We found that 1) Tlr4, Tlr9 and the IFN regulator factors Irf3 and Irf7 showed the highest expression levels under basal conditions in the murine and human heart, 2) regulation of TLR and IRF gene expression differs between the various experimental HF models of diverse etiology and the concomitant inflammatory status, 3) TLR and IRF gene expression is preferentially increased in the infarction zone after myocardial ischemia, whereas no TLR activation was detected in the remote zone, and 4) Irf7 might act as cardiovascular stress-inducible factors in the pathologically stressed heart. This evidence concerns the gene TLR9 and hydrops fetalis.