A paradigm shift in treatment for atrial fibrillation: from electrical to structural therapy?

See doi:10.1016/j.ehj.2003.08.014for the article to which this editorial refers Atrial fibrillation (AF) is associated with increased morbidity and mortality, most notably due to stroke and heart failure. Maintaining sinus rhythm in AF patients is not an easy task, and eventually it will even fail in most leading to permanent AF. Therefore, the therapeutic goal often lies in postponing permanent AF as long as possible. Except from the surgical correction of mitral valve disease, almost all therapeutic approaches have been focused on the electrical problem that is AF. The tools to maintain sinus rhythm, however, are suboptimal, leading to frustration at both the side of the patient and the doctor. Anti-arrhythmic drugs prevent multiple electrical wavelets by interfering with electrical excitation (class-1 drugs) or repolarization (class-3 drugs). Although amiodarone has emerged as the most potent of the pack, its performance is less than stellar and its potential side-effects are well known. Since abundant atrial ectopy may be a dominant trigger of AF, ablation techniques have evolved to eliminate them. Elaborate ablation schemes are deployed now, targeting all four pulmonary veins, but maintenance of sinus rhythm is achieved in only ±70% in the best series. Moreover, only a fraction of the AF population may be ideal candidates for ablation and the procedure carries a definitive risk for veno-occlusive pulmonary hypertension due to pulmonary vein (PV) stenosis or occlusion, a complication without general effective therapy. Autonomic factors definitely play a role in the genesis …