Intra-atrial reentry as a mechanism for atrial flutter induced by acetylcholine and rapid pacing in the dog.

Abstract

In the isolated blood-perfused canine heart we produced episodes of rapid atrial flutter by continuous infusion of acetylcholine and rapid pacing. The spread of excitation during atrial flutter was mapped with the aid of two endocavitary mapping electrodes containing 960 leads and recording from 192 different sites simultaneously. The flutter maps clearly showed that intra-atrial reentry was the mechanism responsible for the arrhythmia. However, the localization and size of the intra-atrial circuits differed from case to case even in the same heart. The orifices of the venae cavae or the atrioventricular ring did not serve as a central anatomic obstacle for circus movement. We also failed to identify a special role of the intemodal pathways in the formation of the loop. Instead, the intra-atrial circuits could be found everywhere, provided sufficient atrial mass was available to accommodate the circuit. The diameter of the circuits varied between 1.5 and 3 cm at a cycle length between 65 and 155 msec. The average conduction velocity of the circulating impulse varied between 60 and 80 cm/sec. Spontaneous termination of atrial flutter frequently occurred and was based on local conduction block in a narrow part of the circuit. Another interesting aspect of these studies is the finding that during continuous circus movement of the impulse, the amount of myocardium that is activated may vary considerably. This marked periodicity in excited tissue mass during atrial flutter could adequately explain the continuously undulating baseline or typical sawtoothlike F waves as seen in the surface electrocardiogram during atrial flutter. Circulation 70, No. 1, 123-135, 1984. THE EXACT MECHANISMS underlying atrial flutter in human beings are still unknown. Detailed clinical studies with intracavitary and intraesophageal leads and programmed electrical stimulation have not resulted in the identification of a single mechanism of human atrial flutter. The results of some studies were explained by assuming the presence of an ectopic focus of abnormal impulse formation, -5 whereas other investigations point to a circus movement involving a large part of the atria.3' 61 Extensive epicardial mapping of the atria in patients with atnal flutter who are subjected to cardiac surgery could be an excellent and direct way to evaluate this condition. However, such studies have been scarce and do not yet allow general conclusions. 12

Effects of activation sequence and anisotropic cellular geometry on the repolarization phase of action potential of dog ventricular muscles.

“…[25][26][27][28][29][30] It is generally accepted that the requirement for reentry is a spatial variation in propagation based on spatial variations in membrane properties.3"-36 We have shown above that the activation sequence and anisotropic cellular geometry can distort the repolarization sequence even when the membrane properties are homogenous throughout the tissue. Such distortion, which may be enhanced at lower conduction velocities, would cause a spatial inhomogeneity of refractoriness and set the stage for reentrant arrhythmias.…”

Heterogeneous Atrial Denervation Creates Substrate for Sustained Atrial Fibrillation

“…Both vagal stimulation and direct application of acetylcholine have been shown to result in AF in dogs. [33][34][35] Spatially disparate effects of vagal stimulation have been demonstrated in the atria. 19,20,36 Although this heterogeneous distribution of vagal effects on electrophysiological properties may contribute to the milieu necessary to maintain multiple-wavelet atrial reentry, it is clearly not sufficient in the baseline state, because spontaneous AF does not occur in the absence of other perturbations (such as vagal stimulation).…”

Atrial Electrophysiological Properties Evaluated by Right and Left Atrial Pacing in Patients with or without Atrial Fibrillation.

“…In the face of short refractory periods and slow conduction, reentry is permissible even in small areas of conduction block. 16,17) Multiple reentering wavelets may start to wander through the available tissue and result in AF, when the wavelength is short enough. Patients with AF have been shown to have a higher tendency to develop slow intraatrial conduction (longer conduction time), as well as a shorter effective refractory period than patients without AF.…”