Natural IgM Blockade Limits Infarct Expansion and Left Ventricular Dysfunction in a Swine Myocardial Infarct Model

摘要

BackgroundAcute coronary syndrome is the leading cause of mortality worldwide. However, treatment of acute coronary occlusion inevitably results in ischemia-reperfusion (I/R) injury. Circulating natural IgM has been shown to play a significant role in mouse models of I/R injury. A highly conserved self-antigen, non-muscle myosin heavy chain II (NMHC-II), has been identified as a target of pathogenic IgM. We hypothesized that a monoclonal antibody (m21G6) directed against NMHC-II may inhibit IgM binding and reduce injury in a pre-clinical model of myocardial infarction (MI). Thus, our objective was to evaluate the efficacy of intravenous m21G6 treatment in limiting infarct expansion, troponin release, and left ventricular dysfunction in a swine MI model.