Abstract: Pyroptosis is programmed cell death characterized by activation or degradation of a series of cytokines. Intracellular inflammasomes are first activated, which induces the activation of caspase-1 and degradation of proinflammatory cytokines interleukin (IL)-1β and IL-18. Subsequently, disruption of cell membranes with fragmentation of nuclear DNA leads to IL-1 and IL-18 release, which finally induces inflammatory reaction. The innate immune cells of the body identify pathogen associated molecular patterns or damage associated molecular patterns via recognition receptor and then remove pathogens or damaged tissue cells by inducing pyroptosis, forming an effective barrier to protect the organism. A growing number of studies related to atherosclerosis have demonstrated that pyroptosis is not only involved in formation of atheromatous plaque, but also is a crucial factor which promotes the development and stability of plaques. In myocardial ischemia-reperfusion injury, pyroptosis is also an important regulatory factor of the inflammatory response in the myocardial infarct and border zones, which can affect myocardial infarct size, fibrosis degree, and cardiac function in the repair period. In summary, pyroptosis may become a novel therapeutic target for atherosclerosis and myocardial ischemia-reperfusion injury.