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It has been tested and found to produce beneficial effects in models of heart failure, ischemic heart disease, AF and VF. It is a multichannel blocker and inhibits INa, ICa, IKr, IKAch, IK1 (for review see (Kaneko et al. 2009)), consequently it also affects the ventricles causing a prolongation of the QTc-interval. However, it was reported not to induce TdP in the methoxamine sensitised rabbit model of TdP (Hasumi et al. 2007). It also suppresses spontaneous Ca2+ release (sparks) from the sarcoplasmic reticulum by inhibiting the sarcoplasmatic reticulum Ca2+-ATPase (SERCA2a/ATP2A2) and the ryanodine receptor (RyR2) (Loughrey et al.

Dronedarone also shows a 100-fold higher potency for blockage of IKACh as compared to amiodarone (Guillemare et al. 2000). There are only a few experimental studies published addressing the atrial effects of dronedarone, and divergent data are found (Manning et al. 1995; Sun et al. 2002; Burashnikov et al. 2010a). Acute superfusion of isolated rabbit atrial tissue with dronedarone abbreviates APD and atrial ERP to a similar extend as for amiodarone. In comparison, four weeks treatment with dronedarone or amiodarone resulted in an increased APD and aERP.

3 to 3 mmol/L Cardiac Ion Channels and Mechanisms for Protection Against Atrial Fibrillation 27 of stroke, increasing the hemodynamic parameters and alleviating the symptoms of atrial fibrillation. As a consequence of these studies one could speculate, that this would spell an end to the era of rhythm control in the treatment of atrial fibrillation. However, this has not been the case. For one thing, the RACE and AFFIRM trials did not address atrial fibrillation in younger, symptomatic patients with little underlying heart disease, and the international guidelines still consider restoration of sinus rhythm by cardioversion with antiarrhythmic drugs or nonpharmacological interventions a useful therapeutic approach in these patients (Fuster et al.