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(Circulation. 2003;107:1460.)
© 2003 American Heart Association, Inc.

Editorial

Proinflammatory Cytokines

Predictors of a Failing Heart?

David R. Murray, MD; Gregory L. Freeman, MD

From the Department of Medicine/Cardiology, University of Texas Health Science Center at San Antonio, and South Texas Veterans Healthcare System, Audie L. Murphy Division, San Antonio.

Correspondence to David R. Murray, MD, Department of Medicine/Cardiology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr, MSC 7872, San Antonio, TX 78229 to 3900. E-mail MurrayD@uthscsa.edu

Key Words: Editorials • heart failure • cytokines • tumor necrosis factor • interleukins

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

Congestive heart failure (CHF) is a complex clinical syndrome characterized by exercise intolerance, fatigability, dyspnea, and volume retention occurring as a consequence of myocardial injury and subsequent dysfunction. Progression of this disease is thought to be mediated by neurohormones, such as norepinephrine and angiotensin II, by virtue of the toxic effects that they exert on the heart and the peripheral vasculature.¹ These mediators are capable of altering the function and structure of the left ventricle (LV), ie, remodeling, via direct effects on cardiomyocyte biology and extracellular matrix composition and via indirect effects on the loading conditions under which the heart must function.¹ Indeed, antagonizing the activation of the renin angiotensin system and the adrenergic system has become the mainstay of contemporary pharmacologic management of patients with this disease.^1,2 ß-blockers and angiotensin converting enzyme inhibitors have been shown to improve ventricular performance and clinical outcomes in patients with symptomatic heart failure due to LV systolic dysfunction, thus supporting the "neurohormonal hypothesis".^1,2

See p 1486

Another group of peptides, the proinflammatory cytokines, are upregulated in patients with CHF and have been implicated in the pathophysiology of this disease. The most well studied of these cytokines is tumor necrosis factor (TNF).³ Comparatively less is known about interleukin (IL)-1, IL-2, IL-6, and interferon- in the setting of heart failure. Cardiomyocytes as well as other nucleated cell types within the myocardium are capable of synthesizing TNF in response to various forms of cardiac stress such as myocardial infarction⁴ and LV pressure or volume overload.⁵ Neither . . . [Full Text of this Article]

Related Article:

Inflammatory Markers and Risk of Heart Failure in Elderly Subjects Without Prior Myocardial Infarction: The Framingham Heart Study

Ramachandran S. Vasan, Lisa M. Sullivan, Ronenn Roubenoff, Charles A. Dinarello, Tamara Harris, Emelia J. Benjamin, Douglas B. Sawyer, Daniel Levy, Peter W.F. Wilson, and Ralph B. D’Agostino
Circulation 2003 107: 1486-1491. [Abstract] [Full Text]

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