Role of the Atrioventricular Node in Atrial Fibrillation

Atrial fibrillation (AF) is probably the most cornmon cardiac arrhythmia in humans, particularly in the elderly (1-3). The irregularity and inequality of the he art beat first described by Hering in 1903 were, and continue to be, the landmark of the clinical diagnosis of AF (4,5). Sir Thomas Lewis (6) observed the gross irregularity ofthe arrhythmia and stated "the pauses betwixt the heart beats bear no relationship to one another." Thanks to work of Lewis (7), Mackenzie (8), Wenckebach (9), and others, the clinical syndrome of AF became well established, and gradually the pathophysiologic mechanisms involved were also recognized (10). In 1915 Einthoven and Korteweg (11) studied the effect of heart cycle duration on the size of the carotid pulse and concluded that the strength of the heart beat was related to the duration of the preceding cycle. Later we repeated those observations by studying in a quantitative fashion the effects of randomly varying RR intervals on the contractions of isolated Langendorff perfused rat hearts (12). Recently Hardmann confirmed the complicated relationship between the randomly irregular rhythm and left ventricular function in patients with AF, confirming the involvement of postextrasystolic potentiation and restitution (13). Animals mayalso develop AF (14,15). lndeed, Lewis (7) observed the arrhythmia in an open-chest horse and used this observation to establish that the irregular pulse noticed in humans was due to fibrillation ofthe atria. Until the 1950s, observations on AF were limited to its etiologic, clinical, and surface EeG manifestations. The beginning of the computer era enabled several groups of investigators to analyze the ventricular rhythm during AF in a more quantitative fashion (16-18). The results of these studies were fascinating and allowed for the development of theories on the behavior of the atrioventricular (AV) node during AF. Sophisticated computer techniques allowed Moe and Abildskov (19,20) to simulate atrial electrical activity during AF, and they formulated the so-called multiple wavelet theory, which was in 1985 supported by experimental evidence (21). Parallel to the growing insight into the electrical behavior of the atria during AF and into the corresponding ventricular rhythm, sophisticated experimental methods were designed to study AV nodal electrophysiology in a variety of circumstances, including induced AF (22,23). This chapter reexamines some of the established concepts of AV no dal function (24) because comparative physiology of the AV node and some specific electrocardiographic observations in patients with AF have demonstrated inexplicable flaws in the current theories of AV no dal function. Alternate mechanisms, which till now have hardly been considered as a basis for explaining AV nodal function during AF, will be discussed. In the first edition ofthis book (25) we postulated that the AV node, rather than acting as an intrinsic part of the cardiac conduction system, is primarily a pacemaker subject to e1ectrotonic influences from other areas in the heart. However, as will be made clear in this chapter, the pacemaker theory cannot explain all clinical phenomena inherent to AF. So a new model based on recently discovered cellular electrophysiologic principles (26,27) has been developed and will be presented.