Hemodynamics, plasma catecholamines, and power spectral analysis of heart rate variability during tilt-evoked neurally mediated hypotension
- 1Clinical Neurosciences Program/Division of Intramural Research (DIR)/National Institute of Neurological Disorders and Stroke (NINDS)/National Institutes of Health (NIH)
- 2Department of Neurology, University of Utah
- 3George E. Wahlen VA Medical Center
Abstract
Background: Syncope workup often includes tilt table testing. One positive result is neurally mediated hypotension (NMH). Mechanisms of NMH are debated.
Objectives: We characterized NMH development in terms of systemic and forearm hemodynamics, plasma catecholamines, and power spectral analysis of heart rate variability.
Methods: We reviewed data from 25 subjects with NMH and 34 controls without NMH who had autonomic testing between 2003 and 2024. Dependent measures included continuously recorded blood pressure (BP), heart rate, stroke volume, cardiac output, respiratory rate (RR), forearm blood flow (FBF), forearm vascular resistance (FVR), systemic vascular resistance (SVR), plasma epinephrine and norepinephrine, and high- and low-frequency power of heart rate variability (HF RR and LF RR ). There were 4 study periods: T0 = supine rest; T1 = start of tilt; T2 = NMH (20 min of tilting in controls); and T3 = supine recovery.
Results: There were significant interaction effects for Group X Study Period for several variables, with a decrease in BP, FVR, SVR, HF RR , and LF RR , and an increase in FBF and epinephrine at a steeper rate in the NMH group compared to the No NMH group. The two groups did not differ in responses of heart rate, RR, stroke volume, cardiac output, or norepinephrine levels. The increment in plasma epinephrine was larger in the NMH group, without a group difference in norepinephrine (i.e., sympathoadrenal imbalance). LF RR was elevated at baseline and decreased markedly in participants developing NMH.
Conclusions: NMH is associated with forearm vasodilation, sympathoadrenal imbalance, and a precipitous fall in LF RR . The results fit with a neurocirculatory-neuroendocrine pattern triggering NMH.
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BibTeX
@article{lamotte2026hemodynamics,
title = {{Hemodynamics, plasma catecholamines, and power spectral analysis of heart rate variability during tilt-evoked neurally mediated hypotension}},
author = {Guillaume Lamotte and Patti Sullivan and David S. Goldstein},
journal = {Frontiers in Neuroscience},
year = {2026},
month = oct,
doi = {10.3389/fnins.2026.1929006},
url = {https://www.frontiersin.org/articles/10.3389/fnins.2026.1929006/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Hemodynamics, plasma catecholamines, and power spectral analysis of heart rate variability during tilt-evoked neurally mediated hypotension
AU - Guillaume Lamotte
AU - Patti Sullivan
AU - David S. Goldstein
PY - 2026
DA - 2026/10/06
JO - Frontiers in Neuroscience
DO - 10.3389/fnins.2026.1929006
UR - https://www.frontiersin.org/articles/10.3389/fnins.2026.1929006/full
AB - Background: Syncope workup often includes tilt table testing. One positive result is neurally mediated hypotension (NMH). Mechanisms of NMH are debated. Objectives: We characterized NMH development in terms of systemic and forearm hemodynamics, plasma catecholamines, and power spectral analysis of heart rate variability. Methods: We reviewed data from 25 subjects with NMH and 34 controls without NMH who had autonomic testing between 2003 and 2024. Dependent measures included continuously recorded blood pressure (BP), heart rate, stroke volume, cardiac output, respiratory rate (RR), forearm blood flow (FBF), forearm vascular resistance (FVR), systemic vascular resistance (SVR), plasma epinephrine and norepinephrine, and high- and low-frequency power of heart rate variability (HF RR and LF RR ). There were 4 study periods: T0 = supine rest; T1 = start of tilt; T2 = NMH (20 min of tilting in controls); and T3 = supine recovery. Results: There were significant interaction effects for Group X Study Period for several variables, with a decrease in BP, FVR, SVR, HF RR , and LF RR , and an increase in FBF and epinephrine at a steeper rate in the NMH group compared to the No NMH group. The two groups did not differ in responses of heart rate, RR, stroke volume, cardiac output, or norepinephrine levels. The increment in plasma epinephrine was larger in the NMH group, without a group difference in norepinephrine (i.e., sympathoadrenal imbalance). LF RR was elevated at baseline and decreased markedly in participants developing NMH. Conclusions: NMH is associated with forearm vasodilation, sympathoadrenal imbalance, and a precipitous fall in LF RR . The results fit with a neurocirculatory-neuroendocrine pattern triggering NMH.
SN - 1662-453X
SN - 1662-4548
ER -