Key result
Electrical ventricular remodeling drives arrhythmogenicity in DCM and presents potential therapeutic targets.
Why the study?
Ventricular arrhythmias significantly contribute to morbidity and mortality in heart failure, driven by myocardial fibrosis and ion channel remodeling whose underlying molecular signaling pathways are increasingly recognized.
This review provides an overview of the pathomechanisms, including myocardial fibrosis and ion channel remodeling, underlying arrhythmogenicity in dilated cardiomyopathy.
Potential targets for arrhythmia prevention in dilated cardiomyopathy warrant testing; leaves open whether remodeling reversal improves outcomes.
Ventricular arrhythmias contribute significantly to morbidity and mortality in patients with heart failure (HF). Pathomechanisms underlying arrhythmogenicity in patients with structural heart disease and impaired cardiac function include myocardial fibrosis and the remodeling of ion channels, affecting electrophysiologic properties of ventricular cardiomyocytes. The dysregulation of ion channel expression has been associated with cardiomyopathy and with the development of arrhythmias. However, the underlying molecular signaling pathways are increasingly recognized. This review summarizes clinical and cellular electrophysiologic characteristics observed in dilated cardiomyopathy (DCM) with ionic and structural alterations at the ventricular level. Furthermore, potential translational strategies and therapeutic options are highlighted.
No takes yet. Share an insight, caveat, or question.
Mages et al. (2021) conducted a review in Dilated Cardiomyopathy. Electrical ventricular remodeling, including myocardial fibrosis and ion channel dysregulation, contributes to arrhythmogenicity in dilated cardiomyopathy and presents potential therapeutic targets.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: