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(Circulation. 1998;98:2640.)
© 1998 American Heart Association, Inc.

Correspondence

Sympathovagal Balance

Peter Sleight, MD

University of Oxford, John Radcliffe Hospital, Oxford, UK

Luciano Bernardi, MD

Department of Internal Medicine, University of Pavia and IRCCS, Ospedale San Matteo, Pavia, Italy

To the Editor:

A letter is inadequate to rebut fully Eckberg's destructive and selectively referenced polemic against sympathovagal balance,¹ which ignored many prior contributions constructively addressing the same points now raised.

Because RR low frequency (LF) is much reduced by atropine, its relation to sympathetic outflow was questioned. De Boer et al² explained the origin of LF oscillations as the interaction of fast vagal and slow sympathetic responses, validated by the LF oscillations that follow a single stimulus to the human carotid sinus.³

Eckberg states that there is no evidence that LF power is related to sympathetic nerve traffic. We⁴ showed that sympathetic reinnervation in transplanted hearts was associated with nonrespiratory LF. Exact quantitative correlations between different sympathetic measures would be surprising.

It was stated by Eckberg that respiratory RR interval variability (high frequency, or HF) "reflects primarily respiratory gating of vagal-cardiac motor neurone responses," whereas there is much evidence that in conscious humans it represents baroreceptor-driven responses to respiratory blood pressure swings.^{5 6} During increasing exercise, and also with denervation, nonneural mechanisms, such as sinus node stretch from increasing respiratory fluctuation in venous return, become important contributors to RR HF.⁷

Fluctuations in nerve traffic were not thought important compared with absolute levels; the widely reported ATRAMI⁸ and UK HEART⁹ studies contradict this view.

The concept of reciprocal changes in sympathetic and vagus output was questioned by citing the diving reflex, in contrast to more physiological states such as standing, arousal, or emotion, in which there is clear reciprocity.

Both HF and LF RR variability are greatly influenced by the gain of the baroreflex.^{2 5} It is not surprising that LF is paradoxically reduced in exercise and heart failure (despite increased sympathetic drive), because baroreflex sensitivity gain for heart rate control is markedly reduced in these conditions.⁵

Eckberg's own study showed a "pivotal, largely ignored role for respiration as a determinant of HF spectral power," but earlier, similar contributions were not quoted.^{7 10}

We agree that heart rate variability (HRV) is complex and highly influenced by respiration^{7 10} but believe it more productive to explore the causes of HRV and its anomalies rather than attempt to destroy Malliani and Pagani's early work while ignoring their later contributions.

Finally, despite this quasi-mathematical review, we notice repeated confusion over the units for spectral power (units²) with spectral power density (units²/Hz), eg, Figures 2 and 4.

References

1. Eckberg DL. Sympathovagal balance: a critical appraisal. Circulation. 1997;96:3224–3232.[Free Full Text]
   
2. De Boer RW, Karemaker JW, Strackee J. Hemodynamic fluctuations and baroreflex sensitivity in humans: a beat-to-beat model. Am J Physiol. 1987;253:680–689.
   
3. Bernardi L, Leuzzi S, Radaelli A, Passino C, Johnston JA, Sleight P. Low-frequency spontaneous fluctuations of RR interval and blood pressure in conscious humans: a baroreceptor or central phenomenon. Clin Sci. 1994;87:649–654.[Medline] [Order article via Infotrieve]
   
4. Bernardi L, Bianchini B, Spadacini G, Leuzzi S, Valle F, Marchesi E, Passino C, Calciati A, Viganó M, Rinaldi M, Martinelli L, Finardi G, Sleight P. Demonstrable cardiac reinnervation after human heart transplantation by carotid baroreflex modulation of RR interval. Circulation. 1995;92:2895–2903.[Abstract/Free Full Text]
   
5. Sleight P, La Rovere MT, Mortara A, Pinna G, Maestri R, Leuzzi S, Bianchini B, Tavazzi L, Bernardi L. Physiology and pathophysiology of heart rate and blood pressure variability in humans: is power spectral analysis largely an index of baroreflex gain? Clin Sci (Colch). 1995;88:103–109.[Medline] [Order article via Infotrieve]
   
6. Piepoli M, Sleight P, Leuzzi S, Valle F, Spadacini G, Passino C, Johnson J, Bernardi L. Origin of respiratory sinus arrhythmia in conscious humans: an important role for arterial carotid baroreceptors. Circulation. 1997;95:1813–1821.[Abstract/Free Full Text]
   
7. Bernardi L, Salvucci F, Suardi R, Soldá, Calciati A, Perlini S, Falcone C, Ricciardi L, Sleight P. Evidence for an intrinsic mechanism regulating heart rate variability in the transplanted and the intact heart during submaximal dynamic exercise? Cardiovasc Res. 1990;24:969–981.[Free Full Text]
   
8. La Rovere MT, Bigger JT Jr, Marcus FI, Mortara A, Schwartz PJ, for the ATRAMI (Autonomic Tone and Reflexes After Myocardial Infarction) Investigators. Baroreflex sensitivity and heart rate variability in prediction of total cardiac mortality after myocardial infarction. Lancet. 1998;351:478–484.[Medline] [Order article via Infotrieve]
   
9. Nolan J, Batin PD, Andrews R, Lindsay SJ, Brooksby P, Mullen M, Baig W, Flapan AD, Cowley A, Prescott RJ, Neilson JMM, Fox KAA. A prospective study of heart rate variability and mortality in chronic heart failure: results of the UK Heart Failure Evaluation and Assessment of Risk Trial (UK-HEART). Circulation. In press.
   
10. Bernardi L, Keller F, Sanders M, Reddy PS, Griffith B, Meno F, Pinsky MR. Respiratory sinus arrhythmia in the denervated human heart. J Appl Physiol. 1989;67:1447–1455.[Abstract/Free Full Text]
    

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