Why the study?
Does T2* mapping quantify acute and chronic myocardial ischemia/reperfusion injury in mice?
Does T2* mapping quantify acute and chronic myocardial ischemia/reperfusion injury in mice?
T2* mapping can discriminate between acute and chronic myocardial infarctions and confirm chronic infarction when late gadolinium enhancement is inconclusive.
T2* mapping may aid preclinical infarct staging in mice; leaves open human translation for ischemia/reperfusion assessment.
Imaging of myocardial infarct composition is essential to assess efficacy of emerging therapeutics. T 2 * mapping has the potential to image myocardial hemorrhage and fibrosis by virtue of its short T 2 * . We aimed to quantify T 2 * in acute and chronic myocardial ischemia/reperfusion (I/R) injury in mice. I/R-injury was induced in C57BL/6 mice (n = 9). Sham-operated mice (n = 8) served as controls. MRI was performed at baseline, and 1, 7 and 28 days after surgery. MRI at 9.4 T consisted of Cine, T 2 * mapping and late-gadolinium-enhancement (LGE). Mice (n = 6) were histologically assessed for hemorrhage and collagen in the fibrotic scar. Baseline T 2 * values were 17.1 ± 2.0 ms. At day 1, LGE displayed a homogeneous infarct enhancement. T 2 * in infarct (12.0 ± 1.1 ms) and remote myocardium (13.9 ± 0.8 ms) was lower than at baseline. On days 7 and 28, LGE was heterogeneous. T 2 * in the infarct decreased to 7.9 ± 0.7 and 6.4 ± 0.7 ms, whereas T 2 * values in the remote myocardium were 14.2 ± 1.1 and 15.6 ± 1.0 ms. Histology revealed deposition of iron and collagen in parallel with decreased T 2 * . T 2 * values are dynamic during infarct development and decrease significantly during scar maturation. In the acute phase, T 2 * values in infarcted myocardium differ significantly from those in the chronic phase. T 2 * mapping was able to confirm the presence of a chronic infarction in cases where LGE was inconclusive. Hence, T 2 * may be used to discriminate between acute and chronic infarctions.
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Aguor et al. (2012) studied this question.
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