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Background  Two days after myocardial infarction (MI), the infarct consists mostly on necrotic tissue, and the myocardium is transformed through granulation tissue to scar in two weeks after the onset of ischemia in mice. In the current work, we determined and optimized cardiovascular magnetic resonance (CMR) methods for the detection of MI size during the scar formation without contrast agents in mice.    Methods  We characterized MI and remote areas with rotating frame relaxation time mapping including relaxation along fictitious field in n th  rotating frame (RAFFn), T 1ρ  and T 2  relaxation time mappings at 1, 3, 7, and 21 days after MI. These results were compared to late gadolinium enhancement (LGE) and Sirius Red-stained histology sections, which were obtained at day 21 after MI.    Results  All relaxation time maps showed significant differences in relaxation time between the MI and remote area. Areas of increased signal intensities after gadolinium injection and areas with increased T RAFF2  relaxation time were highly correlated with the MI area determined from Sirius Red-stained histology sections (LGE: R 2  = 0.92,  P  < 0.01, T RAFF2 : R 2  = 0.95,  P  < 0.001). Infarct area determined based on T 1ρ  relaxation time correlated highly with Sirius Red histology sections (R 2  = 0.97,  P  < 0.01). The smallest overestimation of the LGE-defined MI area was obtained for T RAFF2  (5.6 ± 4.2%) while for T 1ρ  overestimation percentage was > 9% depending on T 1ρ  pulse power.    Conclusion  T 1ρ  and T RAFF2  relaxation time maps can be used to determine accurately MI area at various time points in the mouse heart. Determination of MI size based on T RAFF2  relaxation time maps could be performed without contrast agents, unlike LGE, and with lower specific absorption rate compared to on-resonance T 1ρ  relaxation time mapping.

journal of cardiovascular magnetic resonance

Quantification of myocardial infarct area based on TRAFFn relaxation time maps - comparison with cardiovascular magnetic resonance late gadolinium enhancement, T1ρ and T2 in vivo