Exercise, sex and atrial fibrillation: arrhythmogenesis beyond Y-chromosome?

Although prevailing research trends favour large clinical trials and registries, meticulous observation during daily clinical practice remains a valuable source for hypothesis generation in medical research. Clinical experience has allowed the identification of several risk factors in the cardiovascular field...

Diagnosis, pathophysiology, and management of exercise-induced arrhythmias

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

Exercise and the heart: unmasking Mr Hyde

As physicians, we often face patients with cardiovascular risk factors or different kinds of heart disease. We prescribe statins, ACE inhibitors or β-blockers, but also (should) encourage our patients to engage in regular physical activity to reduce cardiovascular disease burden...

Atrial fibrillation progression: How sick is the atrium?

After many years of lack of interest in the atrium by clinical cardiologists, the evidence of increased morbidity and mortality in patients with atrial fibrillation (AF) relocated the atrium to a central position in cardiology more than 2 decades ago.1 First came the studies showing improved outcome with the use of anticoagulants; later, the ever-lasting controversy on rate vs rhythm control; and at present, new imaging techniques and new therapeutic tools to better define atrial remodeling and improve therapy..

Mechanisms of atrial fibrillation in athletes: what we know and what we do not know.

Exercise is an emerging cause of atrial fibrillation (AF) in young individuals without coexisting cardiovascular risk factors. The causes of exercise-induced atrial fibrillation remain largely unknown, and conclusions are jeopardised by apparently conflicting data. Some components of the athlete's heart are known to be arrhythmogenic in other settings. Bradycardia, atrial dilatation and, possibly, atrial premature beats are therefore biologically plausible contributors to exercise-induced AF. Challenging findings in an animal model suggest that exercise might also prompt the development of atrial fibrosis, possibly due to cumulative minor structural damage after each exercise bout. However, there is very limited, indirect data supporting this hypothesis in athletes. Age, sex, the presence of comorbidities and cardiovascular risk factors, and genetic individual variability might serve to flag those athletes who are at the higher risk of exercise-induced AF. In this review, we will critically address current knowledge on the mechanisms of exercise-induced AF

Validity of the Polar V800 monitor for measuring heart rate variability in mountain running route conditions

PURPOSE: This study was conducted to test, in mountain running route conditions, the accuracy of the Polar V800 monitor as a suitable device for monitoring the heart rate variability (HRV) of runners. METHOD: Eighteen healthy subjects ran a route that included a range of running slopes such as those encountered in trail and ultra-trail races. The comparative study of a V800 and a Holter SEER 12 ECG Recorder included the analysis of RR time series and short-term HRV analysis. A correction algorithm was designed to obtain the corrected Polar RR intervals. Six 5-min segments related to different running slopes were considered for each subject. RESULTS: The correlation between corrected V800 RR intervals and Holter RR intervals was very high (r = 0.99, p  0.05) and were well correlated (r ≥ 0.96, p < 0.001). CONCLUSION: Narrow limits of agreement, high correlations and small effect size suggest that the Polar V800 is a valid tool for the analysis of heart rate variability in athletes while running high endurance events such as marathon, trail, and ultra-trail races. KEYWORDS: HRV; Open field running conditions; Polar V800 heart rate monitor; Validatio

Losartan prevents heart fibrosis induced by long-term intensive exercise in an animal model

Rationale Recently it has been shown that long-term intensive exercise practice is able to induce myocardial fibrosis in an animal model. Angiotensin II is a profibrotic hormone that could be involved in the cardiac remodeling resulting from endurance exercise. Objective This study examined the antifibrotic effect of losartan, an angiotensin II type 1 receptor antagonist, in an animal model of heart fibrosis induced by long-term intense exercise. Methods and Results Male Wistar rats were randomly distributed into 4 experimental groups: Exercise, Exercise plus losartan, Sedentary and Sedentary plus losartan. Exercise groups were conditioned to run vigorously for 16 weeks. Losartan was orally administered daily before each training session (50 mg/kg/day). Time-matched sedentary rats served as controls. After euthanasia, heart hypertrophy was evaluated by histological studies; ventricular collagen deposition was quantified by histological and biochemical studies; and messenger RNA and protein expression of transforming growth factor-β1, fibronectin-1, matrix metalloproteinase-2, tissue inhibitor of metalloproteinase-1, procollagen-I and procollagen-III was evaluated in all 4 cardiac chambers. Daily intensive exercise caused hypertrophy in the left ventricular heart wall and originated collagen deposition in the right ventricle. Additionally long-term intensive exercise induced a significant increase in messenger RNA expression and protein synthesis of the major fibrotic markers in both atria and in the right ventricle. Losartan treatment was able to reduce all increases in messenger RNA expression and protein levels caused by exercise, although it could not completely reverse the heart hypertrophy. Conclusions Losartan treatment prevents the heart fibrosis induced by endurance exercise in training animals

