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(Circulation. 1999;100:e67.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
Department of Cardiology, Leiden University Medical Center, Leiden, Netherlands
| Introduction |
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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
Centro Ricerche Cardiovascolari, CNR, Unità Sincopi, Medicina Interna 2, Ospedale L. Sacco, Università degli Studi di Milano, Milan, Italy
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