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J Appl Physiol 102: 2406, 2007; doi:10.1152/japplphysiol.00283.2007
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POINT-COUNTERPOINT COMMENTS

Comment on Point:Counterpoint: "Cardiovascular variability is/is not an index of autonomic control of circulation"

Catherine F. Notarius and John S. Floras

Clinical Cardiovascular Physiology Research Laboratory
University Health Network and Mount Sinai Hospital
University of Toronto
Toronto, Ontario, Canada
e-mail: c.notarius{at}utoronto.ca

The following letter is in response to Point:Counterpoint "Cardiovascular variability is/is not an index of autonomic control of circulation" that appeared in the August issue (vol. 101, pages 676–682, 2006).

To the Editor: Changes in heart rate variability (HRV) or blood pressure variability (BPV) may well track qualitatively changes in vagal or sympathetic nerve traffic induced by some interventions in experimental models or human volunteers (6). However, contextual and interpretive limitations to their broader application to between-person comparisons or cardiovascular disease states have not been emphasized sufficiently in prior correspondence.

HRV is a marker of sinoatrial node responsiveness to oscillations in sympathetic and vagal nerve traffic, not necessarily of nerve firing rates (5). Thus conditions of high but relatively invariate sympathetic nerve firing and heart rates, such as exercise (2) or advanced heart failure (4), are characterized by loss, rather than gain, of low frequency (LF) HRV spectral power. Even within healthy subjects, a very modest (1.6 mmHg) reduction in central venous pressure without effect on stroke volume or blood pressure elicits marked discordance between muscle sympathetic nerve firing rates (increased) and both LF power and the LF/HF ratio (unchanged; Ref. 3). Although BPV in the LF range tracks sympathetic nerve discharge within healthy subjects (6), it is not increased, but similar in subjects with and without heart failure (1). There is evidence from large population studies that low HRV increases the risk of premature cardiovascular death, but as yet none that such data quantify reliably risk in a specific individual or that selectively increasing HRV pharmacologically or non-pharmacologically without affecting other known modifiable risk markers improves outcome.

Thus HRV and BPV analyses are best reserved for focused within-subject mechanistic investigations.

REFERENCES

  1. Butler GC, Ando S, Floras JS. Fractal component of variability of heart rate and systolic blood pressure in congestive heart failure. Clin Sci (Colch) 92: 543–550, 1997.[Medline]
  2. 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 153: 125–131, 1995.[Web of Science][Medline]
  3. Floras JS, Butler GC, Ando S, Brooks SC, Pollard MJ, Picton P. Differential sympathetic nerve and heart rate spectral effects of nonhypotensive lower body negative pressure. Am J Physiol Regul Integr Comp Physiol 281: R468–R475, 2001.[Abstract/Free Full Text]
  4. Notarius CF, Butler GC, Ando S, Pollard MJ, Senn B, Floras JS. Dissociation between microneurographic and heart rate variability estimates of sympathetic tone in normal subjects and patients with heart failure. Clin Sci (Colch) 96: 557–565, 1999.[Medline]
  5. Notarius CF, Floras JS. Limitations of the use of spectral analysis of heart rate variability for the estimation of cardiac sympathetic activity in heart failure. Europace 3: 29–38, 2001.[Abstract/Free Full Text]
  6. Parati G, Mancia G, Di Rienzo M, Castiglioni J, Taylor A, Studinger P. Point:Counterpoint: Cardiovascular variability is/is not an index of autonomic control of circulation. J Appl Physiol 101: 676–682, 2006.[Abstract/Free Full Text]




This Article
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