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Cardiovascular Research 1999 42(3):557-564; doi:10.1016/S0008-6363(99)00050-4
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

New insights into the pathophysiological role for cytokines in heart failure

Shigetake Sasayama*, Akira Matsumori and Yasuki Kihara

Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan

sasayama@kuhp.kyoto-u.ac.jp

* Corresponding author. Tel.: +81-75-751-3185; Fax:+81-75-752-0856

Received 28 October 1998; accepted 1 February 1999

The first 150 words of the full text of this article appear below.

The syndrome of heart failure may be produced by a variety of disease states. These include dilated cardiomyopathy, mechanically overloaded hypertrophy or ischemic heart disease. We developed experimental models of these cardiac diseases. In the murine model of myocarditis, inflammatory cytokines were induced rapidly in the myocardium and continued to express during the chronic stage when the heart assumed the typical pattern of dilated cardiomyopathy in the absence of inflammatory processes. In the pressure overloaded ventricle, the myocardium first developed adaptive hypertrophy but in the later stage this pattern of hypertrophy underwent a transition to heart failure. Cytokines appeared to play a significant role in this process by accelerating myocyte growth and down-modulating cardiac function. In the ischemic heart, the non-ischemic myocardium developed hypertrophy associated with the progression of scarring in the ischemic area. This remodelling process initially exerts an important compensatory mechanism for ventricular function but later results in . . . [Full Text of this Article]


    1. Cardiomyopathy
 

    2. Mechanical overload
 

    3. Ischemic heart disease
 

    4. Anticytokine therapy for chronic heart failure
 

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