LETTER TO THE EDITOR
Increased randomness of heart rate could explain increased heart rate variability preceding onset of atrial fibrillation
Phyllis K. Stein, PhD
Washington University School of Medicine, HRV Laboratory, 4625 Lindell Boulevard Suite 402, St. Louis, MO 63108, USA
pstein{at}im.wustl.edu
The recent study in JACC by Amar et al. (1) describes significant increases in heart rate variability (HRV) in the period preceding the onset of atrial fibrillation (AF) in postoperative patients. This increase in HRV is interpreted by the investigators as reflecting increased parasympathetic and sympathetic activity. Whereas this is a possible explanation, another equally plausible explanation requires testing. We propose that the increase in HRV is due to an increase in the randomness of the heart-period signal, associated with a marked increase in sympathetic activation. This would be consistent with a study in normals in which increasing doses of norepinephrine produced increased randomness of heart rate patterns (2). This hypothesis could easily be tested using multiple methods. One would be to plot the HRV power spectrum. If there were, indeed, an increase in vagal modulation of heart rate, there would be a clear increase in the size of a clearly seen peak in the high-frequency band. If an increase in randomness occurred, any increase in high-frequency power would be associated with an increasingly broad and abnormal-looking peak.
Alternatively, the Poincaré plot (a plot of each normal-to-normal interval vs. the next) could be generated. Increased randomness would be associated with an increasingly complex-looking plot (3). Finally, nonlinear HRV indices could be calculated. The calculation of the short-term fractal scaling exponent (4) would normally require about 1,000 beat-segments of data. The ratio of the axes of an ellipse fitted to the Poincaré plot (SD12) could be calculated for the same 5-min segments that were used for HRV. Increasing values of SD12, or decreasing values of the short-term scaling exponent, would be consistent with increasing randomness, rather than increased levels of autonomic modulation of the heart. Indeed, this technique has previously been applied to ventricular tachycardias, and increased SD12 was found to precede arrhythmic events (5).
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References
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1. Amar D, Zhang H, Miodownik S, Kadish AH. Competing autonomic mechanisms precede the onset of postoperative atrial fibrillation. J Am Coll Cardiol. 2003;42:1262–1268[Abstract/Free Full Text]
2. Tulppo MP, Mäkikallio TH, Seppänen T, et al. Effects of pharmacological adrenergic and vagal modulation on fractal heart rate dynamics. Clin Physiol. 2001;21:515–523[CrossRef][Medline]
3. Woo MA, Stevenson WG, Moser DK, Middlekauff HR. Complex heart rate variability, and serum norepinephrine levels in patients with advanced heart failure. J Am Coll Cardiol. 1994;23:565–569[Abstract]
4. Goldberger AL, Amaral LAN, Glass L, et al. PhysioBank, PhysioToolkit, and PhysioNet: components of a new research resource for complex physiologic signals. Circulation. 2000;101:e215–220[Abstract/Free Full Text]
5. Huikuri HV, Seppänen T, Koistinen MJ, et al. Abnormalities in beat-to-beat dynamics of heart rate before the spontaneous onset of life-threatening ventricular tachyarrhythmias in patients with prior myocardial infarction. Circulation. 1996;93:1836–1844[Abstract/Free Full Text]
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