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Rhythm and rate strategies are considered equivalent for the management of atrial fibrillation (AF). Moreover, both strategies are intended for improving symptoms and quality of life. Despite the clinical availability of several antiarrhythmic drugs (AAD) the alternatives for the patient with comorbidities are significantly fewer because of the concern regarding many adverse effects, including proarrhythmias. The impetuous development of AF ablation gave rise to a false impression that AAD are a second line therapy. All these statements reflect, in fact, the weakness of the classical paradigm and classification regarding AAD and the gap between the current knowledge of AF mechanism and determinants and the "classical" AAD non-discriminatory action. A new paradigm in development of effective and safe AAD is based on modern knowledge of vulnerable parameters involved in the genesis and perpetuation of AF. New AAD will target specific triggers of AF and ion currents which are expressed preferentially in fibrillatory atrium. Such targets will include repolarizing currents and channels, as ultrarapid potassium current, two pore potassium current, the acetylcholine-gated potassium current, small-conductance calcium-dependent potassium channels, but, also, molecular targets involved in intracellular calcium kinetics, as Ca 2+ -calmodulin-dependent protein kinase, ryanodine receptors and non-coding miRNA. New mechanistic discoveries link AF to inflammation and modern anti-cytokine drugs. There is still a long way to win between basic research and clinical practice, but, without any doubt, antiarrhythmic drug therapy will remain and develop as a cornerstone therapy for AF not in conflict, but complementary and alternative to interventional therapy.

Antiarrhythmic drugs for atrial fibrillation: Imminent impulses are emerging