(Circulation. 1999;100:e67.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
Cardiac Neural Changes Before Vasovagal Syncope
Department of Cardiology, Leiden University Medical Center, Leiden, Netherlands
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To the Editor:
Furlan and colleagues1 present 2 scenarios leading to orthostatically induced syncope in healthy young subjects: "progressive sympathetic activation" and "progressive sympathetic inhibition." Their physiological characterization of the scenarios is based in large part on the observed changes in heart rate variability (HRV).
HRV interpretation is complex. Muscle sympathetic nerve recordings show that sympathetic firing fluctuates on a beat-to-beat basis (see, for example, Reference 2).However, due to the time constants involved, the sinoatrial pacemaker can only follow the low-frequency fluctuations in sympathetic firing (10-second rhythm and slower), whereas faster-changing sympathetic activity is integrated and becomes apparent only in the average heart rate (HR). There is more uncertainty as to the interpretation of low-frequency (LF) HRV, and the Task Force on Heart Rate Variability disagrees as to whether it is sympathetic or sympathetic-plus-vagal modulations that are represented in LF.3
If the sympathovagal balance changes, HR changes too.4 The LF dips and HF peaks that occur several times before the fainting episode in the sudden syncope case depicted in Figure 1 of the article by Furlan et al1 are not reflected in HR itself. In their study, Furlan and colleagues present control subjects and fainting subjects categorized according to the 2 above-mentioned scenarios. HR increases in all groups, no matter the HRV responses (see Tables 2 and 3). The strongest increase is seen in the sudden fainters, the smallest in the control subjects. Therefore, progressive sympathetic inhibition is unlikely in any of the studied groups. An increase in HR while the sympathetic tone is lessening can only be conceived in the setting of simultaneously withdrawing vagal activity, for which the presented data bear no evidence. The assessment of vagal tone, sympathetic tone, or the sympathovagal balance from HRV remains speculative, especially in less common conditions.5
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1. Furlan R, Piazza S, Dell'Orto S, Barbic F, Bianchi A, Mainardi L, Cerutti S, Pagani M, Malliani A. Cardiac autonomic patterns preceding occasional vasovagal reactions in healthy humans. Circulation. 1998;98:1756–1761.
2.
Furlan R, Jacob G, Snell M, Robertson D, Porta A,
Harris P, Mosqueda-Garcia R. Chronic orthostatic
intolerance: a disorder with discordant cardiac and vascular
sympathetic control. Circulation. 1998;98:2154–2159.
3.
Camm AJ, et al. Heart rate variability: standards of
measurement, physiological interpretation, and
clinical use. Circulation. 1996;93:1043–1065.
4. Swenne CA, Bootsma M. Sympathovagal balance and graded orthostatic tilt. Circulation. 1995;91:2292. Letter.
5.
Eckberg DE. Sympathovagal balance: a critical
appraisal. Circulation. 1997;96:3224–3232.
Response
Centro Ricerche Cardiovascolari, CNR, Unità Sincopi, Medicina Interna 2, Ospedale L. Sacco, Università degli Studi di Milano, Milan, Italy
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Swenne and colleagues raise the question of the lack of concomitant fluctuations in heart rate (HR) and in the oscillatory components of its variability (HRV) in subjects before tilt-induced syncope.1
In broad terms, HR depends on pacemaker intrinsic discharge, sympathetic and vagal neural activity, and circulatory neurohormones. Conversely, HRV reflects autonomic modulation of sinoatrial node activity. Thus, HR and HRV cannot be equated.
At least 3 variables (RR, low-frequency RR [LFRR], and high-frequency RR [HFRR]) are necessary to define the individual autonomic profile corresponding to a given posture,2 which suggests that LFRR and HFRR contain information that is not simply inherent in the HR value. In addition, we found that a group of patients with syncope was characterized during tilt by a blunted increase of peroneal sympathetic nerve discharge (MSNA) and plasma norepinephrine levels but an exaggerated enhancement of epinephrine compared with controls.3 Accordingly, HR increased to a similar level in both groups.3
Thus, under certain circumstances (eg, in the presence of an increased concentration of circulating catecholamines before syncope), HR may not parallel the changes of the spectral components of HRV. This seems to also apply to the other statement by Swenne and colleagues that vagal withdrawal is necessary to explain tachycardia while sympathetic tone is lessening.
The time-variant spectral approach enabled us to assess the time course of the changes in the oscillatory components of HRV (ie, the cardiac neural modulation) preceding the onset of syncope that would be otherwise undetectable by simple perusal of HR values. In the example shown in Figure 1,1 the trends of HFRR and LFRR suggest a progressive rise in cardiac vagal modulation and decrease in sympathetic modulation in the case of "syncope with latency" before the onset of bradycardia. Clinical observation of these subjects also detected signs and symptoms of vagal progressive activation, such as increasing nausea, dizziness, and yawning that preceded the loss of consciousness.
Only after a "critical level" is reached, overwhelming the residual neurohormonal adrenergic activation, might vagal excitation and sympathetic inhibition silence the intrinsic sinoatrial node discharge.
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References |
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TopIntroductionReferencesIntroduction References |
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1. Furlan R, Piazza S, Dell'Orto S, Barbic F, Bianchi A, Mainardi L, Cerutti S, Pagani M, Malliani A. Cardiac autonomic patterns preceding occasional vasovagal reactions in healthy humans. Circulation. 1998;98:1756–1761.
2.
Malliani A, Pagani M, Furlan R, Guzzetti S, Lucini D,
Montano N, Cerutti S, Mela S. Individual recognition by heart rate
variability of two different autonomic profiles related to posture.
Circulation. 1997;96:4143–4145.
3. Mosqueda-Garcia R, Furlan R, Fernandez-Violante R, Desai T, Snell M, Jarai Z, Ananthram V, Robertson RM, Robertson D. Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt. J Clin Invest. 1997;99:2736–2744.[Medline] [Order article via Infotrieve]
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