Several mechanisms have been proposed for the sepsis-induced myocardial dysfunction including the overexpression of adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and the production and release of several substances such as cytokines, prostanoids, NO or endothelin-1 (ET-1) (23). This evidence concerns the gene VCAM1 and Sepsis.