Augmented sympathetic neural response to simulated obstructive apnoea in human heart failure

2003 ◽  
Vol 104 (3) ◽  
pp. 231-238 ◽  
Author(s):  
T. Douglas BRADLEY ◽  
Ruzena TKACOVA ◽  
Michael J. HALL ◽  
Shin-ichi ANDO ◽  
John S. FLORAS
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Sympathetic Activity ◽  
Healthy Subjects ◽  
Human Subjects ◽  
Muscle Sympathetic Nerve Activity ◽  
Sleep Apnoea ◽  
Human Heart Failure ◽  
Healthy Human ◽  
Heart Failure Patients

Sleep apnoea in heart failure increases mortality risk, possibly as a result of greater activation of the sympathetic nervous system. In healthy subjects, simulated central apnoeas (holding breath) and obstructive apnoeas (Mueller manoeuvres) increase muscle sympathetic activity equally, primarily through chemoreceptor stimulation. In heart failure, however, Mueller manoeuvres cause greater reductions in blood pressure than breath holds. We hypothesized that in heart failure, the summation of arterial baroreceptor unloading and chemoreceptor stimulation would increase sympathetic activity more during obstructive than central apnoeas. Healthy human subjects and heart failure patients (seven of each) performed 15-s breath holds and 15-s Mueller manoeuvres. Breath holds evoked a progressive increase in muscle sympathetic nerve activity in both groups, but had no effect on blood pressure. In healthy subjects, breath holds and Mueller manoeuvres caused equal peaks in sympathetic activity. In contrast, in heart failure patients, Mueller manoeuvres caused a progressive decrease in blood pressure (P<0.05) and greater increases in sympathetic activity than breath holds (P<0.01). In heart failure, simulated obstructive apnoea elicits greater increases in sympathetic activity than simulated central apnoea, due to its additional hypotensive effect. These present findings offer novel insight into the potential role of sleep apnoea in augmenting sympathetic activity and accelerating disease progression in heart failure.

scholarly journals Muscle sympathetic activity in resting and exercising humans with and without heart failure

2015 ◽  
Vol 40 (11) ◽  
pp. 1107-1115 ◽  
Author(s):  
Catherine F. Notarius ◽  
Philip J. Millar ◽  
John S. Floras
Keyword(s):  
Heart Failure ◽  
Exercise Training ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Cardiovascular Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Muscle Blood Flow ◽  
Exercise Intolerance ◽  
Human Heart Failure ◽  
Healthy Humans

The sympathetic nervous system is critical for coordinating the cardiovascular response to various types of physical exercise. In a number of disease states, including human heart failure with reduced ejection fraction (HFrEF), this regulation can be disturbed and adversely affect outcome. The purpose of this review is to describe sympathetic activity at rest and during exercise in both healthy humans and those with HFrEF and outline factors, which influence these responses. We focus predominately on studies that report direct measurements of efferent sympathetic nerve traffic to skeletal muscle (muscle sympathetic nerve activity; MSNA) using intraneural microneurographic recordings. Differences in MSNA discharge between subjects with and without HFrEF both at rest and during exercise and the influence of exercise training on the sympathetic response to exercise will be discussed. In contrast to healthy controls, MSNA increases during mild to moderate dynamic exercise in the presence of HFrEF. This increase may contribute to the exercise intolerance characteristic of HFrEF by limiting muscle blood flow and may be attenuated by exercise training. Future investigations are needed to clarify the neural afferent mechanisms that contribute to efferent sympathetic activation at rest and during exercise in HFrEF.

Dynamics of muscle sympathetic nerve activity in advanced heart failure patients

1996 ◽  
Vol 271 (5) ◽  
pp. H1962-H1969
Author(s):  
A. H. Nguyen ◽  
A. Garfinkel ◽  
D. O. Walter ◽  
M. A. Hamilton ◽  
G. C. Fonarow ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Frequency Modulation ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Low Frequency ◽  
Nerve Activity ◽  
Heart Failure Patients ◽  
Patients With Heart Failure