Optical Control of Cardiac Function with a Photoswitchable Muscarinic Agonist

Light-triggered reversible modulation of physiological functions offers the promise of enabling on-demand spatiotemporally controlled therapeutic interventions. Optogenetics has been successfully implemented in the heart, but significant barriers to its use in the clinic remain, such as the need for genetic transfection. Herein, we present a method to modulate cardiac function with light through a photoswitchable compound and without genetic manipulation. The molecule, named PAI, was designed by introduction of a photoswitch into the molecular structure of an M2 mAChR agonist. In vitro assays revealed that PAI enables light-dependent activation of M2 mAChRs. To validate the method, we show that PAI photoisomers display different cardiac effects in a mammalian animal model, and demonstrate reversible, real-time photocontrol of cardiac function in translucent wildtype tadpoles. PAI can also effectively activate M2 receptors using two-photon excitation with near-infrared light, which overcomes the scattering and low penetration of short-wave-length illumination, and offers new opportunities for intravital imaging and control of cardiac function

Ventricular tachycardia burden reduction after substrate ablation: predictors of recurrence.

BACKGROUND Substrate-based ventricular tachycardia (VT) ablation is a first-line treatment in patients with structural cardiac disease and sustained VT refractory to medical therapy. Despite technological improvements and increased knowledge of VT substrate, recurrence still is frequent. Published data are lacking on the possible reduction in VT burden after ablation despite recurrence. OBJECTIVE The purpose of this study was to assess VT burden reduction during long-term follow-up after substrate ablation and identify predictors of VT recurrence. METHODS We analyzed 234 consecutive VT ablation procedures in 207 patients (age 63 6 14.9 years; 92% male; ischemic heart disease in 65%) who underwent substrate ablation in a single center from 2013 to 2018. RESULTS After follow-up of 3.14 6 1.8 years, the VT recurrence rate was 41.4%. Overall, a 99.6% reduction in VT burden (median VT episodes per year: preprocedural 3.546 [1.347-13.951] vs postprocedural 0.001 [0-0.689]; P 5 .001) and a 96.3% decrease in implantable cardioverter-defibrillator (ICD) shocks (preprocedural 1.145 [0.118-4.467] vs postprocedural 0.042 [0-0.111] per year; P 5 .017) were observed. In the subgroup of patients who experienced VT recurrences, VT burden decreased by 69.2% (median VT episodes per year: preprocedural 2.876 [1.105-8.801] vs postprocedural 0.882 [0.505-2.283]; P ,.001). Multivariable analysis showed persistence of late potentials (67% vs 19%; hazard ratio 3.18 [2.18- 6.65]; P ,.001) and lower left ventricular ejection fraction (EF) (30 [25-40] vs 39 [30-50]; P 5 .022) as predictors of VT recurrence. CONCLUSION Despite a high recurrence rate during long-term follow-up, substrate-based VT ablation is related to a large reduction in VT burden and a decrease in ICD therapies. Lower EF and persistence of late potentials are predictors of recurrence. KEYWORDS Arrhythmic burden reduction; Implantable cardioverter-defibrillator shock prevention; Ventricular tachycardia ablation; Ventricular tachycardia recurrence predictors; Ventricular tachycardia storm; Ventricular tachycardia substrate ablatio

Accuracy of standard bipolar amplitude voltage thresholds to identify late potential channels in ventricular tachycardia ablation

Background: Ventricular tachycardia (VT) is caused by the presence of a slow conduction channel (CC) of border zone (BZ) tissue inside the scar-core tissue. Electroanatomic mapping can depict this tissue by voltage mapping. Areas of slow conduction can be detected as late potentials (LPs) and their abolition is the most accepted ablation endpoint. In the current guidelines, bipolar voltage thresholds for BZ and core scar are 1.5 and 0.5 mV respectively. The performance of these values is controversial. The aim of the study is to analyze the diagnostic yield of current amplitude thresholds in voltage map to define VT substrate in terms of CCs of LPs. Predictors of usefulness of current thresholds will be analyzed. Methods: All patients with structural heart disease who underwent VT ablation in Hospital Clinic in 2016-2017 were included. Maps with delineation of CCs based on LPs were created with contact force sensor catheter. Thresholds were adjusted for every patient based on CCs. Diagnostic yield and predictors of performance of conventional thresholds were analyzed. Results: During study period, 57 consecutive patients were included (age: 60.4 ± 8.5; 50.2% ischemic cardiomyopathy, LVEF 39.8 ± 13.5%). Cutoff voltages that better identified the scar and BZ according to the LP channels were 0.32 (0.02-2 mV) and 1.84 (0.3-6 mV) respectively. Current voltage thresholds identified correctly core and BZ in 87.7% and 42.1% of the patients respectively. Accuracy was worse in non-ischemic cardiomyopathy (NICM) especially for BZ (28.6% vs 55.2%, p = 0.042). Conclusions: Accuracy of standard voltage thresholds for scar and BZ is poor in terms of LPs detection. Diagnostic yield is worse in NICM patients specially for border zone