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

Atrial fibrillation, the blind man's elephant

This paper seeks to explain that most puzzling of all the forms of irregularity of the heart, where the heart is never regular in its action, where seldom or never two beats of the same character follow one another

Geleidt de atrio-ventriculaire knoop?

De wijze van transport van de boezemimpuls naar de kamers via de AV-knoop en het His-Purkinjesysteem is door de complexe structuur van de AV-knoop niet nauwkeurig bekend. Gegeven de samenhang in tijd tussen boezem- en kamercontracties, die aan het eind van de vorige eeuw door de Utrechtse fysioloog Engelmann werd vastgesteld, lag het voor de hand dat men zich ging afvragen hoe die samenhang dan wel tot stand kwam. Engelmann sprak over 'Ueber die Leitung der Bewegungsreize im Herzen'. Engelmann moet zich gerealiseerd hebben dat er een weg was waarlangs de impuls die de boezem tot contractie had gevoerd, ook de kamer bereikte, maar we kunnen slechts gissen of Engelmann met 'Leitung' verbinding of geleiding heeft bedoeld. Het is evenmin duidelijk wie de term geleiding ('conduction') voor het eerst van toepassing achtte op de transmissie van de atriumimpuls naar de ventrikels. Fye geeft een fraai overzicht van 'the origin of the heart beat', maar verschaft geen zekerheid over het ontstaan of introductie van de term geleiding met betrekking tot de functie van de AV-knoop. De term AV-geleiding en datgene wat men zich daarbij voorstelt, zijn weliswaar stevig geworteld in de pathofysiologie van het hart, echter zonder dat de aard of herkomst van het begrip geheel duidelijk is

Atrioventricular nodal response to retrograde activation in atrial fibrillation

Retrograde (ventriculoatrial) conduction that reaches the atrioventricular node simultaneous with, or just before an atrial impulse can facilitate subsequent anterograde conduction. However, a spontaneous or programmed ventricular extrasystole during atrial fibrillation is generally followed by a compensatory pause indicating subsequent delayed anterograde transmission. This characteristic response was used as a model to study the mechanism of atrioventricular nodal behavior during atrial fibrillation. In eight medically-treated patients with chronic atrial fibrillation and a relatively slow but random ventricular response, single premature right ventricular stimuli were delivered after every eighth spontaneous R wave during at least 1 hour. A fixed coupling interval of the extrastimulus, considerably shorter than the shortest spontaneous RR interval, was used. The histograms of the postextrasystolic intervals were compared with those of the spontaneous noninterrupted RR intervals. The average postextrasystolic interval was 180 to 300 msec longer than the mean control RR interval, and in six of eight patients, the shape of the histogram of the postextrasystolic cycles was insignificantly different from that of the spontaneous RR intervals. This suggests that in those six patients, the retrograde impulse had reset the random timing cycle of atrioventricular nodal discharge during atrial fibrillation. This observation is compatible with the hypothesis that electrotonically-mediated propagation across a weakly coupled junctional area within the atrioventricular node, rather than decremental conduction and extinction of anterograde atrial impulses at different levels within the node, may be the mechanism of atrioventricular transmission in atrial fibrillation

Competitive anterograde and retrograde atrioventricular junctional activation in atrial fibrillation

In eight medically-treated patients with chronic atrial fibrillation and a random ventricular rhythm, we studied the effect of single right ventricular stimuli delivered after each eighth spontaneous R wave during at least 1 hour. The coupling interval of the extrastimulus was fixed and differed marginally from the shortest spontaneous RR interval. The histograms of spontaneous RR intervals and of the "compensatory" pauses following the ventricular extrasystoles were calculated. Analysis of these histograms and simulation of the interaction between anterograde and retrograde impulses in a computer model suggests that in seven of the eight patients the compensatory pause may be caused by two distinctly different mechanisms: (1) reset of the timing cycle of atrioventricular nodal activation by relatively early retrograde impulses; and (2) interception of anterograde impulses by relatively late ventricular extrasystoles. The finding that early retrograde impulses are not blocked by concealed atrioventricular nodal conduction makes the existence of decremental conduction and extinction of atrial impulses at different levels within the node unlikely. The results of this study support the hypothesis that the distal side of a weakly coupled junctional area inside the AV node behaves as a pacemaker for the ventricular rhythm during atrial fibrillation

The electrocardiogram of the Humpback Whale (Megaptera novaeangliae), with specific reference to atrioventricular transmission and ventricular excitation

The objective of the study was to record the electrocardiogram (ECG) of a large whale to obtain crucial data for comparative electrophysiologic analysis. The data were needed to establish the mismatch between heart size and PR interval and QRS duration in mammals. In the waters off the coast of Newfoundland, in two humpback whales (Megaptera novaeangliae) with an estimated weight of 30,000 kg a I-lead ECG was recorded, enabling reliable assessment of P waves and QRS complexes. It was found that both the PR interval (atrioventricular [AV] transmission time) and QRS duration (ventricular excitation) are extremely short for animals of this size. These findings are difficuIt, if not impossible, to explain on the basis of currently accepted electrophysiologic theories. However, the narrow QRS complex may be due to a very dense His-Purkinje network in the ventricular wall of whales. Alternative mechanisms that can explain the function of the mammalian AV node need to be considered and explored. The results of the study may be of value for the understanding of the ECG in humans

Effect of right ventricular pacing on ventricular rhythm during atrial fibrillation

In 13 patients with atrial fibrillation, the effect of right ventricular pacing at various rates on spontaneous RR intervals was studied. Five hundred consecutive RR intervals were recorded and measured before and during varying right ventricular pacing rates. As anticipated, all RR intervals longer than the right ventricular pacing intervals were abolished. However, RR intervals shorter than the right ventricular pacing intervals were also eliminated. It is difficult to explain the elimination of RR intervals shorter than the pacing intervals with the accepted concepts concerning the mechanisms governing the rate and rhythm of the ventricular response to atrial fibrillation. An alternative explanation may be that during atrial fibrillation the atrioventricular node behaves as a nonprotected pacemaker that is electrotonically modulated by the chaotic atrial electrical activity. The result is a random ventricular rhythm. With right ventricular pacing, the automatic focus is depolarized by the retrogradely concealed conducted ventricular impulses, the short RR intervals are not generated as a consequence and the rhythm becomes pacemaker dependent

Where to draw the mitral isthmus line in catheter ablation of atrial fibrillation: histological analysis.

Item does not contain fulltextAIMS: A linear lesion between the left inferior pulmonary vein orifice and mitral annulus, the so-called mitral isthmus, may improve the success of catheter ablation for atrial fibrillation. Gaps in the lesion line, however, may facilitate left atrial flutter. The aim of the study was to determine the optimal location of the lesion line by serial sectioning of the isthmus area. METHODS AND RESULTS: In a post-mortem study of 16 patients with normal left atria, serial sections of the isthmus area from 10 mm superior to and 30 mm inferior to the isthmus were studied by light microscopy. The length of the isthmus was 35+/-7 mm. On average, the muscle sleeve around the coronary sinus ended 10 mm inferior to the isthmus. The prevalence of a ramus circumflexus <5 mm from the endocardial surface, decreased from 60% in the most superior section to 0% in the most inferior section. Atrial arteries were frequently present in all sections. CONCLUSIONS: The thickness of atrial myocardium, the ramus circumflexus sometimes very close to the endocardium, a myocardial sleeve around the coronary sinus, and local cooling by atrial arteries and veins may complicate the creation of conduction block in the mitral isthmus