Typical hallmarks for the involvement of immune mechanisms in CHF pathogenesis are the activation/migration of leukocytes from the circulation to the areas of myocardial inflammation and an increased expression of proinflammatory cytokines, such as tumor necrosis factor α, interleukin-1, and interleukin-6 from a damaged myocardium [3-6]. This evidence concerns the gene TNF and congestive heart failure.