Abstract
Chronic heart failure is a clinical syndrome with multiple etiologies, associated with significant morbidity and mortality. Cardiac arrhythmias, including ventricular tachyarrhythmias and atrial fibrillation, are common in heart failure. A number of cardiac diseases including heart failure alter the expression and regulation of ion channels and transporters leading to arrhythmogenic electrical remodeling. Myocardial hypertrophy, fibrosis and scar formation are key elements of arrhythmogenic structural remodeling in heart failure. In this article, the mechanisms responsible for increased arrhythmia susceptibility as well as the underlying changes in ion channel, transporter expression and function as well as alterations in calcium handling in heart failure are discussed. Understanding the mechanisms of arrhythmogenic remodeling is key to improving arrhythmia management and the prevention of sudden cardiac death in patients with heart failure.
Highlights
Chronic heart failure is a clinical syndrome with multiple etiologies, associated with significant morbidity and mortality
Heart failure is a clinical syndrome with multiple etiologies leading to cardiac function impairment and it is associated with significant morbidity and mortality
In a recent analysis of 12 clinical trials (1995–2014), sudden cardiac death (SCD) occurred in 8.9% of patients with HF with reduced ejection fraction (HFrEF; EF ≤ 40%) [5]
Summary
Conduction in the heart is fast (1–2 m/s) and action potential durations in myocardial cells are long (200–300 ms). An early trigger mimicking potential durations using codes during bradycardia and d-sotalol (red arrow) can only conduct via pathways where the tissue is not depolarized, and its refractoriness is over, whereas the decreased repolarization reserve in the canine wedge long QT syndrome 2 model. Arrows mark mal impulse can travel inpotentials a complicated pathwayfrom through reentry paths created heterogeneous repolarization significant differences in the action potential withinperiod, relatively short transmural conduction. Early trigger (red arrow) can conduct viathe pathways where the tissue is jority of reports indicate significant lengthening of cardiac ventricular action potential dunot depolarized, and its refractoriness is over, whereas the conduction is blocked in other directions ration (APD) regardless of the investigated species and its pathophysiological origin in where the tissue is not fully repolarized and cells are refractory.
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