The Mechanism of Cardiac Sympathetic Activity Assessment Methods: Current Knowledge

Abstract

This review has summarized the methods currently available for cardiac sympathetic assessment in clinical or under research, with emphasis on the principles behind these methodologies. Heart rate variability (HRV) and other methods based on heart rate pattern analysis can reflect the dominance of sympathetic nerve to sinoatrial node function and indirectly show the average activity level of cardiac sympathetic nerve in a period of time. Sympathetic neurotransmitters play a key role of signal transduction after sympathetic nerve discharges. Plasma or local sympathetic neurotransmitter detection can mediately display sympathetic nerve activity. Given cardiac sympathetic nerve innervation, i.e., the distribution of stellate ganglion and its nerve fibers, stellate ganglion activity can be recorded either directly or subcutaneously, or through the surface of the skin using a neurophysiological approach. Stellate ganglion nerve activity (SGNA), subcutaneous nerve activity (SCNA), and skin sympathetic nerve activity (SKNA) can reflect immediate stellate ganglion discharge activity, i.e., cardiac sympathetic nerve activity. These cardiac sympathetic activity assessment methods are all based on the anatomy and physiology of the heart, especially the sympathetic innervation and the sympathetic regulation of the heart. Technological advances, discipline overlapping, and more understanding of the sympathetic innervation and sympathetic regulation of the heart will promote the development of cardiac sympathetic activity assessment methods.

Impact of music performance anxiety on cardiovascular blood pressure responses, autonomic tone and baroreceptor sensitivity to a western classical music piano-concert

“…In order to assess cardiac autonomic modulation, we performed Wavelet analysis using the Wigner-Ville transform (W-V) for time/frequency domain analysis with standard MatLab software. We determined sympathetic and parasympathetic modulation of RR intervals (RRI) in the low frequency (LF; 0.04–0.14 Hz) and high frequency (HF; 0.15–0.50 Hz) ranges ( Task Force of the European Society of Cardiology the North A, 1996 ; Hilz and Dütsch, 2006 ; Li and Zheng, 2022 ). LF modulation of RRI reflects mainly sympathetic tone and, to an undetermined degree, also parasympathetic modulation; HF oscillations of RRIs reflect parasympathetic modulation ( Task Force of the European Society of Cardiology the North A, 1996 ; Hilz and Dütsch, 2006 ; Li and Zheng, 2022 ).…”

“…We determined sympathetic and parasympathetic modulation of RR intervals (RRI) in the low frequency (LF; 0.04–0.14 Hz) and high frequency (HF; 0.15–0.50 Hz) ranges ( Task Force of the European Society of Cardiology the North A, 1996 ; Hilz and Dütsch, 2006 ; Li and Zheng, 2022 ). LF modulation of RRI reflects mainly sympathetic tone and, to an undetermined degree, also parasympathetic modulation; HF oscillations of RRIs reflect parasympathetic modulation ( Task Force of the European Society of Cardiology the North A, 1996 ; Hilz and Dütsch, 2006 ; Li and Zheng, 2022 ). We also calculated the ratios between RRI modulations in the LF and HF ranges, using the LF/HF ratios as index of the sympathetic-parasympathetic balance ( Task Force of the European Society of Cardiology the North A, 1996 ; Hilz and Dütsch, 2006 ; Li and Zheng, 2022 ).…”

“…LF modulation of RRI reflects mainly sympathetic tone and, to an undetermined degree, also parasympathetic modulation; HF oscillations of RRIs reflect parasympathetic modulation ( Task Force of the European Society of Cardiology the North A, 1996 ; Hilz and Dütsch, 2006 ; Li and Zheng, 2022 ). We also calculated the ratios between RRI modulations in the LF and HF ranges, using the LF/HF ratios as index of the sympathetic-parasympathetic balance ( Task Force of the European Society of Cardiology the North A, 1996 ; Hilz and Dütsch, 2006 ; Li and Zheng, 2022 ). To reduce the parasympathetic component of LF modulation, we normalized LF and HF powers of RRI by calculating percentage values of LF and HF powers, with RRI LFnu = [LF/(LF + HF)] × 100%, and RRIHFnu = [HF/(LF + HF)] × 100% ( Task Force of the European Society of Cardiology the North A, 1996 ; Hilz and Dütsch, 2006 ; Li and Zheng, 2022 ).…”

Etiological Diagnosis and Personalized Therapy for Hypertension: A Hypothesis of the REASOH Classification

“…At present, for the screening of SAH, some clinical assessments for SA have been proved to be effective, including clinical features, neurotransmitter detection, metabolic biochemical-index detection, sympathetic-nerve-potential detection, and hemodynamic detection [ 42 ]. Studies have shown that patients who meet the following description are suggestive of the possibility of SAH, requiring further examination and early intervention: (1).…”

Stellate Ganglia and Cardiac Sympathetic Overactivation in Heart Failure

“…Regions of cardiac sympathetic nerve terminal denervation and hyperinnervation are present in the same failed heart to form the heterogeneity of the cardiac sympathetic nerve distribution [ 119 , 120 ]. Iodine-123 meta-iodobenzylguanidine ( 123 I-MIBG) or other radiolabeled neurotransmitter analogs (including the recently used F-18 meta-fluorobenzylguanidine) and cardiac neurotransmission imaging with single-photon emission computed tomography (SPECT) and positron emission tomography (PET) have been employed to noninvasively assess the integrity of human NET and further evaluate cardiac sympathetic nerve innervation [ 121 , 122 , 123 ]. However, poor imaging quality, difficulty in distinguishing different cardiac structures, and high cost limit this technique’s application in animal studies, especially small animal studies.…”