Select Articles Published on the Topic of Arrhythmia and Electrophysiogy in 2013

Noninvasive atrial fibrillation (AF) therapies are based on 2 separate strategies: rate or rhythm control aiming to slow ventricular rate to normal or to restore sinus rhythm, respectively. Hence, in rate control, AF itself is not resolved, whereas the curtailment of ventricular frequency reduces exercise tolerance. Rhythm control, on the other hand, is hampered by adverse effects such as ventricular proarrhythmia. Therefore, better insight into the contribution of ion channels, present in the atria but not the ventricles, to AF and the concordant exploration of possible atrium-specific therapies are essential if we are to diminish the burden of adverse effects in AF treatment. Previous studies showed that the acetylcholine-dependent potassium current (I K,ACh ), governed by the atrium-specific Kir3.x channels, can become constitutively active (I K,ACh-C ) in patients with AF. In the present study, we demonstrate the contribution of I K,ACh-C and Kir3.x to the initiation, maintenance, and termination of AF. We show for the first time that I K,ACh-C increases the chance of AF initiation through its steepening effects on the action potential duration and conduction velocity restitution curves, causing action potential duration and amplitude alternans. In addition, I K,ACh-C is shown to facilitate AF maintenance by stabilizing rotor dynamics, whereas AF termination can be elicited by blockade of I K,ACh-C , causing alternans-mediated rotor destabilization. Our findings provide evidence for a causal relationship between I K,ACh-C , alternans, and the initiation, maintenance, and termination of AF. Thus, not only I K,ACh-C or Kir3.x but also its consequent alternans might be an interesting atrium-specific target for future AF rhythm control or pharmacological cardioversion.