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Volume 81, Issue 8, Pages 950-955 (August 2010)


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Circadian variation of human ventricular fibrillation dominant frequency

Philip LangleyaCorresponding Author Informationemail address, Guy A. MacGowanb, Alan Murrayc

Received 27 January 2010; received in revised form 2 March 2010; accepted 14 March 2010. published online 26 April 2010.

Abstract 

Aim

Circadian variation in human ventricular fibrillation (VF) dominant frequency is unknown. If present this would provide evidence of physiological influence on VF. The objective was to quantify the circadian variation in human VF dominant frequency.

Methods

Eight-lead Holter ECG recordings were obtained from a patient with severe myocarditis and chronic VF who was supported by a biventricular assist device. Recordings of up to 24h duration were obtained on 6 days with an average interval between recordings of 7 days. Dominant frequency and amplitude were obtained using spectral analysis and assessed for (i) circadian (ii) inter-recording and (iii) inter-lead differences.

Results

There was a significant circadian variation in amplitude (night: 0.027±0.004mVHz vs day: 0.044±0.006mVHz, p<0.0001) but not dominant frequency (night: 7.85±0.62Hz vs day: 7.93±0.54Hz, p>0.05). There were significant differences between recordings in dominant frequency which ranged from 6.80±0.29Hz to 8.36±0.38Hz (p<0.0001) and dominant frequency spectral amplitude which ranged from 0.033±0.014mVHz to 0.043±0.017mVHz (p<0.0001). Histograms of dominant frequencies in leads exhibited strikingly different distributions, particularly in V2 that was characterised by a bimodal distribution, while the other leads were characterised by predominantly unimodal distributions.

Conclusion

VF dominant frequency spectral amplitude exhibited circadian variability. In a patient with severe myocarditis, supported with a biventricular assist device and in chronic VF, these results provide evidence for modulation of VF, probably induced by changes in posture and physical activity.

a Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, NE7 7DN, UK

b Department of Cardiology, Freeman Hospital, Newcastle upon Tyne, UK

c Medical Physics Department, Freeman Hospital, Newcastle upon Tyne, UK

Corresponding Author InformationCorresponding author at: Medical Physics Department, Freeman Hospital, Newcastle upon Tyne, NE7 7DN, UK. Tel.: +44 0 1912231664; fax: +44 0 1912130290.

 A Spanish translated version of the summary of this article appears as Appendix in the online version at doi:10.1016/j.resuscitation.2010.03.026.

PII: S0300-9572(10)00182-6

doi:10.1016/j.resuscitation.2010.03.026


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