Muscle sympathetic nerve activity (MSNA) is increased in patients with heart failure compared with healthy subjects. We applied spectral and correlation techniques to determine if qualitative as well as quantitative differences in MSNA differentiate heart failure patients from healthy subjects. We recorded MSNA, heart rate, and respiration in 11 heart failure patients and 10 healthy humans. Our results are as follows. 1) Statistically significant low-frequency modulation of MSNA at 0.029 +/- 0.002 Hz (mean +/- SE; range 0.026-0.038 Hz) was found in 10 of 11 heart failure patients but in only 2 of 10 healthy controls (differences between groups, P < 0.01; chi 2 test). 2) Heart rate and respiration also demonstrated significant low-frequency modulation in a similar range. 3) Spectral and correlation techniques revealed that low-frequency modulation of MSNA was highly correlated with low-frequency modulation of respiration in heart failure patients, but not in healthy subjects. In contrast, low-frequency modulation of MSNA did not correlate well with low-frequency modulation of heart rate. In summary, low-frequency modulation of respiration is coupled to low-frequency modulation of MSNA in heart failure patients, but not in normal subjects. We speculate that this low-frequency modulation of respiration may represent subclinical Cheyne-Stokes breathing, which has marked qualitative effects on MSNA in patients with heart failure.

scholarly journals The prognostic significance of cardiac sympathetic activity and dyssynchrony in cardiac resynchronization therapy in ischemic and non-ischemic heart failure patients

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
A Mishkina ◽  
K Zavadovsky ◽  
V Saushkin ◽  
D Lebedev ◽  
Y Lishmanov
Keyword(s):  
Heart Failure ◽  
Cardiac Resynchronization Therapy ◽  
Sympathetic Activity ◽  
Gated Spect ◽  
Prognostic Significance ◽  
Cardiac Resynchronization ◽  
Resynchronization Therapy ◽  
Cardiac Sympathetic Activity ◽  
Heart Failure Patients ◽  
Crt Response

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Russian Foundation for Basic Research Introduction Impaired cardiac sympathetic activity and contractility are associated with poor prognosis in patients with heart failure after cardiac resynchronization therapy (CRT). There are few prognostic data of the cardiac sympathetic activity and dyssynchrony in patients with chronic heart failure of various etiologies. Purpose To examine the prognostic significance of scintigraphic cardiac sympathetic activity and contractility in predicting the response to CRT and to assess the differences between patients with ischemic (IHF) and non-ischemic (NIHF) heart failure. Methods This study included 38 heart failure patients (24 male; mean age of 56 ± 11 years; 16 patients with ischemic etiology), who were submitted to CRT. Before CRT all patients underwent 123I-metaiodobenzylguanidine (123I-MIBG) imaging for cardiac sympathetic activity evaluating: early and delay heart to mediastinum ratio (eH/M and dH/M), summed MIBG Score (eSMS and dSMS). Moreover all patients underwent gated SPECT with the assessments of left ventricle dyssynchrony indexes: standard deviation (SD) and histogram bandwidth (HBW). In addition, all patients underwent gated blood-pool SPECT (GBPS) to assessed ejection fraction (EF) and stroke volume (SV) of both ventricles. Results One year after CRT response defined as LV ESV decreased by≥15% and/or LV EF increase by≥5%. Baseline cardiac sympathetic activity parameters showed significant differences between responders and non-responders only in NIHF patients: eH/M: 2.27 (2.02–2.41) vs. 1.64 (1.32–2.16); dH/M: 2.18 (2.11–2.19) vs. 1.45 (1.23 – 1.61); eSMS: 7 (5-7) vs. 15.5 (10–28.5); dSMS: 10 (10–13) vs. 16.5 (15.5–29). Significant differences in baseline LV dyssynchrony indexes between responders and non-responders were in patients of both group: in NIHF patients - SD: 54.3 (43–58) degree vs. 65 (62–66) degree; HBW: 179.5 (140–198) degree vs. 211 (208-213) degree, p &lt; 0.054 in IHF patients - HBW: 162 (115.2–180) degree vs.  115.2 (79.2–136.8) degree. Contractility of RV was significantly differed between responders and non-responders in IHF patients: RV EF: 54.5 (41-56) % vs. 44.5 (37–49.5) %; RV SV: 80 (69-101) ml vs. 55.5 (50–72.5) ml. According to univariate logistic regression analyses in IHF patients LV dyssynchrony indexes – SD (OR = 1.55; 95% CI 1.09-2.2; p &lt; 0.5) and HBW (OR = 1.13; 95% CI 1.02-1.24; p &lt; 0.5), as well as RV indexes – RV EF (OR = 1.11; 95% CI 1.001-1.23; p &lt; 0.5), RV SV (OR = 1.07; 95% CI 1.003-1.138; p &lt; 0.5) were predictors of CRT response. In the group of NIHF patients, dH/M (OR = 1.47; 95% CI 1.08-2; p &lt; 0.5), SD (OR = 0.83; 95% CI 0.73-0.95; p &lt; 0.5), HBW (OR = 0.96; 95% CI 0.93-0.99; p &lt; 0.5) showed the predictive value in terms of CRT response. Conclusion  Scintigraphic methods can be used to select patients for CRT. Cardiac 123I-MIBG scintigraphy and gated SPECT may be used for predicting CRT response in NIHF patients. Whereas in IHF patients ECG-gated SPECT and GBPS may be valuable for predicting the response to CRT.

