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(Circulation Research. 2000;86:369.)
© 2000 American Heart Association, Inc.

Editorials

Fibrillating Myocardium

Rabbit Warren or Beehive?

Jack M. Rogers, Raymond E. Ideker

From the Departments of Biomedical Engineering and Medicine, University of Alabama at Birmingham.

Correspondence to Jack M. Rogers, 1670 University Blvd, Volker Hall, B140, Birmingham, AL 35294. E-mail jmr@crml.uab.edu

Key Words: fibrillation • Fourier analysis • reentry • mapping

	Introduction

 
Until 20 years ago, it was thought that atrial and ventricular fibrillation were highly disorganized, with tens or hundreds of tiny wandering wavelets simultaneously present and following ever-changing pathways.¹ In this model, the disorganization is due to intrinsic heterogeneity of refractory periods that causes transitory islets of refractoriness about which wavelets circulate.

However, about two decades ago, a new view emerged. This model was based on the theoretical^{2 3 4 5} and experimental⁶ finding that the heart could support electrical waves that rotate about a functional, rather than anatomical, obstacle. These so-called rotors were thought to be the primary "organizing centers" for fibrillation, and refractory period heterogeneity was a secondary factor, possibly modulating and masking the activity of rotors, but not driving the rhythm.⁷

Indeed, electrical and optical mapping have demonstrated a considerable organization during ventricular fibrillation (VF).^{8 9 10 11 12 13} These studies indicate that activation fronts are frequently large during fibrillation and follow pathways that are centimeters in length. In addition, many of these activation fronts follow similar pathways. Surprisingly, however, after the first few seconds of VF, rotors are rarely observed. In several recent mapping studies, only 2% to 8% of activation fronts were identified as parts of reentrant circuits.^{13 14 15} In addition, most of the reentrant circuits were short-lived, lasting typically only slightly more than one cycle.

Consistent with these findings, many recently proposed mechanisms for fibrillation have focused on rotors as transient, unstable objects, and VF is explained in terms of how rotors break up to form the turbulent state seen in epicardial . . . [Full Text of this Article]

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