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European Journal of Heart Failure 1999 1(4):309-312; doi:10.1016/S1388-9842(99)00049-5
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© 1999 European Society of Cardiology

How are cytokines activated in heart failure?

Walter J. Paulus

Cardiovascular Center O.L.V. Ziekenhuis, Moorselbaan 164, B 9300 Aalst, Belgium

Received June 28, 1999; Revised July 15, 1999; Accepted August 9, 1999

The first 10% of the full text of this article appears below.


   1. Introduction
 
Proinflammatory cytokines such as interleukin 1, interleukin 6 and tumor necrosis factor {alpha} (TNF{alpha}) were recently identified as contributors to the syndrome of chronic heart failure [1] and to the underlying cardiomyopathic process of adverse left ventricular remodeling and of progressive left ventricular dysfunction [2,3]. Due to this role of proinflammatory cytokines, ‘the cardioinflammatory response to heart failure’ was recently proposed as a new heart failure paradigm with implications for both prognosis and treatment [4]. The origin of these proinflammatory cytokines in heart failure patients remains unclear so far and has been the subject of controversy. Two divergent explanations have been proposed, namely endotoxin-induced immune activation because of bowel oedema and myocardial cytokine production because of hemodynamic overload. Due to the therapeutic implications, such as sterilisation of the gut with antibiotics or inhibition of endotoxin-induced cytokine expression with . . . [Full Text of this Article]


   2. Endotoxin-induced cytokine production
 

   3. Myocardial cytokine production
 

   4. Extramyocardial cytokine production
 

   5. Summary
 

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