(Circulation. 1998;98:2643-2644.)
© 1998 American Heart Association, Inc.
Correspondence |
Sympathovagal Balance: A Critical Appraisal
Department of Cardiological Sciences St. George's Hospital Medical School, London, England
To the Editor:
With interest, I read Dr Eckberg's review,1 but some of his views need clarification. There are 2 principal methods for spectral analysis of heart rate variability (HRV) that differ in the determination of spectral components. Either integrals of power spectrum density over specific bands or automatic determination of components by autoregressive algorithms is used. We do not know whether 1 of these methods is superior, let alone whether 1 is the "correct" way. Although the sum of high- and low-frequency components accounts for the majority of spectral power in short-term recordings with both approaches, both methods may provide different values for individual components.
Standardization efforts were organized to propose the optimum methods for spectral and other analyses of HRV and interpretation of the results.2 3 Dr Eckberg was involved in some of these discussions and knows that no consensus on the "correct" spectral analysis was reached because no study exists comparing the 2 methods in a comprehensive variety of conditions. The assumption that spectral frequency components as integrals of specific bands are equal to their automatic autoregressive detection is an unsound speculation; I would be very surprised if it were not wrong. Consequently, the claims that some results by Dr Pagani et al (Reference 4 and others) are unreproducible are unfounded. Dr Eckberg compares these studies with investigations (Reference 5 and others) that used data obtained under similar circumstances but analyzed them differently.
There are numerous difficulties in the interpretation of any spectral analysis of biological data. These technologies were mathematically and technically developed for different purposes, and we conveniently ignore the mathematical premises of spectral methods that are very frequently, if not always, unfulfilled. Therefore, it is not too extreme to speculate that the high- and low-frequency components obtained with 1 method have, in some cases, different physiological interpretation than the results of the other method. Indeed, the discrepancy pointed out by Dr Eckberg points precisely in this direction.
Dr Eckberg will surely agree that it is more important to realize the unknown rather than dismiss it because it does not fit our theories. A study comparing the 2 approaches and studying the effects of ignoring some presumptions of spectral methods is very much needed. Only when we understand what the differences in technology mean will the comparisons attempted by Dr Eckberg be possible.
Finally, I find it difficult to understand why Dr Eckberg (for whom I have a high regard) proposes that the study by Pagani et al was not conducted properly. Such an approach to criticism will not help us obtain a consensus between research groups that is badly needed.
References
1.
Eckberg DL. Sympathovagal balance: a critical
appraisal. Circulation. 1997;96:3224–3232.
2.
Task Force of the European Society of
Cardiology and the North American Society of Pacing and
Electrophysiology: Heart rate variability: standards of measurement,
physiological interpretation, and clinical use.
Circulation. 1996;93:1043–1065; Eur Heart
J. 1996;17:353–380; Ann Noninvas Electrocardiol.
1966;1:151–181.
3. Berntson GG, Bigger JT Jr, Eckberg DL, Grossman P, Kaufmann PG, Malik M, Nagaraja HN, Porges SW, Saul JP, Stone PH, van der Molen MW. Heart rate variability: origins, methods, and interpretive caveats. Psychophysiology. 1997;34:623–648.[Medline] [Order article via Infotrieve]
4.
Pagani M, Montano N, Porta A, Malliani A, Abboud FM,
Birkett C, Somers VK. Relationship between spectral components of
cardiovascular variabilities and direct measures of
muscle sympathetic nerve activity in humans. Circulation. 1997;95:1441–1448.
5.
Saul JP, Rea RF, Eckberg DL, Berger RD, Cohen RJ.
Heart rate and muscle sympathetic activity during reflex changes of
autonomic activity. Am J Physiol. 1990;258:H713–H721.
Response
Medical College of Virginia at Virginia Commonwealth University and Hunter Holmes McGuire Department of Veterans Affairs Medical Center Richmond, Va
I thank my friends for their thoughtful responses to my article.
The legend to Figure 5 of the article by Malliani et al1 states that "A predominant low frequency (LF) characterizes RR and SND [sympathetic neural discharge] autospectra, whereas a greater respiratory high-frequency (HF) component is present in VND [vagal nerve discharge]." Introna et al2 showed that high spinal anesthesia does not reduce absolute LF RR-interval spectral power, and van de Borne et al3 showed that normalized LF RR-interval spectral power is low notwithstanding high sympathetic nerve activity in heart failure patients. Both studies undermine the view that LF RR-interval fluctuations reflect sympathetic-cardiac nerve traffic.
I did not cite literature critical of "sympathovagal balance"4 5 6 because I focused on physiology. The observation by Brown et al7 that tidal volumes and breathing rates are rarely controlled in heart rate variability studies is unique. I cited more recent than old studies from the Milan group. Highly variable, positive, synchronous, or negative systolic pressure–RR-interval phase relations8 and reductions of arterial pressure fluctuations by fixed-rate atrial pacing9 argue against a baroreflex explanation for respiratory frequency autonomic rhythms. Badilini et al10 reported good correlations between autoregressive and fast Fourier transform power spectra during upright tilt.
Malliani's criticism that I made no mention that his group has recognized limitations of "sympathovagal balance" is unfair. In my review,11 I said that "The sympathovagal-balance literature is replete with assertions that spectral power reflects fluctuations, not absolute levels of autonomic nerve traffic."
Use of models imposes philosophy on physiology. The "sympathovagal balance" model holds that baseline LF/LF+HF is a sympathetic marker; however, published studies show that this relation bears no significant (never mind "exact") correlation with any index of sympathetic activity.3 12 13 The model correctly holds that during graded upright tilt, the autonomic "balance" shifts from vagal to sympathetic; however, this shift is due entirely to reductions of vagally mediated respiratory sinus arrhythmia.14 In this case, the model is wrong in positing proportionality between LF RR-interval fluctuations and sympathetic nerve traffic. The model implicitly requires that reciprocal vagal and sympathetic changes be expressed equally; however, any vagal activity may prevent expression of sympathetic responses.15
For my part, I prefer actual measurements to calculations based on theories about how the autonomic nervous system works. For example, if I were given some measure of absolute respiratory frequency RR-interval fluctuations, I could draw my own conclusions about whether the higher levels of LF/LF+HF reported in hypertensive16 and postinfarction17 patients reflect "sympathetic predominance," as proposed, or merely reduced vagally mediated respiratory sinus arrhythmia.
I disagree that it is wrong to criticize science; debate of scientific issues is integral to the process of doing science. Scientific debate has intrinsic merit, independent of outcome. Authors who advance new ideas deserve great credit; the ideas themselves deserve close scrutiny.
References
1.
Malliani A, Pagani M, Lombardi F, Cerutti S.
Cardiovascular neural regulation explored in the
frequency domain. Circulation. 1991;84:482–492.
2. Introna R, Yodlowski E, Pruett J, Montano N, Porta A, Crumrine R. Sympathovagal effects of spinal anesthesia assessed by heart rate variability analysis. Anesth Analg. 1995;80:315–321.[Abstract]
3.
Van de Borne P, Montano N, Pagani M, Oren R, Somers
VK. Absence of low-frequency variability of sympathetic nerve activity
in severe heart failure. Circulation. 1997;95:1449–1454.
4. Casadei B, Cochrane S, Johnston J, Conway J, Sleight P. Pitfalls in the interpretation of spectral analysis of the heart rate variability during exercise in humans. Acta Physiol Scand. 1995;153:125–131.[Medline] [Order article via Infotrieve]
5.
Parati G, Saul JP, DiRienzo M, Mancia G. Spectral
analysis of blood pressure and heart rate variability in
evaluating cardiovascular regulation: a critical
appraisal. Hypertension. 1995;25:1276–1286.
6. Berntson GG, Bigger JT Jr, Eckberg DL, Grossman P, Kaufmann PG, Malik M, Nagaraja HN, Porges SW, Saul JP, Stone PH, van der Molen M. Heart rate variability: origins, methods, and interpretive caveats. Psychophysiology. 1997;34:623–648.
7.
Brown TE, Beightol LA, Koh J, Eckberg DL. Important
influence of respiration on human R-R interval power spectra is largely
ignored. J Appl Physiol. 1993;75:2310–2317.
8. Airaksinen KEJ, Tahvanainen KUO, Kuusela TA, Huikuri HV, Niemelä MJ, Karjalainen P, Eckberg DL. Cross spectral analysis in assessment of baroreflex gain in patients with coronary artery disease. Ann Noninvas Electrocardiol. 1997;2:229–235.[Medline] [Order article via Infotrieve]
9.
Taylor JA, Eckberg DL. Fundamental relations between
short-term RR interval and arterial pressure
oscillations in humans. Circulation. 1996;93:1527–1532.
10. Badilini F, Maison-Blanche P, Coumel P. Heart rate variability in passive tilt test: comparative evaluation of autoregressive and FFT spectral analyses. Pacing Clin Electrophysiol. 1998;21:1122–1132.[Medline] [Order article via Infotrieve]
11. Eckberg DL. Sympathovagal balance: a critical appraisal. Circulation. 1997;96:3224–3232.
12. Saul JP, Rea RF, Eckberg DL, Berger RD, Cohen RJ. Heart rate and muscle sympathetic nerve variability during reflex changes of autonomic activity. Am J Physiol. 1990;258:H713–H721.
13.
Kingwell BA, Thompson JM, Kaye DM, McPherson GA,
Jennings GL, Esler MD. Heart rate spectral analysis, cardiac
norepinephrine spillover, and muscle sympathetic nerve
activity during human sympathetic nervous activation and failure.
Circulation. 1994;90:234–240.
14.
Mukai S, Hayano J. Heart rate and blood pressure
variabilities during graded head-up tilt. J Appl
Physiol. 1995;78:212–216.
15. Samaan A. The antagonistic cardiac nerves and heart rate. J Physiol (Lond). 1935;83:332–340.
16. Guzzetti S, Piccaluga E, Casati R, Cerutti S, Lombardi F, Pagani M, Malliani A. Sympathetic predominance in essential hypertension: a study employing spectral analysis of heart rate variability. J Hypertens. 1988;6:711–717.[Medline] [Order article via Infotrieve]
17. Lombardi F, Sandrone G, Pernpruner S, Sala R, Garimoldi M, Cerutti S, Baselli G, Pagani M, Malliani A. Heart rate variability as an index of sympathovagal interaction after acute myocardial infarction. Am J Cardiol. 1987;60:1239–1245.[Medline] [Order article via Infotrieve]
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