Heart failure is a complex neurohumoral and inflammatory syndrome. Recent s
tudies have shown that proinflammatory cytokines (interleukin-1, interleuki
n-2, interleukin-6, interleukin-10, and tumor necrosis factor) are involved
in cardiac depression and in the complex syndrome of heart failure. Unders
tanding the involvement of these cytokines may enable us to reverse cardiac
depression and heart failure by the use of monoclonal antibodies directed
against specific cytokines to block the downhill progression of heart failu
re.