Short-term intermittent hypoxia enhances sympathetic responses to continuous hypoxia in humans

2007 ◽  
Vol 103 (3) ◽  
pp. 835-842 ◽  
Author(s):  
Urs A. Leuenberger ◽  
Cynthia S. Hogeman ◽  
Sadeq Quraishi ◽  
Latoya Linton-Frazier ◽  
Kristen S. Gray
Keyword(s):  
Blood Pressure ◽  
Sleep Apnea ◽  
Sympathetic Activity ◽  
Intermittent Hypoxia ◽  
Muscle Sympathetic Nerve Activity ◽  
Acute Hypoxia ◽  
Short Term ◽  
Healthy Humans ◽  
Obstructive Sleep ◽  
Normal Humans

Short-term intermittent hypoxia leads to sustained sympathetic activation and a small increase in blood pressure in healthy humans. Because obstructive sleep apnea, a condition associated with intermittent hypoxia, is accompanied by elevated sympathetic activity and enhanced sympathetic chemoreflex responses to acute hypoxia, we sought to determine whether intermittent hypoxia also enhances chemoreflex activity in healthy humans. To this end, we measured the responses of muscle sympathetic nerve activity (MSNA, peroneal microneurography) to arterial chemoreflex stimulation and deactivation before and following exposure to a paradigm of repetitive hypoxic apnea (20 s/min for 30 min; O2 saturation nadir 81.4 ± 0.9%). Compared with baseline, repetitive hypoxic apnea increased MSNA from 113 ± 11 to 159 ± 21 units/min ( P = 0.001) and mean blood pressure from 92.1 ± 2.9 to 95.5 ± 2.9 mmHg ( P = 0.01; n = 19). Furthermore, compared with before, following intermittent hypoxia the MSNA (units/min) responses to acute hypoxia [fraction of inspired O2 (FiO2) 0.1, for 5 min] were enhanced (pre- vs. post-intermittent hypoxia: +16 ± 4 vs. +49 ± 10%; P = 0.02; n = 11), whereas the responses to hyperoxia (FiO2 0.5, for 5 min) were not changed significantly ( P = NS; n = 8). Thus 30 min of intermittent hypoxia is capable of increasing sympathetic activity and sensitizing the sympathetic reflex responses to hypoxia in normal humans. Enhanced sympathetic chemoreflex activity induced by intermittent hypoxia may contribute to altered neurocirculatory control and adverse cardiovascular consequences in sleep apnea.

Feedback effects of circulating norepinephrine on sympathetic outflow in healthy subjects

2005 ◽  
Vol 288 (2) ◽  
pp. H710-H715 ◽  
Author(s):  
Mikko P. Tulppo ◽  
Heikki V. Huikuri ◽  
Elli Tutungi ◽  
Derek S. Kimmerly ◽  
Adrian W. Gelb ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Sympathetic Activity ◽  
Healthy Subjects ◽  
Blood Pressure Variability ◽  
Feedback Inhibition ◽  
Adrenergic Blockade ◽  
Sympathetic Outflow ◽  
Systolic Blood Pressure Variability ◽  
Normalized Units

The amplitude of low-frequency (LF) oscillations of heart rate (HR) usually reflects the magnitude of sympathetic activity, but during some conditions, e.g., physical exercise, high sympathetic activity results in a paradoxical decrease of LF oscillations of HR. We tested the hypothesis that this phenomenon may result from a feedback inhibition of sympathetic outflow caused by circulating norepinephrine (NE). A physiological dose of NE (100 ng·kg−1·min−1) was infused into eight healthy subjects, and infusion was continued after α-adrenergic blockade [with phentolamine (Phe)]. Muscle sympathetic nervous activity (MSNA) from the peroneal nerve, LF (0.04–0.15 Hz) and high frequency (HF; 0.15–0.40 Hz) spectral components of HR variability, and systolic blood pressure variability were analyzed at baseline, during NE infusion, and during NE infusion after Phe administration. The NE infusion increased the mean blood pressure and decreased the average HR ( P < 0.01 for both). MSNA (10 ± 2 vs. 2 ± 1 bursts/min, P < 0.01), LF oscillations of HR (43 ± 13 vs. 35 ± 13 normalized units, P < 0.05), and systolic blood pressure (3.1 ± 2.3 vs. 2.0 ± 1.1 mmHg2, P < 0.05) decreased significantly during the NE infusion. During the NE infusion after PHE, average HR and mean blood pressure returned to baseline levels. However, MSNA (4 ± 2 bursts/min), LF power of HR (33 ± 9 normalized units), and systolic blood pressure variability (1.7 ± 1.1 mmHg2) remained significantly ( P < 0.05 for all) below baseline values. Baroreflex gain did not change significantly during the interventions. Elevated levels of circulating NE cause a feedback inhibition on sympathetic outflow in healthy subjects. These inhibitory effects do not seem to be mediated by pressor effects on the baroreflex loop but perhaps by a presynaptic autoregulatory feedback mechanism or some other mechanism that is not prevented by a nonselective α-adrenergic blockade.

