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(Circulation. 2004;110:e34.)
© 2004 American Heart Association, Inc.

Correspondence

Vagal Nerve Stimulation in Chronic Heart Failure: An Antiinflammatory Intervention?

Jochen Springer, PhD

Division of Applied Cachexia Research, Department of Cardiology, Charité Campus Virchow-Klinikum, Berlin, Germany

Darlington O. Okonko, BSc, MRCP; Stefan D. Anker, MD, PhD

Clinical Cardiology, National Heart & Lung Institute, Imperial College, London, UK, s.anker@imperial.ac.uk

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

Li et al¹ recently reported that vagal nerve stimulation improved survival in otherwise untreated rats with heart failure secondary to left coronary artery ligation. Although this finding is indeed intriguing and of potential therapeutic importance, the authors are understandably speculative about the possible mechanisms underlying this observation.

The authors discuss that the beneficial effects seen in their study cannot solely be ascribed to vagal inhibition of myocardial presynaptic norepinephrine release or to the attenuation of cardiomyocyte G-protein interactions that normally augment ß-adrenergic tone. Although the inhibition of sympathetic activity may partly account for the benefits observed, there are likely to be, we suggest, additional and important effects on the chronic inflammation seen in chronic heart failure (CHF).

It is increasingly appreciated that efferent vagal nerve stimulation can directly and rapidly regulate immune responses. Vagal nerve stimulation can inhibit the release of cytokines like tumor necrosis factor; interleukins-1, -6, and -18 (but not interleukin-10); and intracellular high-mobility group B1 protein. In particular, vagal nerve stimulation protects against endotoxemia² and ischemia-reperfusion injury.³ Tracey has termed this the "cholinergic anti-inflammatory pathway" or "the inflammatory reflex."³ Mechanistically, the process seems to depend on the nicotinic acetylcholine receptor -7 subunit.⁴

In edematous human CHF patients, increased levels of proinflammatory endotoxin (LPS) have been detected.⁵ Plausibly, we propose that increased levels of LPS may have been present in the studied rats with untreated CHF. These rats were treated from 2 weeks onward. At this time, >60% had died, and many were severely ill, . . . [Full Text of this Article]

Meihua Li, PhD; Can Zheng, PhD; Toru Kawada, MD; Masaru Sugimachi, MD; Kenji Sunagawa, MD

Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Suita, Japan

Takayuki Sato, MD

Department of Cardiovascular Control, Kochi Medical School, Nankoku, Japan, tacsato-kochimed@umin.ac.jp

This article has been cited by other articles:

				B. Olshansky, H. N. Sabbah, P. J. Hauptman, and W. S. Colucci Parasympathetic Nervous System and Heart Failure: Pathophysiology and Potential Implications for Therapy Circulation, August 19, 2008; 118(8): 863 - 871. [Full Text] [PDF]