Tumor necrosis factor-α (TNF-α) in particular has been shown to have negative inotropic effects by exerting oxidative stress on the cardiomyocyte, and studies have shown that overexpression of the TNF-α transgene is associated with increased mortality.12, 13, 14 Several studies have suggested the use of TNF-α and interleukin (IL)-6 as markers of HF.15 This evidence concerns the gene TNF and hydrops fetalis.