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Inflammatory cytokines have been related to the pathogenesis and progression of heart failure.1 Cytokines can modulate cardiovascular function through different mechanisms, such as depressing contractile function, promoting left ventricular remodelling, uncoupling myocardial β adrenergic receptors, and inducing apoptosis. Loss of myocytes caused by apoptosis or programmed cell death occurs in patients with heart failure and may contribute to progressive myocardial dysfunction.2 Fas is an apoptosis signalling surface receptor known to trigger programmed cell death in a variety of cell types,3 and increased plasma concentrations of soluble Fas receptors have been reported in patients with heart failure. Pentoxifylline is a xanthine derived agent known to inhibit the production of tumour necrosis factor α (TNFα). It was also found to inhibit apoptosis in different human cell types in vitro and in vivo.4 However, the effects of pentoxifylline on apoptosis signalling receptors in patients with heart failure has not been investigated. We have previously reported beneficial effects of pentoxifylline in patients with idiopathic dilated cardiomyopathy.5 Treatment with pentoxifylline resulted in a significant improvement in functional class and left ventricular function, and was associated with a reduction in TNFα plasma …