13th International Congress
THE "NEW FRONTIERS"
OF ARRHYTHMIAS 1998

January 24-31, 1998
Marilleva, Trento, Italy

RT-75

Identification of the electrophysiologic substrate for the initiation of idiopathic atrial fibrillation episodes in man

R.N.W. Hauer, H. Ramanna.
Heart-Lung Institute, University Hospital Utrecht, The Netherlands

Studies in patients

Our knowledge of the electrophysiologic substrate for initiation of atrial fibrillation in patients is still very limited. Evidence that atrial electrical remodeling due to atrial fibrillation itself may also occur in patients is infered from several clinical observations: 1) paroxysmal atrial fibrillation often progresses to chronic atrial fibrillation; 2) longer duration of fibrillation episodes facilitates transition to the chronic form; 3) lower success rate of chemical or electrical cardioversion after longer duration of atrial fibrillation. One may argue that these observations can be explained by progression of the underlying disease. However, similar observations have been obtained in patients with idiopathic atrial fibrillation. It seems likely that in some categories of patients atrial fibrillation begets atrial fibrillation is the most important mechanism, whereas in others progression of structural disease may contribute importantly. Finally, recent observations in chronic fibrillating goat atria showed histologic changes⁵. Thus, the arrhythmia may become the cause of structural changes.

From animal experiments discussed above, we know that shortening of the refractory period by sustained atrial fibrillation promotes perpetuation of the arrhythmia. This shortening also facilitates its initiation. From other animal experiments we know that conduction block is crucial for initiation. In vitro observations in human atria showed similar results⁶. Superfused strips of the right atrial appendage from patients with chronic atrial fibrillation showed a shorter refractory period and a significantly greater dispersion in atrial refractory period than from patients without this arrhythmia.

Ramdat Misier and coworkers⁷ studied the substrate for atrial fibrillation in patients in vivo during cardiac surgery. These authors used atrial fibrillation intervals as index of atrial refractoriness. Intervals were measured from multiple epicardial sites. To exclude other causes of atrial fibrillation only patients with idiopathic atrial fibrillation and a control group were included. Both, shorter refractoriness and a larger dispersion of refractoriness were found in the atrial fibrillation group. This is an important study. However, appropriate interpretation of the results is hampered by several limitations. Since the time of onset of the episode of atrial fibrillation used for the measurements is not reported, nor the incidence of the arrhythmia, we are not informed about the contribution of electrical remodeling. In addition, the study group was rather small and the patients were studied under rather unphysiologic conditions during cardiac surgery and under general anesthesia.