Role of the Atrioventricular Node in Atrial Fibrillation (1997)

Atrial fibrillation (AF) is probably the most cornmon cardiac arrhythmia in humans, particularly\nin the elderly (1-3). The irregularity and inequality of the he art beat first\ndescribed by Hering in 1903 were, and continue to be, the landmark of the clinical diagnosis\nof AF (4,5). Sir Thomas Lewis (6) observed the gross irregularity ofthe arrhythmia\nand stated "the pauses betwixt the heart beats bear no relationship to one another."\nThanks to work of Lewis (7), Mackenzie (8), Wenckebach (9), and others, the clinical\nsyndrome of AF became well established, and gradually the pathophysiologic mechanisms\ninvolved were also recognized (10). In 1915 Einthoven and Korteweg (11) studied\nthe effect of heart cycle duration on the size of the carotid pulse and concluded that the\nstrength of the heart beat was related to the duration of the preceding cycle. Later we\nrepeated those observations by studying in a quantitative fashion the effects of randomly\nvarying RR intervals on the contractions of isolated Langendorff perfused rat hearts (12).\nRecently Hardmann confirmed the complicated relationship between the randomly irregular\nrhythm and left ventricular function in patients with AF, confirming the involvement\nof postextrasystolic potentiation and restitution (13).\nAnimals mayalso develop AF (14,15). lndeed, Lewis (7) observed the arrhythmia in an\nopen-chest horse and used this observation to establish that the irregular pulse noticed in\nhumans was due to fibrillation ofthe atria. Until the 1950s, observations on AF were limited\nto its etiologic, clinical, and surface EeG manifestations. The beginning of the computer\nera enabled several groups of investigators to analyze the ventricular rhythm during\nAF in a more quantitative fashion (16-18). The results of these studies were fascinating\nand allowed for the development of theories on the behavior of the atrioventricular (AV)\nnode during AF. Sophisticated computer techniques allowed Moe and Abildskov (19,20)\nto simulate atrial electrical activity during AF, and they formulated the so-called multiple\nwavelet theory, which was in 1985 supported by experimental evidence (21). Parallel to\nthe growing insight into the electrical behavior of the atria during AF and into the corresponding\nventricular rhythm, sophisticated experimental methods were designed to study\nAV nodal electrophysiology in a variety of circumstances, including induced AF (22,23).\nThis chapter reexamines some of the established concepts of AV no dal function (24)\nbecause comparative physiology of the AV node and some specific electrocardiographic\nobservations in patients with AF have demonstrated inexplicable flaws in the current theories\nof AV no dal function. Alternate mechanisms, which till now have hardly been considered\nas 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\nas an intrinsic part of the cardiac conduction system, is primarily a pacemaker subject to\ne1ectrotonic influences from other areas in the heart. However, as will be made clear in\nthis chapter, the pacemaker theory cannot explain all clinical phenomena inherent to AF.\nSo a new model based on recently discovered cellular electrophysiologic principles\n(26,27) has been developed and will be presented.