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Atrial fibrillation (AF) is the most common supraventricular tachyarrhythmia and is associated with increased cardiovascular complications and mortality. The current patient management paradigm is shifting from a rate control strategy to early and proactive rhythm control, as supported by large randomized trials and current European and Russian guidelines. This review examines the pathophysiological basis of arrhythmogenesis in AF, including the levels of electrical, mechanical, structural, and autonomic atrial remodeling, as well as the key mechanisms of arrhythmia initiation and maintenance (ectopic activity, reentry, trigger activity/delayed afterdepolarizations). Particular attention is paid to the pharmacological strategy of rhythm control using following Vaughan-Williams class I and III antiarrhythmic agents: the molecular targets, pharmacokinetics, clinical efficacy, and safety profile of propafenone, flecainide, lappaconitine hydrobromide (allapinin), ethacizine, amiodarone, sotalol, and others are analyzed, including drugs primarily available in Russia. Based on current data and guidelines, an algorithmic approach to the selection of anti-relapse therapy is proposed, taking into account the patient’s phenotype (paroxysmal or persistent AF, structural myocardial pathology, heart failure coronary artery disease, left ventricular hypertrophy), the level of atrial remodeling, conduction system characteristics, comorbidities, and drug interactions. The characteristics of antiarrhythmic therapy in the early period after cardioversion and after pulmonary vein catheter isolation as part of a hybrid strategy (invasive+drug therapy) are separately discussed. This review is intended for practicing cardiologists and arrhythmologists and aims to facilitate the individualization of antiarrhythmic drug selection within the safe and effective rhythm control strategy for AF.
Published in: Russian Journal of Cardiology
Volume 30, Issue 4S, pp. 6709-6709