A2 Vertaisarvioitu katsausartikkeli tieteellisessä lehdessä
Molecular Imaging of Heart Failure : An Update and Future Trends
Tekijät: Saraste Antti, Ståhle Mia, Roivainen Anne, Knuuti Juhani
Kustantaja: Elsevier
Julkaisuvuosi: 2024
Journal: Seminars in Nuclear Medicine
Tietokannassa oleva lehden nimi: Seminars in Nuclear Medicine
Vuosikerta: 54
Numero: 5
Aloitussivu: 674
Lopetussivu: 685
ISSN: 0001-2998
eISSN: 1558-4623
DOI: https://doi.org/10.1053/j.semnuclmed.2024.03.005
Verkko-osoite: https://doi.org/10.1053/j.semnuclmed.2024.03.005
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/387650247
Molecular imaging can detect and quantify pathophysiological processes underlying heart failure, complementing evaluation of cardiac structure and function with other imaging modalities. Targeted tracers have enabled assessment of various cellular and subcellular mechanisms of heart failure aiming for improved phenotyping, risk stratification, and personalized therapy. This review outlines the current status of molecular imaging in heart failure, accompanied with discussion on novel developments. The focus is on radionuclide methods with data from clinical studies. Imaging of myocardial metabolism can identify left ventricle dysfunction caused by myocardial ischemia that may be reversible after revascularization in the presence of viable myocardium. In vivo imaging of active inflammation and amyloid deposition have an established role in the detection of cardiac sarcoidosis and transthyretin amyloidosis. Innervation imaging has well documented prognostic value in predicting heart failure progression and arrhythmias. Tracers specific for inflammation, angiogenesis and myocardial fibrotic activity are in earlier stages of development, but have demonstrated potential value in early characterization of the response to myocardial injury and prediction of cardiac function over time. Early detection of disease activity is a key for transition from medical treatment of clinically overt heart failure towards a personalized approach aimed at supporting repair and preventing progressive cardiac dysfunction.
Ladattava julkaisu This is an electronic reprint of the original article. |  |
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Authors acknowledge financial support by grants from the Research Council of Finland, the Finnish Foundation for Cardiovascular Research, the Sigrid Jusélius Foundation, and the State Research Funding of Turku University Hospital. Mia Ståhle was supported by the European Atherosclerosis Society, Orion Research Foundation, and Turku Collegium for Science, Medicine and Technology, University of Turku. Antti Saraste discloses speaker or consultancy fees from Abbott, Astra Zeneca, BMS, Janssen, Novartis and Pfizer outside of the submitted work. Juhani Knuuti discloses consultancy fees from GE Healthcare and Synektik and speaker fees from GE Healthcare, Bayer, Lundbeck, Boehringer-Ingelheim, Pfizer and Merck, outside of the submitted work.
