Vigorous endurance training results in prolongation of cardiac repolarization and increased repolarization instability, mild ventricular fibrosis associated with decrease of the transient outward potassium current, and enhanced arrhythmia susceptibility in canine model.

In models reconstructed from MRI scans of patients with embolic stroke of undetermined source, computational simulations reveal that fibrosis has the intrinsic capacity to sustain arrhythmia drivers when subjected to triggered activity known to exist in patients with atrial fibrillation.

Customization of ion channel gating enhances homeostatic regulation through automatic detection and correction of abnormal physiological changes, as illustrated by self-restoration of excitation rhythm in cardiac arrhythmias.

A novel mathematical method for screening new drugs for pro-arrhythmic cardiotoxicity without using animals or costly drug-specific computer simulations is proposed.

Ex vivo, in vitro, and computational modeling studies indicate a persistence of myofibroblast senescence in the infarct border zone with age which can disrupt conduction and promote arrhythmias via senescent myofibroblast-cardiomyocyte coupling.

Important mechanistic details on Duchenne Muscular Dystrophy arrhythmogenesis are revealed, providing a crucial lead for investigators interested in developing therapeutic solutions for this deadly disease.

4,6-Sulfation of chondroitin sulfate proteoglycans prevents sympathetic nerve regeneration into the infarct after myocardial ischemia/reperfusion, and reducing this sulfation promotes nerve regeneration and decreases arrhythmia susceptibility.

The ion channel accessory subunit KChIP2 has a transcriptional role that provides regulation over miRNA targets, driving the adverse remodeling of key ion channels during cardiac stress and leading to the development of arrhythmia.

Modest changes in expression of interacting dose-dependent transcription factors Tbx5 and Prrx1, caused by disease-associated common regulatory variants, significantly impact on the cardiac gene regulatory network and disease susceptibility.

Long-term increased risks of arrhythmia and heart failure were found in breast cancer patients, while systemic adjuvant therapies including trastuzumab and anthracyclines were associated with the increased risk of heart failure.