Significance Myocardial infarction (MI) is one of the leading causes of death worldwide and is characterized by apoptosis and inflammation. While increased adrenomedullin (ADM) levels after MI are associated with disease severity, ADM infusion leads to antiapoptotic effects, suggesting a self-protective mechanism. ADM is cleaved from a full‐length precursor protein (ProADM), a putatively inactive prohormone. Our data show that ProADM is biologically active by reducing apoptosis to a similar extent as ADM. In contrast to ADM, ProADM has proinflammatory effects on cardiac fibroblasts but antiinflammatory effects on activated leukocytes. We assume that ProADM induces local inflammation but attenuates exaggerated inflammation. Our data suggest that both proteins are beneficial during MI by regulating inflammation and reducing apoptosis of cardiomyocytes.