Circulation. 1998;97:1340-1341
(Circulation. 1998;97:1340-1341.)
© 1998 American Heart Association, Inc.
Tumor Necrosis Factor-
and Cardiomyopathy
Michael R. Bristow, MD, PhD
From the Division of Cardiology, University of Colorado HSC, Denver.
Correspondence to Michael R. Bristow, MD, PhD, Division of Cardiology, University of Colorado HSC, 4200 E 9th Ave, Denver, CO 80262. (Circulation. 1998;97:1340-1341.)
Key Words: Editorials • TNF- • cytokines • remodeling • heart failure
The
myocardium has limited options for responding to an injury
sufficient to cause decreased global contractile function. Myocardial
pump performance can be quickly stabilized by increased
adrenergic drive, which through ß-adrenergic mechanisms increases
cardiac output via positive chronotropic and inotropic effects. In a
kinetic sense, the next available option for stabilizing pump function
is the Frank-Starling mechanism, whereby volume expansion places the
ventricles at a higher position in the preload-performance
relationship. The renin-angiotensin and ß-adrenergic
systems appear to exert most of the signaling in this regard. The third
and slowest-to-develop option is to create more contractile elements
through a hypertrophic response involving new synthesis of sarcomeres
in individual cardiac myocytes. The first two compensatory adjustments
are very powerful in humans and have probably evolved as protective
responses to trauma and blood loss. The hypertrophic response may also
be considered in this context but in more of a wound-healing paradigm
that incorporates features of a generalized inflammatory response. As
such, a host of proinflammatory cytokines have been shown to be
increased systemically or in the myocardium of subjects
with heart failure. The first of these was tumor necrosis factor-
(TNF-),1 a 17-kD protein that acts through two
distinct receptors, TNFR1 and
TNFR2. TNF- produces a series of powerful
biological effects that include immunostimulation, mediation of host
resistance to bacteria, activation of protein kinase C, and activation
of the expression of a wide variety of genes generally involved in
inflammation or cell growth.2 In an acute or
subacute setting, most . . . [Full Text of this Article]
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