A trial fibrillation (AF) is a common clinical problem that is increasing in prevalence 1 and is inextricably linked to another burgeoning cardiovascular problem, namely, congestive heart failure. 2 There is increasing evidence that AF, at least in some population subsets, may be part of a spectrum of atherosclerotic vascular disease, hypertension, inflammation, diastolic dysfunction, and the metabolic syndromes. AF is part of a family of atrial tachyarrhythmias (Figure 1). A panel of experts has recently characterized the definition and position of AF within this group of tachyarrhythmias. 3 Nonetheless, this family of tachyarrhythmias is closely interrelated, and the individual tachyarrhythmias often coexist in the same patient. Although the present discussion focuses on AF, many of the points made with regard to AF apply to these other tachyarrhythmias to varying degrees.Recently, international panels of experts have also created clinical practice guidelines 4 and perspectives on future research directions 5 for AF. These documents are a rich source of reference to the vast literature on AF. It is not the intention of the present article to review this literature, and, in particular, it is not intended that the reader will use the present article as a manual for managing AF. However, the perspective is intended to provide a framework for rational thinking about the management of AF.
Inside the Basic Scientist's BoxA schema of how a basic scientist might currently view AF is presented in Figure 2. In this schema, modulating factors surround the basic elements of arrhythmogenesis, and the focus is on the mechanisms for initiation and perpetuation of AF. In this particular paradigm, a trigger and substrate interact to form a reentrant circuit or circuits, but provision is also provided for a trigger to lead directly to AF. The consequences of the interaction between triggers and substrate are dependent in part on the milieu created by multiple modulating factors and in particular the autonomic nervous system. The relative influence of these pathways in the pathogenesis of AF has always been controversial, and their deemed importance has waxed and waned over the years. Until recently, reentry based on the multiple wavelet hypothesis, attributed to Moe and Abildskov, 6 has held predominance, partly because of the mapping experiments of Allessie and colleagues. 7 However, the multiple wavelet hypothesis was preceded by hypotheses that invoked single or multiple rapidly firing foci and other reentry concepts (see Waldo 8 for a review). Recent observations on the initiation of AF from the area of the pulmonary veins 9 and the concepts of fibrillatory conduction and of rotors 10 have rekindled consideration of some of the older concepts, presented some new options, and lessened the dominance of the multiple wavelet hypothesis. However, the relative roles of abnormal automaticity and reentry in the pulmonary vein region for initiation and perpetuation, respectively, of AF are entirely unclear at the present time. Furth...