In contrast to the prior studies investigating anti-inflammatory interventions targeting downstream NLRP3 mediators of inflammation (IL-1 receptors, IL-1β, IL-6), this present study was designed to utilize OLT1177® as a selective NLRP3 inhibitor of which the mechanism of action targets the NLRP3 ATPase activity that contributes to the NLRP3 oligomerization of the NLRP3 inflammasome [32], thereby resulting in less caspase-1 being activated and less IL-1β being produced, thus preserving the contractile reserve and diastolic function following a non-reperfused myocardial infarction [20,28]. This evidence concerns the gene CASP1 and myocardial infarction.