F Bönner1, M W Merx2, K Klingel3, P Begovatz4, U Flögel5, M Sager6, S Temme7, C Jacoby1, M Salehi Ravesh4, C Grapentin8, R Schubert8, J Bunke9, M Roden10, M Kelm11, J Schrader12. 1. Department of Cardiology, Pulmonology and Vascular Medicine, Heinrich Heine University, Düsseldorf, Germany Department of Molecular Cardiology, Heinrich Heine University, Universitätsstr. 1, Düsseldorf 40225, Germany. 2. Department of Cardiology, Pulmonology and Vascular Medicine, Heinrich Heine University, Düsseldorf, Germany. 3. Department of Molecular Pathology, Eberhard Karls University, Tübingen, Germany. 4. Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Düsseldorf, Germany German Center for Diabetes Research, Partner Düsseldorf, Germany. 5. Department of Molecular Cardiology, Heinrich Heine University, Universitätsstr. 1, Düsseldorf 40225, Germany Cardiovascular Research Institute Düsseldorf (CARID), Medical Faculty, University Düsseldorf, Germany. 6. Central Animal Research Facility, Heinrich Heine University, Düsseldorf, Germany. 7. Department of Molecular Cardiology, Heinrich Heine University, Universitätsstr. 1, Düsseldorf 40225, Germany. 8. Department of Pharmaceutical Technology, Albert-Ludwigs University, Freiburg, Germany. 9. Philips Healthcare, Hamburg, Germany. 10. Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Düsseldorf, Germany German Center for Diabetes Research, Partner Düsseldorf, Germany Department of Endocrinology and Diabetology, Heinrich Heine University, Düsseldorf, Germany. 11. Department of Cardiology, Pulmonology and Vascular Medicine, Heinrich Heine University, Düsseldorf, Germany Cardiovascular Research Institute Düsseldorf (CARID), Medical Faculty, University Düsseldorf, Germany. 12. Department of Molecular Cardiology, Heinrich Heine University, Universitätsstr. 1, Düsseldorf 40225, Germany schrader@uni-duesseldorf.de.
Abstract
AIM: Inflammation is a hallmark of cardiac healing after myocardial infarction and it determines subsequent cardiovascular morbidity and mortality. The aim of the present study was to explore whether inflammation imaging with two perfluorocarbon (PFC) nanoemulsions and fluorine magnetic resonance imaging ((19)F MRI) is feasible at 3.0 T with sufficient signal-to-noise ratio (SNR) using explanted hearts, an (19)F surface coil and dedicated MR sequences. METHODS AND RESULTS: Acute myocardial infarction (AMI) was induced by balloon angioplasty (50 min) of the distal left anterior descending artery in 12 pigs. One day thereafter, PFCs were injected intravenously to label circulating monocytes. Either emulsified perfluoro-15-crown-5 ether or already clinically applied perfluorooctyl bromide (PFOB) was applied. Four days after AMI and immediately after gadolinium administration, hearts were explanted and imaged with a 3.0 T Achieva MRI scanner. (19)F MRI could be acquired with an SNR of >15 using an in-plane resolution of 2 × 2 mm(2) within <20 min for both agents. Combined late gadolinium enhancement (LGE) and (19)F MRI revealed that (19)F signal was inhomogenously distributed across LGE myocardium reflecting patchy macrophage infiltration as confirmed by histology. In whole hearts, we found an apico-basal (19)F gradient within LGE-positive myocardium. The (19)F-positive volume was always smaller than LGE volume. Ex vivo experiments on isolated monocytes revealed that pig and human cells phagocytize PFCs even more avidly than mouse monocytes. CONCLUSION: This pilot study demonstrates that (19)F MRI at 3.0 T with clinically applicable PFOB is feasible, thus highlighting the potential of (19)F MRI to monitor the inflammatory response after AMI. Published on behalf of the European Society of Cardiology. All rights reserved.
AIM: Inflammation is a hallmark of cardiac healing after myocardial infarction and it determines subsequent cardiovascular morbidity and mortality. The aim of the present study was to explore whether inflammation imaging with two perfluorocarbon (PFC) nanoemulsions and fluorine magnetic resonance imaging ((19)F MRI) is feasible at 3.0 T with sufficient signal-to-noise ratio (SNR) using explanted hearts, an (19)F surface coil and dedicated MR sequences. METHODS AND RESULTS:Acute myocardial infarction (AMI) was induced by balloon angioplasty (50 min) of the distal left anterior descending artery in 12 pigs. One day thereafter, PFCs were injected intravenously to label circulating monocytes. Either emulsified perfluoro-15-crown-5 ether or already clinically applied perfluorooctyl bromide (PFOB) was applied. Four days after AMI and immediately after gadolinium administration, hearts were explanted and imaged with a 3.0 T Achieva MRI scanner. (19)F MRI could be acquired with an SNR of >15 using an in-plane resolution of 2 × 2 mm(2) within <20 min for both agents. Combined late gadolinium enhancement (LGE) and (19)F MRI revealed that (19)F signal was inhomogenously distributed across LGE myocardium reflecting patchy macrophage infiltration as confirmed by histology. In whole hearts, we found an apico-basal (19)F gradient within LGE-positive myocardium. The (19)F-positive volume was always smaller than LGE volume. Ex vivo experiments on isolated monocytes revealed that pig and human cells phagocytize PFCs even more avidly than mouse monocytes. CONCLUSION: This pilot study demonstrates that (19)F MRI at 3.0 T with clinically applicable PFOB is feasible, thus highlighting the potential of (19)F MRI to monitor the inflammatory response after AMI. Published on behalf of the European Society of Cardiology. All rights reserved.
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