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Open Access 01-12-2018 | Research
Quantitative cardiovascular magnetic resonance: extracellular volume, native T1 and 18F-FDG PET/CMR imaging in patients after revascularized myocardial infarction and association with markers of myocardial damage and systemic inflammation
Published in: Journal of Cardiovascular Magnetic Resonance | Issue 1/2018
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Background
Characterization of tissue integrity and inflammatory processes after acute myocardial infarction (AMI) using non-invasive imaging is predictive of patient outcome. Quantitative cardiovascular magnetic resonance (CMR) techniques such as native T1 and extracellular volume (ECV) mapping as well as 18F-FDG positron emission tomography (PET) imaging targeting inflammatory cell populations are gaining acceptance, but are often applied without assessing their quantitative potential. Using simultaneously acquired PET/CMR data from patients early after AMI, this study quantitatively compares these three imaging markers and investigates links to blood markers of myocardial injury and systemic inflammatory activity.
Methods
A total of 25 patients without microvascular obstruction were retrospectively recruited. All imaging was simultaneously performed 5 ± 1 days after revascularization following AMI on an integrated 3T PET/MRI scanner. Native and post-contrast T1 data were acquired using a modified Look-Locker inversion recovery (MOLLI) sequence, ECV maps were calculated using individually sampled hematocrit. 18F-FDG PET was executed after 1 day of dietary preparation, 12 h of fasting, and administration of heparin. ECV, 18F-FDG and native T1 data were compared mutually as well as to peak counts of peripheral blood markers (creatine kinase, creatine kinase-MB, troponin, leukocytes, monocytes) and infarct size.
Results
High intra-patient correlations of relative ECV, 18F-FDG PET and native T1 signal increases were observed in combination with no inter-patient correlation of maximum absolute values at the infarct center, suggesting well-colocalized but physiologically diverse processes begetting the respective image signals. Comparison of maximum image signals to markers of myocardial damage and systemic inflammation yielded highly significant correlations of ECV to peak creatine kinase-MB and overall infarct size as well as between native T1 and peak monocyte counts.
Conclusions
Absolute native T1 values at the infarct core early after AMI can be linked to the systemic inflammatory response independent of infarct size. Absolute ECV at the infarct core is related to both infarct size and blood markers of myocardial damage.