Although infarction sizes were significantly smaller in MINOCA animals, plasma levels of pro-inflammatory, innate immune cytokines monitored including tumor necrosis factor-alpha (TNF-α) as well as interleukin-1α (IL-1α) and IL-1β, which are crucial inflammatory mediators of myocardial ischemia reperfusion injury (IRI), were equally increased over time in both groups (Fig. 4a). This evidence concerns the gene IL1B and infarction.