scholarly journals What Is the Ideal Blood Pressure Goal for Heart Failure Patients?

2018 ◽  
Vol 6 (10) ◽  
pp. 889-890
Author(s):  
Mostafa Ghanim ◽  
Maxwell Eyram Afari ◽  
Lana Tsao
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Blood Pressure Goal ◽  
Heart Failure Patients ◽  
The Ideal

scholarly journals Daytime periodic breathing during short-term laboratory recordings in heart failure patients: the iceberg tip of central sleep apnoea?

2017 ◽  
Vol 20 (5) ◽  
pp. 934-936 ◽  
Author(s):  
Maria Teresa La Rovere ◽  
Roberto Maestri ◽  
Elena Robbi ◽  
Angelo Caporotondi ◽  
Giampaolo Guazzotti ◽  
...  
Keyword(s):  
Heart Failure ◽  
Periodic Breathing ◽  
Sleep Apnoea ◽  
Short Term ◽  
Heart Failure Patients ◽  
Central Sleep Apnoea

Abstract 2470: Augmented Tonic Activation Of Chemoreceptors May Contribute To Sympathetic Overactivity In Patients With Essential Hypertension

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Maciej Sinski ◽  
Jacek Lewandowski ◽  
Joanna Bidiuk ◽  
Piotr Abramczyk ◽  
Anna Dobosiewicz ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Sympathetic Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Hemoglobin Saturation ◽  
Ambient Oxygen ◽  
Young Subjects ◽  
End Tidal ◽  
Carotid Body Chemoreceptors

Rationale : Peripheral chemoreflex contributes to regulation of arterial blood pressure and chemoreceptors respond not only to hypoxia but they are also continuously activated by normal ambient oxygen concentration. Stimulation of chemoreceptors activates sympathetic traffic and this response may be altered in subjects with essential hypertension.. Objective: The aim of our study was to investigate the effect of deactivation of carotid body chemoreceptors on sympathetic activity directly measured as MSNA (muscle sympathetic nerve activity) in young subjects with mild to moderate untreated hypertension. Methods: Twelve patients with essential hypertension (36±9 years, all men, BMI 29±4 kg/m 2 ,) and 8 controls (37±7, men BMI 27±5kg/m 2 ) participated in the study. None of the patients or controls received any medications. MSNA (burst/minute and mean burst amplitude - au), systolic blood pressure (SBP) and diastolic blood pressure (DBP), heart rate (HR), ECG, hemoglobin saturation with oxygen (Sat%), end tidal CO 2 and respiratory movements were monitored and measured after 10 minute of respiration by non-rebreathing mask with 100% 0 2 or 21% O 2 applied in blinded fashion. Results: Hypertensives had higher resting MSNA (38.6 ±8.6 burst/min vs. 30.3±.7 burst/min, p<0.05), SBP (149.1± 9.9 vs. 124.1 ±11.6, p < 0.05) and DBP (92.1 ±8.6 vs. 78.1 ± 8.9, p< 0.05) than controls. Breathing with 100% oxygen caused significant decrease in MSNA in hypertensives (from 38.6 ± 8.6 burst/min to 26.3 burst/min ± 6.8 and from 100 ± 0 au to 86 ± 18 au, p< 0.05) and no change in MSNA in controls (30.3 ± 5.7 burst/min initially and 27.3 burst/min ± 6.2 after 100% 0 2 , 100 ± 0 au vs. 98 ± 11 au). Blood pressure, end tidal CO 2 , respiration frequency did not change significantly after hyperoxia while HR decreased (from 69.6 ± 9 to 64.1 ± 7 in hypertensives p<0.05 and from 67± 8 to 62.5 ± 7 in controls, p< 0.05). Sat% increased significantly in both groups to 99%. Conclusions: Increased sympathetic activity in young, untreated hypertensives may be caused by the elevated tonic chemoreflex activation.

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