Introduction: It is not known whether ventricular fibrillation (VF) is always caused by multiple wavelet reentry, or if it could also be caused by a single wandering reentrant wavefront. Activation mapping of the entire ventricles during VF is practically impossible.

Methods and results: We studied VF in a two-dimensional sheet of left ventricular subepicardial tissue of isolated, Langendorff-perfused pig hearts. Left and right endocardial cryoablation via probes filled with liquid nitrogen caused coagulation necrosis of the right ventricle, interventricular septum, and most of the left ventricular wall, leaving a thin subepicardial layer intact. Left ventricular epicardial activation patterns were constructed based on simultaneous recording of 128 unipolar extracellular electrograms. Regular pacing through a central electrode before and after freezing revealed that, following cryoablation, the activation pattern no longer showed evidence of involvement of the Purkinje system, and that it was compatible with propagation through a two-dimensional anisotropic tissue sheet. VF was induced by burst pacing. When the mass of surviving subepicardium was < 10 g, no VF could be induced; when it was between 10 and 20 g, VF was nonsustained; when it was > 20 g, VF was sustained. Unipolar extracellular electrograms during VF before and after cryablation could not be distinguished from each other; however, epicardial activation patterns were markedly different. In the intact left ventricle, up to six different wavefronts were simultaneously present during a 100-msec time window. In the "frozen heart," during a period of about 0.5 seconds, at most two wandering reentrant waves were simultaneously present; sometimes only one reentrant wave was seen in a 100-msec time window.

Conclusion: The extracellular waveform during VF can be caused by different forms of reentry: multiple wavelet reentry (on the order of six different wavefronts), two independent wandering reentrant waves, and a single wandering reentrant wave.