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Atrial fibrillation is the most prevalent cardiac arrhythmia, affecting 0.9% of the general population, including 6% of those over 65 years of age,1 and its prevalence is increasing.2 Although structural heart disease underlies most cases, the pathogenesis of atrial fibrillation in the otherwise normal heart—lone atrial fibrillation—is largely unknown. Atrial fibrillation in an apparently normal heart may account for up to one third of all cases, particularly in younger patients.2Despite substantial mortality, morbidity, and consumption of health care resources, specific treatment of the arrhythmic source in atrial fibrillation, and the maintenance of sinus rhythm, have remained elusive. Other tachyarrhythmias may be amenable to percutaneous catheter ablation by application of radiofrequency energy to destroy a small region of endomyocardium that is critical to initiation or maintenance of the arrhythmia.
Initiation of atrial fibrillation
Recently, clinical and experimental studies have indicated that rapid repetitive activation of the atrial myocardium may play a role in the genesis of atrial fibrillation.3 It has long been recognised that patients with a variety of regular tachycardias involving the atria, such as accessory pathway mediated junctional reentrant tachycardia, can have an associated tendency to atrial fibrillation, which may be abolished by successfully ablating the underlying arrhythmia. Although this observation has remained largely unexplained, it raises the question of whether the tendency to atrial fibrillation may be causally related to the frequency of atrial myocardial activation during tachycardia. This concept is reinforced by a recent …