Cholinergic agonists and vagal stimulation potentiate the inducibility of atrial fibrillation. To describe the activation patterns and determine the mechanisms that sustain cholinergic fibrillation, tachyarrhythmias were induced with a single extrastimulus in the isolated Krebs-Henseleit-perfused canine right atrium (n = 11) at increasing concentrations of acetylcholine (from 10(-7.5) to 10(-4.5) M). Bipolar electrograms were recorded from 250 epicardial sites simultaneously during control conditions and during extrastimulation (S1S1, 300 msec; S1S2, effective refractory period+5 msec) with and without acetylcholine. Activation sequence maps were constructed from each recording. Without acetylcholine, no tachyarrhythmias were induced. With increasing concentrations of acetylcholine, the refractory period decreased, and nonsustained (< 2 seconds) rapid repetitive responses were induced. At higher concentrations, a sustained (> 2-minute) fibrillation was induced. Activation sequence maps revealed that the rapid repetitive responses were characterized by multiple reentrant circuits. The number of circuits and wavelets increased in a dose-dependent fashion. However, unexpectedly, this trend did not continue when the tachyarrhythmia became sustained. Instead, the reentry tended to stabilize to a small, single, relatively stable reentrant circuit. In conclusion, the data suggest that, in this model, below a critical level of refractory period (< 95 msec) atrial reentrant circuits, unassociated with anatomic obstacles, can become stable and dominate activation.

The findings of this study demonstrate that epicardial and endocardial activation can be discordant in specific regions and that discordance increases with abnormal activation sequences. Many of the differences in the epicardial and endocardial activation can be correlated with the heterogeneity of the anatomic architecture of the right atrium. The study also demonstrates that reentry can occur in a three-dimensional plane using the epicardial and endocardial surfaces connected by transmural muscle fibers.

Cardiac arrest was the only distinguishing clinical feature between high and low risk groups and the first manifestation in 80% of the children of an accessory pathway that can precipitate a life-threatening arrhythmia. In this series, the largest reported to date of children with Wolff-Parkinson-White syndrome having a cardiac arrest, a shortest pre-excited RR interval <220 ms was more sensitive than clinical history for identifying those at risk for sudden death.

It was generally accepted that the site of normal impulse origin within the atria was a single static focus within the sinus node. This review will examine how this model of impulse origin came about and has evolved. Early on, conflicting data suggested that the sinus node focus was not static and changed with interventions that changed heart rate, such as vagal stimulation. Furthermore, even with removal of the sinus node, a normal atrial rhythm was generated. High-resolution mapping in humans and dogs showed that the initiation of the impulse was dynamic and could be multicentric, with more than one focus initiating a single beat. Shifts in the site of origin correlated with changes in rate and were consistent with P wave changes routinely observed in the standard ECG. These studies suggested multiple pacemakers were responsible for impulse initiation. However, it was not clear how these widespread pacemakers were coordinated to function synchronously. Recent canine data suggest that the node may be partially insulated from the surrounding atrium, resulting in multicentric origin starting from a single site within the node. What has evolved is a model of impulse origin with a sinus node having discrete exit sites and a dominant pacemaker within the node that can shift to other nodal sites. Complex and changing conduction out of the node, coupled with extranodal pacemakers, which can assume dominance over the node, combine with the autonomic nervous system to control heart rate and the pattern of impulse origin within the atria.

Activation sequence maps derived during normal sinus rhythm from extracellular potentials in the canine right atrium exhibit widely separated sites of origin. The objectives of this study were to characterize the distribution of pacemakers within the right atrium and to determine the relationship of pacemaker action potentials to sites of earliest surface activation as well as to local extracellular electrograms. The right atria of six adult mongrel dogs were rapidly excised under deep pentobarbital sodium anesthesia and perfused with 95% O2-5% CO2 Krebs-Henseleit solution. Action potentials from the epicardial surface were recorded throughout the region bounded by the crista terminalis laterally and the atrial septum medially. Simultaneously, unipolar extracellular electrograms were recorded from 250 endocardial sites. The earliest pacemakers preceded the earliest electrogram by 63 +/- 34 ms; the latest pacemakers followed the earliest electrogram by 71 +/- 40 ms. Primary negativity in the extracellular electro gram did not predict the site of the earliest or dominant pace maker and in some cases was associated with the latest pace makers. We conclude that primary negativity and/or the sites of earliest activation reflect the point at which the impulse engages atrial myocardium, not the site of earliest pacemaker activity. As such, early extracellular activation appears to represent sites of exit from a relatively insulated sinus node.