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(Circulation. 2002;105:276.)
© 2002 American Heart Association, Inc.

Editorials

New Antiarrhythmic Drugs for Atrial Flutter and Atrial Fibrillation

A Conceptual Breakthrough at Last?

Francisco G. Cosío, MD, FESC; Eva Delpón, BPharm, PhD

From Cardiology Service (F.G.C.), Hospital Universitario de Getafe and Pharmacology Department (E.D.), Universidad Complutense, Madrid, Spain.

Correspondence to Francisco G. Cosío, MD, FACC, FESC, Chief Cardiology Service, Hospital Universitario de Getafe, Carretera de Toledo, km 12.5, 28905 Getafe, Madrid, Spain. E-mail fcosio@vitanet.euroredes.es

Key Words: Editorials • antiarrhythmia agents • atrial fibrillation • atrial flutter

Antiarrhythmic drug (AAD) use in the clinical setting remains an often frustrating empirical exercise, despite significant advances in understanding the effect of AADs on myocardial ion channels and action potential. Not only is efficacy lower than desired, but prediction of antiarrhythmic versus arrhythmogenic effects of AADs in a particular case is nearly impossible. Vaughan Williams classification¹ helped to describe and group AADs and to differentiate between AADs mainly acting on the low diastolic polarization cells (sinoatrial and atrioventricular nodes) for their effect on ß-adrenergic receptors and Ca²⁺ channels and those capable of slowing conduction velocity and/or prolonging the action potential duration of the working myocardium and Purkinje cells. Unfortunately, usefulness of the Vaughan Williams classification for clinicians was limited because it provided incomplete links among AAD actions, arrhythmia mechanisms, and therapeutic results.

Modern arrhythmology is dominated by the concept of reentry as the bases of most clinical tachyarrhythmias. Reentry has been conceived generally as continuous activation rotating around a central obstacle, be it fixed or functional, and the equilibrium necessary between refractory period, conduction velocity, and circuit circumference to maintain reentry has been nicely synthesized in the wavelength (WL) concept. WL is the circuit length covered by the activation front in the time lapse of refractory period duration (Figure 1) and, obviously, it must be shorter than total circuit length in order to leave an excitable gap; otherwise, activation would be extinguished by meeting a barrier of refractory tissue. In animal experiments, the WL of the initiating premature . . . [Full Text of this Article]

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