Lipomatous metaplasia (LM) of myocardial infarctions (MI) is typically observed in the peripheral zone of chronic MI and has been linked to major adverse clinical outcomes. To date, the mechanisms driving LM of MI remain unknown. A common feature of many disease processes associated with pathological fat accumulation is the iron-induced foam cell formation. Growing body of evidence now shows that iron deposits within hemorrhagic MI drive the prolonged recruitment of phagocytes into the infarcted territory. Herein, we investigated the spatial distribution and temporal accumulation of fatty infiltration in hemorrhagic MIs.