This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Request Permissions Google Scholar Articles by Mason, P. K. Articles by DiMarco, J. P. PubMed Articles by Mason, P. K. Articles by DiMarco, J. P. Related Collections Arrhythmias, clinical electrophysiology, drugs Cardiovascular Pharmacology

Advances in Arrhythmia and Electrophysiology

New Pharmacological Agents for Arrhythmias

Pamela K. Mason, MD and John P. DiMarco, MD, PhD

From the Division of Cardiovascular Medicine, University of Virginia Health System, Charlottesville, Va.

Correspondence to John P. DiMarco, MD, PhD, Box 800158, Division of Cardiovascular Medicine, University of Virginia Health System, Charlottesville, VA 22908. E-mail jpd4h@virginia.edu

Key Words: antiarrhythmia agents • fibrillation • tachyarrhythmias • arrhythmia

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Despite advances in catheter ablation techniques and device-based therapies for cardiac arrhythmias, antiarrhythmic drugs remain essential components of any comprehensive therapeutic strategy. Antiarrhythmic drug therapy, however, has been limited by both incomplete efficacy and a substantial potential for cardiac and extracardiac toxicity. As a result, only a few new antiarrhythmic agents have successfully completed clinical development programs and reached routine clinical usage over the past 20 years.

Antiarrhythmic drugs may be indicated for ventricular tachycardia, sudden death prevention, or specific types of supraventricular arrhythmia. Implantable cardioverter-defibrillator (ICD) therapy has evolved as the primary treatment for most life-threatening ventricular arrhythmias, and antiarrhythmic drugs for these rhythms are currently mostly used either as acute interventions or as adjuncts to chronic ICD therapy. Although numerous trials have evaluated the effect of antiarrhythmic drugs to decrease ICD shocks or therapies, such data have yet to provide the sole basis for approval for any new agent. At the same time, drug therapy for atrial arrhythmias is often limited by the drug’s simultaneous effects on the ventricles, which has led to efforts to identify ionic channel targets specific to or preferentially located in the atria. The sustained outward K⁺ current (I_Kur, encoded by the K_v 1.5 subunit), the acetylcholine-activated outward K⁺ current (I_KAch), and both peak and late atrial Na⁺ currents have therefore become potential targets for antiarrhythmic drug developers.^1–4 Another approach has been to seek agents that synergistically affect multiple channels simultaneously, resulting in a net beneficial effect while minimizing toxicity. Other nontraditional . . . [Full Text of this Article]