. Rate or rhythm control leads to relief in symptoms, fewer hospitalizations, and an improvement in quality of life. Invasive methods, such as catheter ablation, are the new frontier of treatment in maintaining an even sinus rhythm in this particular population.

Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. Several conventional and novel predictors of AF development and progression (from paroxysmal to persistent and permanent types) have been reported. The most important predictor of AF progression is possibly the arrhythmia itself. The electrical, mechanical and structural remodeling determines the perpetuation of AF and the progression from paroxysmal to persistent and permanent forms. Common clinical scores such as the hypertension, age ≥ 75 years, transient ischemic attack or stroke, chronic obstructive pulmonary disease, and heart failure and the congestive heart failure, hypertension, age ≥ 75 years, diabetes mellitus, stroke/transient ischemic attack, vascular disease, age 65-74 years, sex category scores as well as biomarkers related to inflammation may also add important information on this topic. There is now increasing evidence that even in patients with so-called lone or idiopathic AF, the arrhythmia is the manifestation of a structural atrial disease which has recently been defined and described as fibrotic atrial cardiomyopathy. Fibrosis results from a broad range of factors related to AF inducing pathologies such as cell stretch, neurohumoral activation, and oxidative stress. The extent of fibrosis as detected either by late gadolinium enhancement-magnetic resonance imaging or electroanatomic voltage mapping may guide the therapeutic approach based on the arrhythmia substrate. The knowledge of these risk factors may not only delay arrhythmia progression, but also reduce the arrhythmia burden in patients with first detected AF. The present review highlights on the conventional and novel risk factors of development and progression of AF.