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(Circulation. 2002;106:2417.)
© 2002 American Heart Association, Inc.

Editorial

Sympathetic Nervous System in Heart Failure

Jay N. Cohn, MD

From the Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis.

Correspondence to Jay N. Cohn, MD, Cardiovascular Division, Mayo Mail Code 508, University of Minnesota, 420 Delaware St SE, Minneapolis, MN 55455. E-mail cohnx001@umn.edu

Key Words: Editorials • nervous system, sympathetic • heart failure

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

For those who have comfortably accepted the mechanistic link between sympathetic nervous system activation and poor outcome in heart failure, the study by Brede et al¹ in this issue of Circulation is a welcome confirmation. The authors appear to have demonstrated in a murine model that absence of sympathoinhibitory ₂ adrenoreceptors is associated with overactive catecholamine release, aggressive remodeling of the left ventricle, worsening signs of heart failure, and shortened life expectancy. Provocatively, deletion polymorphism of the ₂ receptor in patients with heart failure also appears to be associated with worse heart failure and poorer outcome.

See p 2491

One may, of course, quibble with some experimental shortcomings. The number of animals is small, and surgical mortality is neither addressed nor accounted for. The magnitude of circulating norepinephrine increase in the at-risk receptor-deficient mice is surprisingly modest. The clinical material has been assessed retrospectively from a database that is poorly described and not available for scrutiny. Furthermore, the experimental model of pressure overload from aortic banding bears little similarity to the syndrome of heart failure observed clinically. Nonetheless, the apparent link between poor outcome and ₂ receptor dysfunction certainly provides support for an adverse effect of unfettered sympathetic stimulation on the progression of the syndrome. Indeed, our early observations of a relationship between plasma norepinephrine and mortality in heart failure,² buttressed by the survival benefit of ß-blocker therapy^3,4 appear to have been mechanistically validated.

Or have they? Nothing is simple when dealing with the ₂ receptor. It has traditionally been recognized to have at . . . [Full Text of this Article]

Related Article:

Feedback Inhibition of Catecholamine Release by Two Different ₂-Adrenoceptor Subtypes Prevents Progression of Heart Failure

Marc Brede, Frank Wiesmann, Roland Jahns, Kerstin Hadamek, Carsten Arnolt, Stefan Neubauer, Martin J. Lohse, and Lutz Hein
Circulation 2002 106: 2491-2496. [Abstract] [Full Text]

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