Frontiers in neuroscience · 2026
Hemodynamics, plasma catecholamines, and power spectral analysis of heart rate variability during tilt-evoked neurally mediated hypotension.
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Lamotte Guillaume, Sullivan Patti, Goldstein David S
Аннотация
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 (HFRR and LFRR). 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, HFRR, and LFRR, 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). LFRR 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 LFRR. The results fit with a neurocirculatory-neuroendocrine pattern triggering NMH.
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 (HFRR and LFRR). 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, HFRR, and LFRR, 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). LFRR 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 LFRR. The results fit with a neurocirculatory-neuroendocrine pattern triggering NMH.