It has been suggested that sepsis-induced myocardial dysfunction involves pro-inflammatory cytokines including tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6,19 nitrite oxide, alteration of beta-adrenergic receptors,20 apoptosis and calcium abnormalities particularly a decreased myocardial fibers sensibility.5 This evidence concerns the gene IL1B and Sepsis.