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Natural IgM Blockade Limits Infarct Expansion and Left Ventricular Dysfunction in a Swine Myocardial Infarct Model
Dec 27, 2018
Authors: Smita Sihag, MD,1, Michael S. Haas, PhD,3, Karen M. Kim, MD,5 J. Luis Guerrero, BS,2 Jonathan Beaudoin, MD,2 Elisabeth M. Alicot, PharmD,3 Franziska Schuerpf, BS,3 James D. Gottschall, BS,1 Robyn J. Puro, PhD,3 Joren C. Madsen, MD,1 David H. Sachs, MD,1 Walter Newman, PhD,3 Michael C. Carroll, PhD,4 and James S. Allan, MD1,2
Citation: Sihag, S., Haas, M. S., Kim, K. M., Guerrero, J. L., Beaudoin, J., Alicot, E. M., Schuerpf, F., Gottschall, J. D., Puro, R. J., Madsen, J. C., Sachs, D. H., Newman, W., Carroll, M. C., … Allan, J. S. (2016). Natural IgM Blockade Limits Infarct Expansion and Left Ventricular Dysfunction in a Swine Myocardial Infarct Model. Circulation. Cardiovascular interventions, 9(1), e002547.
Summary By: Alan Arrieta, ICEP Member
The article revolves around the topic of myocardial infarction, and the study of how left ventricular dysfunctionality and infarction expansion can be limited using a monoclonal antibody. When a myocardial infarction occurs, a chain of reactions takes place which involve the nonmuscle myosin heavy chain II (NMHC II). Due to the revascularization of the area affected, cytokines can cause myocyte damage. In order to limit the damage and abnormal function of the left ventricle, it involves the epitope of the NMHC II recognized by the IgM. According to Sihag et al. (2015), monoclonal antibody (Mab) m21G6 is an effective way to reduce infarction expansion. Basically, what the Mab M21G6 does is block the pathway where the pathogenic Immunoglobulin M (IgM) binds to the N2 peptide of the NMHC II. For their study, thirty swine showed left anterior descending artery (LAD) occlusion and the results were positive, showing reduced levels of cardiac troponin-T and reduced percentages of the infarct dimensions from the area at risk (Figure 2). There are other treatments that help with myocardial infarction, but they are not that effective since the ischemic reperfusion still leaves damage to myocytes. Results from their murine models have driven the cardiovascular team to a conclusion that the Mab m21G6 has the potential of binding to the NMHC II, thus blocking the function of IgM and reducing infarction size. IgM with injury-inducing capabilities for the NMHC II is found in all species that have been investigated (Sihag et al., 2015), this means that the possibilities of creating a Mab m21G6 for humans is very likely and it will help people with preventing ischemic reperfusion injuries in the future.
Keywords: Myocardial Infarction, Left Ventricular Dysfunction, Nonmuscle Myosin Heavy Chain II,NMHC II, Immunoglobulin M, IgM, Monoclonal Antibody m21G6, Mab m21G6, Coronary Arteries, Ischemic Reperfusion, Preventive Cardiology
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Natural IgM Blockade Limits Infarct Expansion and Left Ventricular Dysfunction in a Swine Myocardial Infarct Model
Dec 27, 2018
Authors: Smita Sihag, MD,1, Michael S. Haas, PhD,3, Karen M. Kim, MD,5 J. Luis Guerrero, BS,2 Jonathan Beaudoin, MD,2 Elisabeth M. Alicot, PharmD,3 Franziska Schuerpf, BS,3 James D. Gottschall, BS,1 Robyn J. Puro, PhD,3 Joren C. Madsen, MD,1 David H. Sachs, MD,1 Walter Newman, PhD,3 Michael C. Carroll, PhD,4 and James S. Allan, MD1,2
Citation: Sihag, S., Haas, M. S., Kim, K. M., Guerrero, J. L., Beaudoin, J., Alicot, E. M., Schuerpf, F., Gottschall, J. D., Puro, R. J., Madsen, J. C., Sachs, D. H., Newman, W., Carroll, M. C., … Allan, J. S. (2016). Natural IgM Blockade Limits Infarct Expansion and Left Ventricular Dysfunction in a Swine Myocardial Infarct Model. Circulation. Cardiovascular interventions, 9(1), e002547.
Summary By: Alan Arrieta, ICEP Member
The article revolves around the topic of myocardial infarction, and the study of how left ventricular dysfunctionality and infarction expansion can be limited using a monoclonal antibody. When a myocardial infarction occurs, a chain of reactions takes place which involve the nonmuscle myosin heavy chain II (NMHC II). Due to the revascularization of the area affected, cytokines can cause myocyte damage. In order to limit the damage and abnormal function of the left ventricle, it involves the epitope of the NMHC II recognized by the IgM. According to Sihag et al. (2015), monoclonal antibody (Mab) m21G6 is an effective way to reduce infarction expansion. Basically, what the Mab M21G6 does is block the pathway where the pathogenic Immunoglobulin M (IgM) binds to the N2 peptide of the NMHC II. For their study, thirty swine showed left anterior descending artery (LAD) occlusion and the results were positive, showing reduced levels of cardiac troponin-T and reduced percentages of the infarct dimensions from the area at risk (Figure 2). There are other treatments that help with myocardial infarction, but they are not that effective since the ischemic reperfusion still leaves damage to myocytes. Results from their murine models have driven the cardiovascular team to a conclusion that the Mab m21G6 has the potential of binding to the NMHC II, thus blocking the function of IgM and reducing infarction size. IgM with injury-inducing capabilities for the NMHC II is found in all species that have been investigated (Sihag et al., 2015), this means that the possibilities of creating a Mab m21G6 for humans is very likely and it will help people with preventing ischemic reperfusion injuries in the future.
Keywords: Myocardial Infarction, Left Ventricular Dysfunction, Nonmuscle Myosin Heavy Chain II,NMHC II, Immunoglobulin M, IgM, Monoclonal Antibody m21G6, Mab m21G6, Coronary Arteries, Ischemic Reperfusion, Preventive Cardiology
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