Christoph Rischpler1, Ralf J Dirschinger1, Stephan G Nekolla1, Hans Kossmann1, Stefania Nicolosi1, Franziska Hanus1, Sandra van Marwick1, Karl P Kunze1, Alexander Meinicke1, Katharina Götze1, Adnan Kastrati1, Nicolas Langwieser1, Tareq Ibrahim1, Matthias Nahrendorf1, Markus Schwaiger1, Karl-Ludwig Laugwitz2. 1. From the Nuklearmedizinische Klinik und Poliklinik, Klinikum rechts der Isar (C.R., S.G.N., S.N., S.v.M., K.P.K., A.M., M.S.), Medizinische Klinik und Poliklinik I, Klinikum rechts der Isar (R.J.D., H.K., F.H., N.L., T.I., K.-L.L.), Medizinische Klinik und Poliklinik III, Klinikum rechts der Isar (K.G.), and Deutsches Herzzentrum (A.K.), Technische Universität München, Munich, Germany; DZKH (Deutsches Zentrum für Herz-Kreislauf-Forschung e.V.), partner site Munich Heart Alliance, Munich, Germany (C.R., S.G.N., A.K., M.S., K.-L.L.); and Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston (M.N.). 2. From the Nuklearmedizinische Klinik und Poliklinik, Klinikum rechts der Isar (C.R., S.G.N., S.N., S.v.M., K.P.K., A.M., M.S.), Medizinische Klinik und Poliklinik I, Klinikum rechts der Isar (R.J.D., H.K., F.H., N.L., T.I., K.-L.L.), Medizinische Klinik und Poliklinik III, Klinikum rechts der Isar (K.G.), and Deutsches Herzzentrum (A.K.), Technische Universität München, Munich, Germany; DZKH (Deutsches Zentrum für Herz-Kreislauf-Forschung e.V.), partner site Munich Heart Alliance, Munich, Germany (C.R., S.G.N., A.K., M.S., K.-L.L.); and Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston (M.N.). laugwitz@mytum.de.
Abstract
BACKGROUND: The immune system orchestrates the repair of infarcted myocardium. Imaging of the cellular inflammatory response by (18)F-fluorodeoxyglucose ((18)F-FDG) positron emission tomography/magnetic resonance imaging in the heart has been demonstrated in preclinical and clinical studies. However, the clinical relevance of post-MI (18)F-FDG uptake in the heart has not been elucidated. The objective of this study was to explore the value of (18)F-FDG positron emission tomography/magnetic resonance imaging in patients after acute myocardial infarction as a biosignal for left ventricular functional outcome. METHODS AND RESULTS: We prospectively enrolled 49 patients with ST-segment-elevation myocardial infarction and performed (18)F-FDG positron emission tomography/magnetic resonance imaging 5 days after percutaneous coronary intervention and follow-up cardiac magnetic resonance imaging after 6 to 9 months. In a subset of patients, (99m)Tc-sestamibi single-photon emission computed tomography was performed with tracer injection before revascularization. Cellular innate immune response was analyzed at multiple time points. Segmental comparison of (18)F-FDG-uptake and late gadolinium enhancement showed substantial overlap (κ=0.66), whereas quantitative analysis demonstrated that (18)F-FDG extent exceeded late gadolinium enhancement extent (33.2±16.2% left ventricular myocardium versus 20.4±10.6% left ventricular myocardium, P<0.0001) and corresponded to the area at risk (r=0.87, P<0.0001). The peripheral blood count of CD14(high)/CD16(+) monocytes correlated with the infarction size and (18)F-FDG signal extent (r=0.53, P<0.002 and r=0.42, P<0.02, respectively). (18)F-FDG uptake in the infarcted myocardium was highest in areas with transmural scar, and the standardized uptake valuemean was associated with left ventricular functional outcome independent of infarct size (Δ ejection fraction: P<0.04, Δ end-diastolic volume: P<0.02, Δ end-systolic volume: P<0.005). CONCLUSIONS: In this study, the intensity of (18)F-FDG uptake in the myocardium after acute myocardial infarction correlated inversely with functional outcome at 6 months. Thus, (18)F-FDG uptake in infarcted myocardium may represent a novel biosignal of myocardial injury.
BACKGROUND: The immune system orchestrates the repair of infarcted myocardium. Imaging of the cellular inflammatory response by (18)F-fluorodeoxyglucose ((18)F-FDG) positron emission tomography/magnetic resonance imaging in the heart has been demonstrated in preclinical and clinical studies. However, the clinical relevance of post-MI (18)F-FDG uptake in the heart has not been elucidated. The objective of this study was to explore the value of (18)F-FDG positron emission tomography/magnetic resonance imaging in patients after acute myocardial infarction as a biosignal for left ventricular functional outcome. METHODS AND RESULTS: We prospectively enrolled 49 patients with ST-segment-elevation myocardial infarction and performed (18)F-FDG positron emission tomography/magnetic resonance imaging 5 days after percutaneous coronary intervention and follow-up cardiac magnetic resonance imaging after 6 to 9 months. In a subset of patients, (99m)Tc-sestamibi single-photon emission computed tomography was performed with tracer injection before revascularization. Cellular innate immune response was analyzed at multiple time points. Segmental comparison of (18)F-FDG-uptake and late gadolinium enhancement showed substantial overlap (κ=0.66), whereas quantitative analysis demonstrated that (18)F-FDG extent exceeded late gadolinium enhancement extent (33.2±16.2% left ventricular myocardium versus 20.4±10.6% left ventricular myocardium, P<0.0001) and corresponded to the area at risk (r=0.87, P<0.0001). The peripheral blood count of CD14(high)/CD16(+) monocytes correlated with the infarction size and (18)F-FDG signal extent (r=0.53, P<0.002 and r=0.42, P<0.02, respectively). (18)F-FDG uptake in the infarcted myocardium was highest in areas with transmural scar, and the standardized uptake valuemean was associated with left ventricular functional outcome independent of infarct size (Δ ejection fraction: P<0.04, Δ end-diastolic volume: P<0.02, Δ end-systolic volume: P<0.005). CONCLUSIONS: In this study, the intensity of (18)F-FDG uptake in the myocardium after acute myocardial infarction correlated inversely with functional outcome at 6 months. Thus, (18)F-FDG uptake in infarcted myocardium may represent a novel biosignal of myocardial injury.
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