|
Atrial fibrillation may occur in the absence of
detectable structural heart disease. From animal experiments we have learnt that atrial
fibrillation begets atrial fibrillation1. This means
that after a longer period of atrial fibrillation the duration of the arrhythmia episode
will increase. The mechanism of this electrical remodeling appeared to be due to
shortening of the refractory period. Since the atrial wavelength is the product of
refractory period and conduction velocity and since the conduction did not change
significantly, the wave-length shortened as well. A shorter wavelength allows more
reentrant circuits within a certain amount of atrial tissue. Allessie and coworkers2 reported that a critical number of 4-6 wavelets are
needed for sustained atrial fibrillation. Thus, a longer duration of an atrial
fibrillation episode will give shortening of the refractory period, which shortens the
wave-length, which may increase the number of wavelets up to above that critical value.
A previous episode of sustained atrial fibrillation may not only promote perpetuation
of the arrhythmia, but also its inducibility by programmed electrical stimulation. This
was demonstrated in goats by Wijffels et al1, using
single extrastimuli during regular pacing. Although this response was associated with the
described shortening of the refractory period, it may be questioned if this shortening is
the only precipitating factor. Several factors characterizing the substrate are needed for
initiation of reentrant arrhythmias: 1) an anatomical or functional circuit with enough
length to enable a cycle length of the rotating excitation to be longer than the longest
local refractory period in that circuit; 2) this implies that shorter local refractory
periods and lower conduction velocities, and thus a shorter wavelength, will enhance the
possibility of reentry as well; 3) unidirectional conduction block in at least part of the
circuit. Whereas most factors are also prerequisites for maintenance of reentry, the last
factor is crucial specifically for its initiation3.
Conduction block in the atria can be explained by inhomogeneity of the
electrophysiologic substrate. In the presence of structural heart disease this may be due
to fibrosis, stretch, or ischemia. Fibrosis may also occur as a degenerative process
during aging. None of these conditions appeared to be present in the goats of Wijffels1. In the absence of structural heart disease
inhomogeneity may be due to increased local differences in refractory period4. This was studied in the goats in a limited way by
measuring the difference in refractory periods of only the right and left atrial appendage
and comparing data obtained during control (sinus rhythm) and after 24 and 48 hours of
maintained atrial fibrillation. In addition, atrial fibrillatory intervals as index of
refractoriness at 10-13 atrial sites were measured to estimate spatial differences after
respectively 1 and 14 days of maintained atrial fibrillation, but unfortunately no control
data were reported. Nevertheless, given the limitations, no evidence of enhanced spatial
dispersion of refractoriness after various periods of atrial fibrillation could be
obtained. Thus, the increased inducibility of atrial fibrillation after a prolonged
previous fibrillation episode is not completely understood from this goat model.
|
