Role of Inflammatory Cytokines in the Development and Progression of Ischemic Heart Diseases-Experimental and Clinical Studies-

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(A)Basic Research(1) Chrocic Treatment with interleukin (IL) -1beta causes arteriosclerotic changes and vasospastic responses to autacoids in porcine coronary arteries in vivo.(2) Chronic treatment with IL-1alpha or tumor necrosis factor-alpha (TNF-alpha) also caused similar changes of the coronary artery, showing the redundant effects of inflammatory cytokines.(3) The histological and functiona changes of the coronary artery induced by IL-1beta were mediated by both platelet-derived growth factor and fibroblast growth factor-2.(4) A selective tyrosine kinase inhibitor, ST638, markedly suppressed the histological and functional changes of the coronary artery induced by IL-1beta.(5) In the pathogenesis of coronary artery spasm at the inflammatory coronary lesions, a PKC-mediated pathway plays an important role, while the contribution of Ca^<2+>release from the intracellular store site may be minimal.(B)Clinical Research(6) Three types of changes in the plasma levels of cytokines were noted in patients with acute myocardial infarction ; transient increase (plasma levels of IL-6, generation capacity for IL-1alpha), sustained increase (plasma levels of macrophagecolony stimulating factor and generation capacity for IL-1beta), and late increase (plasma levels of interferon-gamma).(7) In patients with ischemic heart disease, plasma levels of macrophage colony stimulating factor were increased, while those of transforming growth factor-beta were decreased.