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Endogenous assessment of chronic myocardial infarction with T1ρ mapping in patients

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Figure

Figure 1 Spin lock pulse sequence used to obtain T1ρ weighted images. The pulse sequence consists of 2 continuous RF pulses with oppositephase to compensate for B1 variations, and a refocusing pulse between the spin-locking halves to compensate for B0 errors, followed by the readout.
Figure 2 In vivo T1ρ relaxation time versus ex vivo histology. A: T1ρ relaxation time measured in vivo in a porcine animal model issignificantly higher in infarct area (57 ± 11 ms) compared to healthy myocardium (37 ± 4 ms) (p < 0.001) B: The amount of fibrosis in the infarctarea (44.9 ± 13.2%) was also significantly higher compared to the remote myocardium (6.6 ± 7.1%) (p < 0.0001).
Figure 4 T1ρ dispersion measured in ex vivo porcine hearts (n = 5) 8 weeks after MI. Errorbars indicate standard deviation.
Figure 5 T1ρ relaxation time measured in patients with chronic MIis significantly higher in the infarct area (79 ± 11 ms) compared tohealthy myocardium (54 ± 6 ms) (p < 0.0005), and compared tomyocardium in healthy young volunteers (50 ± 3 ms) (p < 0.0005).
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