Drug therapy for prevention of atrial fibrillation

Atrial fibrillation is not a homogeneous entity, and many factors are responsible for a number of different behaviors, clinical consequences, and reactions to therapy. Therefore, the conventional evaluation of preventive treatments is not really adapted to provide the correct answers to difficult problems of therapeutic indications, as the 2 components of the benefit-risk ratio are not really known. Like ventricular fibrillation, atrial fibrillation may be primary or secondary to organized tachyarrhythmias, and reentrant flutter or automatic atrial tachycardia may well form the actual target for treatment. The automatic nervous system is never absent as a determinant of the onset of arrhythmia, and the vagal as well as the sympathetic action may predominate and explain why a treatment may or may not be effective in situations that are identical only in appearance. The electrophysiologic milieu formed by the atrial tissue probably accounts for the perpetuation of the process of atrial fibrillation or its self-termination, and drugs themselves may contribute to modify the milieu in a way that in the end may be favorable or not. Finally, the presence or the absence of heart disease and heart failure largely contributes to the state of the vagosympathetic balance, to the hemodynamic consequences of atrial fibrillation, and ultimately to the proper toxic effects of drugs. The overall consequence of these complex situations is that any precise therapeutic decision algorithm for atrial fibrillation is always simplistic and that any global evaluation of drug efficacy or toxicity is not really meaningful as long as the category of patients treated is not precisely determined: no drug appears better or worse than others, but simply more or less adapted to various situations.