In the infarcted myocardium, necrotic cardiomyocytes release danger signals activating an intense inflammatory reaction that serves to clear the wound from dead cells and matrix debris, but may also extend injury. A growing body of evidence suggests an important role for members of the Interleukin (IL)-1 family in injury, repair and remodeling of the infarcted heart. This review manuscript discusses the pathophysiologic functions of IL-1 in the infarcted and remodeling myocardium and its potential role as a therapeutic target in patients with myocardial infarction. Dead cardiomyocytes release IL-1a that may function as a crucial alarmin triggering the post-infarction inflammatory reaction. IL-1b is markedly upregulated in the infarcted myocardium; activation of the inflammasome in both cardiomyocytes and interstitial cells results in release of bioactive IL-1b in the infarcted area. Binding of IL-1 to the type 1 receptor triggers an inflammatory cascade, inducing recruitment of pro-inflammatory leukocytes and stimulating a matrix-degrading program in fibroblasts, while delaying myofibroblast conversion. IL-1 mediates dilative remodeling following infarction and may play a role in the pathogenesis of post-infarction heart failure. As the wound is cleared from dead cells and matrix debris, endogenous inhibitory signals suppress the IL-1 response resulting in repression of inflammation and resolution of the inflammatory infiltrate. Other members of the IL-1 family (such as IL-18 and IL-33) are also implicated in regulation of the inflammatory and reparative response following myocardial infarction. IL-18 may participate in pro-inflammatory signaling, whereas IL-33 may exert cytoprotective effects. Early clinical trials suggest that IL-1 blockade may be a promising therapeutic strategy for patients with myocardial infarction.