Current strategies in the care of patients with acute myocardial infarction seem to be insufficient to modify the inflammatory pathway mediated by interleukin-6. Higher concentrations of this cytokine appear to be associated with decreased left ventricular ejection fraction. Therapies targeting interleukin-6 seem promising for their additional decrease in residual inflammatory risk in subjects with acute myocardial infarction. The great challenge for reducing residual inflammatory risk lies in the development of safe and affordable therapies.