Runaway pacemakers in ventricular fibrillation.

Arunaway pacemaker is a malfunctioning pacemaker that paces the heart at rapid rates. A report from Australia 30 years ago1 described a patient with runaway pacemaker that paced the ventricles at 280 bpm. The patient survived only because one of the coauthors alertly cut the pacemaker wires to disconnect the high-frequency focal source from the myocardium. In this issue of Circulation, Thomas et al2 report that they occasionally detected sustained high-frequency sources during ventricular fibrillation (VF) in sheep with myocardial infarction (MI). Specifically, in 3 of 12 hearts, they detected periodic high-frequency activations at 1.3% of the intramural electrodes sampled. The authors propose that these findings support the hypothesis3 that a relatively stable periodic source (“mother rotor”), with fibrillatory conduction block occurring in the remainder of the ventricle, may be the mechanism of VF in this model. This mother rotor mechanism of fibrillation contrasts with the multiple wavelet mechanism, in which all rotors are unstable and wavebreak is the engine driving fibrillation. Both mechanisms of fibrillation have been documented in various settings,4 but controversy exists over which is the most common in and clinically relevant to diseased human hearts. This issue has therapeutic implications because it has been suggested that ablation of the mother rotor may be a strategy to abolish VF. At the same time, ablation of the mother rotor may just allow the next-fastest daughter rotor to take its place because fibrillatory wavebreaks act as niduses for new rotors. In any case, however, to even test this intriguing therapeutic strategy, it is first necessary to identify the location of the mother rotor, which has been elusive to date, especially in large animals.5 The findings of the present study, in a large-animal diseased heart model, are therefore significant. They also raise important questions. For example, were mother rotors also present in the remaining 75% of hearts but undetected because of the limited area accessible to mapping? Or was the mechanism of fibrillation different in these hearts? Were the high-frequency focal sources that the authors detected really rotors that activate the ventricles in the form of scroll waves, or some other mechanism such as automatic foci or triggered activity? See p 157