NLRP3 and myocardial infarction: Thus, we have assessed RIP3 in the context of the RIP3‐NLRP3‐csp‐1‐IL‐1β axis promoting inflammation.29, 32 Such csp‐1‐mediated IL‐1β production has been found to stimulate chronic pro‐inflammatory tissue response and adverse ventricular remodeling after MI.46, 47, 48 In both LV zones of failing hearts, increased proIL‐1β cleavage has been demonstrated with the infarcted area being affected to a greater degree.