Accumulating studies have proved that systemic inflammation is one of the important pathophysiologic mechanisms of heart failure. This article focuses on the sources of inflammation mediators and the causes of inflammation activation in heart failure including hemodynamic changes and oxidative stress, Toll-like receptors, microbial antigens and microorganisms, endotoxin hypothesis and neurohormonal activation. Furthermore, the effects of inflammation mediators such as cytokines and chemokines on heart failure are introduced. All lead to the conclusion that heart failure is a process with complex inflammation.