The intense inflammatory response that follows myocardial infarction is associated with increased infarct size and impaired cardiac function. IL-1β and IL-18 are important mediators of this response and are controlled by the NLRP3 inflammasome. Female pigs (n = 30) were subjected to 75 min of transluminal balloon occlusion of the left anterior descending coronary artery to mimic myocardial infarction, and were then randomly assigned to receive MCC950 (a novel, small-molecule inhibitor of the NLRP3 inflammasome) or placebo for 7 days. The infarct size and area at risk, assessed using 3D echocardiography and histological staining, were lower with MCC950 than with placebo. MCC950 treatment was associated with preserved left ventricular ejection fraction and reduced myocardial neutrophil influx. “Interference with NLRP3-inflammasome-mediated signalling therefore has become a promising target to reduce infarct size and preserve cardiac function in MI patients,” conclude the investigators.