Ventricular fibrillation articles from across Nature Portfolio

Romero-Becerra et al. report that stress kinases p38γ and p38δ are activated in ventricles of old mice and in arrhythmogenic conditions, and they demonstrate that p38γ/δ -driven phosphorylation of RyR2 and SAP97 is a trigger for ventricular fibrillation.

Genome-wide association analyses identify new susceptibility loci for Brugada syndrome. Functional studies implicate microtubule-related trafficking effects on sodium channel expression as an underlying molecular mechanism.

Ventricular arrhythmias are associated with aging and are a leading cause of sudden cardiac death. A new study shows that hyperactivation of p38γ/δ MAPKs is a key driver of stress-induced ventricular arrhythmias via increased phosphorylation of ryanodine receptor 2 at Ser2367 and impaired localization of potassium voltage-gated channel K_v4.3.

In the CASTLE HTx trial, patients with symptomatic atrial fibrillation and end-stage heart failure who underwent catheter ablation and received medical therapy had improved outcomes compared with patients who received medical therapy only.

Alternative strategies for defibrillation improve outcomes in patients with refractory ventricular fibrillation, according to findings from the DOSE VF trial.

Extravascular implantable cardioverter–defibrillators are safe and effective at detecting and terminating ventricular arrhythmias induced at the time of implantation.

In a new mouse model of spontaneous ventricular tachycardia after myocardial infarction, cardiac neutrophils increased the likelihood of arrhythmia, whereas cardiac macrophages protected against arrhythmia.