Sympathovagal Balance
1998; Lippincott Williams & Wilkins; Volume: 98; Issue: 23 Linguagem: Inglês
10.1161/01.cir.98.23.2640
ISSN1524-4539
AutoresPeter Sleight, Luciano Bernardi,
Tópico(s)Cardiac Health and Mental Health
ResumoHomeCirculationVol. 98, No. 23Sympathovagal Balance Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBSympathovagal Balance Peter Sleight Luciano Bernardi Peter SleightPeter Sleight University of Oxford, John Radcliffe Hospital, Oxford, UK Luciano BernardiLuciano Bernardi Department of Internal Medicine, University of Pavia and IRCCS, Ospedale San Matteo, Pavia, Italy Originally published8 Dec 1998https://doi.org/10.1161/01.CIR.98.23.2640Circulation. 1998;98:2640To 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.3Eckberg 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.56 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.7Fluctuations 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.25 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.5Eckberg'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.710We agree that heart rate variability (HRV) is complex and highly influenced by respiration710 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.CrossrefMedlineGoogle Scholar2 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.MedlineGoogle Scholar3 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.CrossrefMedlineGoogle Scholar4 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.CrossrefMedlineGoogle Scholar5 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.CrossrefGoogle Scholar6 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.CrossrefMedlineGoogle Scholar7 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.CrossrefMedlineGoogle Scholar8 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.CrossrefMedlineGoogle Scholar9 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.Google Scholar10 Bernardi L, Keller F, Sanders M, Reddy PS, Griffith B, Meno F, Pinsky MR. Respiratory sinus arrhythmia in the denervated human heart. 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