Abstract
Myocardial dilatation and dysfunction in the absence of significant
coronary heart disease has been termed "idiopathic" dilated cardiomyopathy
(iDCM), which--according to the 1995 task force report on the classification
of cardiomyopathies-besides genetic, toxic or infectious causes also
includes immune-mediated heart muscle damage in the spectrum of putative
DCM etiologies. Incremental research on this topic particularly in
the past few years has significantly contributed evidence to the
hypothesis that autoimmune reactions against certain myocyte antigens
may play a pivotal role in the initiation and/or progression of DCM.
Recent transfer experiments in animals (mostly rodents) performed
by various groups throughout the world and some preliminary clinical
data even indicate that a few of these autoantibodies are indeed
"pathogenic", inferring that they can actually cause cardiac dysfunction
and heart failure by their own. Dependent on the individual genetic
predisposition such harmful autoimmune reactions are supposed to
emerge as a consequence of heart muscle damage induced by viral triggers,
ischemia or exposure to cardiotoxins leading to myocyte apoptosis
(and/or necrosis) and subsequent liberation of a "critical amount"
of self-antigens previously hidden to the immune system. The following
article will summarize the so far available evidence for an implication
of a confined number of harmful autoantibodies directed against specific
cardiac antigens in the pathogenesis of DCM.
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