Drug Therapy for Ventricular Tachyarrhythmia in Heart Failure

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Sudden cardiac death (SCD) accounts for approximately one-third of all deaths in patients with heart failure, and is generally the result of ventricular tachycardia (VT) and/or ventricular fibrillation (VF). The mechanisms of VT/VF associated with heart failure are complex and heterogeneous; they include functional and structural remodeling, as well as neurohormonal activation. The implantable cardioverter-defibrillator is very useful for preventing SCD, but the improvement of outcome is limited in patients with cardiac dysfunction and advanced heart failure. This article reviews the current status of drug therapy for the treatment of VT/VF in patients with heart failure. Chronic β-blocker therapy reduces SCD and improves survival. Angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers and aldosterone antagonists are thought to reduce SCD by preventing ventricular remodeling. Amiodarone is potentially effective for preventing VT/VF in patients at high risk, especially those with nonischemic heart failure. This may be a result of the complex pharmacodynamics of amiodarone, which affects many kinds of ion channels/transporters, as well as thyroid function. The pure class III antiarrhythmic drug, nifekalant, is useful in the emergency treatment of VT/VF. (Circ J 2007; Suppl A: A-90 - A-96)