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

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POINT-COUNTERPOINT COMMENTSComment on Point:Counterpoint: “Cardiovascular variability is/is not an index of autonomic control of circulation”Catherine F. Notarius, and John S. FlorasCatherine F. Notarius, and John S. FlorasPublished Online:01 Jun 2007https://doi.org/10.1152/japplphysiol.00283.2007MoreSectionsPDF (27 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations 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.REFERENCES1 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.Crossref | Google Scholar2 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.Crossref | PubMed | Google Scholar3 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.Link | ISI | Google Scholar4 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.Crossref | Google Scholar5 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.Crossref | PubMed | ISI | Google Scholar6 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.Link | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation Cited ByDifferent equestrian sports horses’ reactivity to startleJournal of Veterinary Behavior, Vol. 57Mild Hypothermia Attenuates Circulatory and Pulmonary Dysfunction During Experimental Endotoxemia*Critical Care Medicine, Vol. 41, No. 12 More from this issue > Volume 102Issue 6June 2007Pages 2406-2406 Copyright & PermissionsCopyright © 2007 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00283.2007PubMed17551108History Published online 1 June 2007 Published in print 1 June 2007 Metrics