The Sympathetic Nervous System in Heart Failure
Open accessAbstract
Heart failure is a syndrome characterized initially by left ventricular dysfunction that triggers countermeasures aimed to restore cardiac output. These responses are compensatory at first but eventually become part of the disease process itself leading to further worsening cardiac function. Among these responses is the activation of the sympathetic nervous system (SNS) that provides inotropic support to the failing heart increasing stroke volume, and peripheral vasoconstriction to maintain mean arterial perfusion pressure, but eventually accelerates disease progression affecting survival. Activation of SNS has been attributed to withdrawal of normal restraining influences and enhancement of excitatory inputs including changes in: 1) peripheral baroreceptor and chemoreceptor reflexes; 2) chemical mediators that control sympathetic outflow; and 3) central integratory sites. The interface between the sympathetic fibers and the cardiovascular system is formed by the adrenergic receptors (ARs). Dysregulation of cardiac beta(1)-AR signaling and transduction are key features of heart failure progression. In contrast, cardiac beta(2)-ARs and alpha(1)-ARs may function in a compensatory fashion to maintain cardiac inotropy. Adrenergic receptor polymorphisms may have an impact on the adaptive mechanisms, susceptibilities, and pharmacological responses of SNS. The beta-AR blockers and the inhibitors of the renin-angiotensin-aldosterone axis form the mainstay of current medical management of chronic heart failure. Conversely, central sympatholytics have proved harmful, whereas sympathomimetic inotropes are still used in selected patients with hemodynamic instability. This review summarizes the changes in SNS in heart failure and examines how modulation of SNS activity may affect morbidity and mortality from this syndrome.
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Decreased cardiac output and sympathetic vasoconstriction in heart failure stimulates adaptive redistribution of the systemic circulation, leading to congestion in multiple end organs including the bowel wall.
“Decreased cardiac output and the resulting sympathetic vasoconstriction in heart failure stimulates adaptive re-distribution of the systemic circulation, leading to congestion in multiple end organs, including the bowel wall31.”
From Dietary metabolism, the gut microbiome, and heart failure (2019) · cites this paper as [31]
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- Authors
- Triposkiadis, F., Karayannis, G., Giamouzis, G., Skoularigis, J., Louridas, G., & Butler, J.
- Affiliations
- University Hospital of Larissa (GR)
- Emory University (US)
- AHEPA University Hospital (GR)
- Corresponding author
- Butler, Javed
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 2009-11
- Volume
- 54
- Issue
- 19
- Pages
- 1747-1762
- ISSN
- 0735-1097 (ISSN-L)
- OpenAlex
- W2097757382
- Cited by
- 978
- References
- 171
- Citations by year
- 2026: 40 · 2025: 44 · 2024: 69 · 2023: 46 · 2022: 74 · 2021: 54 · 2020: 59 · 2019: 77 · 2018: 59 · 2017: 62 · 2016: 71 · 2015: 66 · 2014: 63 · 2013: 58 · 2012: 61
- FWCI
- 6.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of the American College of Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Failure Treatment and Management
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart rate and cardiovascular health
- Keywords
- heart failure, sympathetic nervous system, sympathetic activation, left ventricular dysfunction, beta1-adrenergic receptor, beta2-adrenergic receptor, alpha1-adrenoceptors, baroreflex, chemoreceptor reflex, beta-blockers, renin-angiotensin-aldosterone system inhibitors, cardiac inotropy, disease progression
- MeSH terms
- Adrenergic alpha-Antagonists, Adrenergic beta-Antagonists, Cardiotonic Agents, Digoxin, Heart Failure, Hemodynamics, Humans, Parasympathetic Nervous System, Polymorphism, Genetic, Receptors, Adrenergic, Renin-Angiotensin System, Sympathetic Nervous System, Sympatholytics, Sympathomimetics, Randomized Controlled Trials as Topic, Exercise Tolerance, Receptors, Adrenergic, alpha-1, Receptors, Adrenergic, beta-2
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