Hyperpolarization-activated cyclic nucleotide-gated channels and ventricular arrhythmias in heart failure: a novel target for therapy? J Am Heart Assoc (2013

A rrhythmias are a common and often fatal complication ofheart failure accounting for 50 % to 70 % of cardiac deaths due to tachyarrhythmic mechanisms.1 In the failing heart, disturbances in cardiac rhythm are the likely result of cardiac remodeling consisting of structural and/or electro-physiological abnormalities. The structural heterogeneities provide a substrate for triggered activity from which ventric-ular arrhythmias can be initiated. Pathological alterations in ion channel properties and gap junction intercellular commu-nication lead to changes in the action potential profile and cellular excitability, serving as a trigger for arrhythmias. Although extensive pharmacological therapies have been developed for the treatment of arrhythmias, efficacy of the drugs remains limited due to the complex remodeling processes underlying heart failure. Among the ionic mechanisms that contribute to ventricula