This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chen, P.-S. Articles by Weiss, J. N. Search for Related Content PubMed PubMed Citation Articles by Chen, P.-S. Articles by Weiss, J. N. Pubmed/NCBI databases Medline Plus Health Information Pacemakers and Implantable Defibrillators Related Collections Electrophysiology Animal models of human disease Arrhythmias, clinical electrophysiology, drugs Related Article

(Circulation. 2005;112:148-150.)
© 2005 American Heart Association, Inc.

Editorial

Runaway Pacemakers in Ventricular Fibrillation

Peng-Sheng Chen, MD; James N. Weiss, MD

From the Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center and the David Geffen School of Medicine, University of California–Los Angeles, Los Angeles, Calif.

Correspondence to Peng-Sheng Chen, MD, Room 5342, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA 90048. E-mail chenp@cshs.org

Key Words: Editorials • pacemakers • arrhythmia • death, sudden • fibrillation

An extract of the first 250 words of the full text is provided, because this article has no abstract.

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 . . . [Full Text of this Article]

Related Article:

Organization of Myocardial Activation During Ventricular Fibrillation After Myocardial Infarction: Evidence for Sustained High-Frequency Sources

Stuart P. Thomas, Aravinda Thiagalingam, Elisabeth Wallace, Pramesh Kovoor, and David L. Ross
Circulation 2005 112: 157-163. [Abstract] [Full Text]

This article has been cited by other articles:

				M. W. Kay, G. P. Walcott, J. D. Gladden, S. B. Melnick, and J. M. Rogers Lifetimes of epicardial rotors in panoramic optical maps of fibrillating swine ventricles Am J Physiol Heart Circ Physiol, October 1, 2006; 291(4): H1935 - H1941. [Abstract] [Full Text] [PDF]