BackgroundQuantitative measurement of T1 in the myocardium may be used to detect both focal and diffuse disease processes such as interstitial fibrosis or edema. A partial volume problem exists when a voxel in the myocardium also contains fat. Partial volume with fat occurs at tissue boundaries or within the myocardium in the case of lipomatous metaplasia of replacement fibrosis, which is commonly seen in chronic myocardial infarction. The presence of fat leads to a bias in T1 measurement. The mechanism for this artifact for widely used T1 mapping protocols using balanced steady state free precession readout and the dependence on off-resonance frequency are described in this paper.MethodsSimulations were performed to illustrate the behavior of mono-exponential fitting to bi-exponential mixtures of myocardium and fat with varying fat fractions. Both inversion recovery and saturation recovery imaging protocols using balanced steady state free precession are considered. In-vivo imaging with T1-mapping, water/fat separated imaging, and late enhancement imaging was performed on subjects with chronic myocardial infarction.ResultsIn n = 17 subjects with chronic myocardial infarction, lipomatous metaplasia is evident in 8 patients (47%). Fat fractions as low as 5% caused approximately 6% T1 elevation for the out-of-phase condition, and approximately 5% reduction of T1 for the in-phase condition. T1 bias in excess of 1000 ms was observed in lipomatous metaplasia with fat fraction of 38% in close agreement with simulation of the specific imaging protocols.ConclusionsMeasurement of the myocardial T1 by widely used balanced steady state free precession mapping methods is subject to bias when there is a mixture of water and fat in the myocardium. Intramyocardial fat is frequently present in myocardial scar tissue due lipomatous metaplasia, a process affecting myocardial infarction and some non-ischemic cardiomyopathies. In cases of lipomatous metaplasia, the T1 biases will be additive or subtractive depending on whether the center frequency corresponds to the myocardium and fat being in-phase or out-of-phase, respectively. It is important to understand this mechanism, which may otherwise lead to erroneous interpretation.
T2 relaxation parameters are different in the infarcted and salvaged myocardium, and both are significantly longer than remote. Furthermore, the magnitude of increase in T2 was less in the salvaged myocardium after longer reperfusion, indicating partial resolution of oedema in the first 48 h after reperfusion.
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