Immunomodulatory and Immunoadsorptive Treatments

Abstract

Patients with myocarditis and dilated cardiomyopathy (DCM) demonstrate abnormalities of the cellular and humoral immune system. Data from experimental and clinical sources indicate a causal relationship between myocarditis and DCM. It has not yet been possible, however, to establish the relative contributions of cellular and humoral immune disturbances to the pathogenesis and progression of myocarditis and of DCM. An experimental model of autoimmune myocarditis induced by myosin has revealed that activated autoreactive T lymphocytes may mediate myocardial damage [1]. Further, T-cell depletion can modify or abort myosin-induced myocarditis. The transfer of peripheral blood leucocytes can transmit impairment in left ventricular function in patients suffering from myocarditis to mice with severe combined immune deficiency [2]. Publications have indicated that indices of T-cell activation, such as soluble interleukin-2 receptor or b2-microglobulin, are elevated in a substantial proportion of DCM cases [3,4]. Other studies, in contrast, have identified various cardiac autoantibodies against cardiac cellular proteins in patients with myocarditis and DCM. These antibodies include those against mitochondrial proteins, contractile proteins, cardiac–b1-adrenergic receptors, and muscarinergic receptors [5–9]. Elucidation remains to be provided, however, of the functional role of cardiac autoantibodies in the development of DCM and possibly myocarditis. Further clarification is required as to whether these autoantibodies are directly pathogenic, or whether they reflect an in-