S100A8 and myocardial infarction: Acute inhibition of S100A8/A9 in murine MI and myocarditis models lessens macrophage/neutrophil infiltration, decreases fibrosis, improves neovascularization, and protects against decline in LV function, which is crucial for harnessing the anti-inflammatory benefit, including in S100A8/A9-derived arrhythmogenesis (65).