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Ann Thorac Surg 1996;61:111-112
© 1996 The Society of Thoracic Surgeons


Invited Commentary

Invited Commentary

John P. Boineau, MD

Division of Cardiothoracic Surgery, Department of Surgery, Box 8234-3308 CSRB, Washington University School of Medicine, 660 S Euclid Ave, St. Louis, MO 63110

See also page 104.

This article by Harada and associates is an important contribution to the literature on atrial fibrillation because it confirms in patients with clinical atrial fibrillation previous observations made in greater detail in experimental atrial fibrillation in animal models. Previously, my colleagues and I had demonstrated in certain forms of experimental atrial fibrillation that the complex and irregular patterns of activation could result from a single, regular, repeating reentrant circuit (RC). The necessary conditions were an RC with a cycle time of 100 ± 10 milliseconds plus a passive conduction time from RC to the furthest aspects of the remaining atrium that was longer than the RC cycle time. For example, if the RC cycle time was 100 milliseconds and the passive activation time needed to complete the atrial depolarization was 220 milliseconds, then wavefronts from the present and two previous reentrant cycles could coexist simultaneously in the right atrium (three separate wavefronts). This factor, coupled with the uneven dispersion of repolarization, resulted in a complex and irregular pattern of atrial electrograms in large regions of the atria together with regular, repeating electrograms in the area adjacent to the RC. However, these patterns, which superficially resembled atrial fibrillation, could be readily accounted for by the two factors indicated above. This represents a form of passive dissociation and not multiple changing reentrant circuits. The significance of this report by Harada and associates is that it confirms that this phenomenon can also occur in patients with true or spontaneous atrial fibrillation and thus may represent a more simple form, or first-degree atrial fibrillation, amenable to therapy directed at the site of the single RC.

However, enthusiasm for direct ablative approaches should be tempered by the knowledge that this may not be the only potential RC, but simply the predominant one at the moment. We have also observed that multiple potential sites of reentry may be present, with one predominating at a time. In addition, if one records for long enough, one may observe two (or more) separate RCs, with one and then the other dominating. In other words, the conditions of repolarization dispersion and conduction may give rise to one type of reentry, and if those conditions change during the arrhythmia, then another site may emerge and dominate. Thus, any future approaches to control of atrial fibrillation must take this factor into account.

Finally, it should be pointed out that two of the authors of this article spent several years in our laboratory. I hope they learned as much from us as we learned from them.

References

  1. Yamauchi S, Sato S, Schuessler RB, Boineau JP, Matsunaga Y, Cox JL. Induced atrial arrhythmias in a canine model of left atrial enlargement [Abstract]. PACE 1990;13:556.
  2. Schuessler RB, Grayson TM, Bromberg BI, Cox JL, Boineau JP. Cholinergically mediated tachyarrhythmias induced by a single extrastimulus in the isolated canine right atrium. Circ Res 1992;71:1254–67.[Abstract/Free Full Text]

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Ann. Thorac. Surg. 1996 61: 104-112. [Abstract] [Full Text]



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