• interleukin-18
• congestive heart failure
• cytokine
• tumour necrosis factor α

• CHF, congestive heart failure
• DCM, dilated cardiomyopathy
• IGIF, interferon γ inducing factor
• IL, interleukin
• OMI, old myocardial infarction
• SAP, stable angina pectoris without CHF
• TNF, tumour necrosis factor

Accumulating evidence suggests that proinflammatory cytokines such as tumour necrosis factor (TNF) α, interleukin (IL)-1β, and IL-6 are likely to be involved in the pathogenesis of advanced cardiac failure. Cytokine actions directly identified to date include promotion of systemic catabolism, myocardial depression, cardiac hypertrophy, and apoptosis of myocytes in congestive heart failure (CHF).

IL-18, a new member of the IL-1 family, is a proinflammatory cytokine with multiple biologic functions.¹ In concert with IL-12, IL-18 stimulates Th1 mediated immune responses; by itself, IL-18 can stimulate Th2 cytokine production. IL-18, originally named as an interferon γ inducing factor (IGIF),² can induce TNFα and IL-6 in murine macrophages.³ Pomerantz and colleagues demonstrated that IL-18 is expressed in vascular endothelial cells and macrophages in human heart, and that IL-18 binding protein, which is derived from a gene distinct from the IL-18 receptor gene and can neutralise IL-18 actions, reduces human myocardial reperfusion injury after 30 minutes of ischaemia.^4,5 We hypothesised that IL-18 might contribute to immune activation and cardiac dysfunction in congestive heart failure. In this study we examined serum concentrations of IL-18 in patients with CHF to examine whether the cytokine was involved in the pathophysiology of this syndrome.