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1 Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka, Japan; Department of Autonomic Neuroscience, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan
2 Core Laboratory, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan
3 Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka, Japan
4 Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka, Japan; Department of Cardiovascular Medicine, Kyusyu University Graduate School of Medical Sciences, Fukuoka, Japan
* To whom correspondence should be addressed. E-mail: kamiya{at}ri.ncvc.go.jp.
Sympathetic activation under orthostatic stress is accompanied by a marked increase of low frequency (LF, approximately 0.1 Hz) oscillation of sympathetic nerve activity (SNA) when arterial pressure is well maintained. However, the LF oscillation of SNA during the development of orthostatic neurally mediated syncope remains unknown. Ten healthy subjects who developed head-up tilt-induced neurally mediated syncope and 10 age-matched nonsyncopal control subjects were studied. Non-stationary time-dependent changes in calf muscle SNA (MSNA, microneurography), R-R interval and arterial pressure (finger photoplethysmography) variability were assessed during a 15-min 60° head-up tilt test (HUT) using complex demodulation. In both groups, HUT during the first 5 min increased the heart rate, magnitude of MSNA, LF and respiratory high frequency (HF) amplitudes of MSNA variability, as well as LF and HF amplitudes of arterial pressure variability, but decreased the HF amplitude of R-R interval variability (index of cardiac vagal nerve activity). In the non-syncopal group, these changes were sustained throughout the HUT. In the syncopal group, however, systolic arterial pressure decreased from 100 s to 60 s before onset of syncope; the LF amplitude of MSNA variability decreased, whereas the magnitude of MSNA and the LF amplitude of arterial pressure variability remained elevated. From 60s before syncope onset, MSNA and heart rate decreased, the index of cardiac vagal nerve activity increased, and arterial pressure further decreased to syncopal level. The LF oscillation of MSNA variability decreased during the development of orthostatic neurally mediated syncope, preceding sympathetic withdrawal, bradycardia and severe hypotension to syncope level.
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