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Arch Cardiovasc Dis. 2009 Aug-Sep;102(8-9):633-9. doi: 10.1016/j.acvd.2009.05.006. Epub 2009 Sep 10.

Cardiac magnetic resonance demonstrates myocardial oedema in remote tissue early after reperfused myocardial infarction.

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Department of Human Investigations, GIP Cyceron, boulevard Henri-Becquerel, BP 5229, 14074 Caen Cedex 05, France.



Cardiac magnetic resonance can detect myocardial oedema using myocardial transverse relaxation time (T2)-weighted sequences but quantitative data are lacking in patients evaluated early after acute myocardial infarction.


To assess the spatial distribution of T2 in patients with recent acute myocardial infarction.


Twenty-four consecutive patients (mean age 60+/-11 years) with acute myocardial infarction (anterior, n=12; inferior, n=12) were evaluated prospectively. T2 was determined using a series of breath-hold T2-weighted segmented half-Fourier turbo-spin echo sequences. No-reflow was defined as the association of early hypoenhancement and delayed enhancement in an akinetic region after a bolus injection of DOTA-Gd (0.2 mmol/kg).


No-reflow was present in 13 (54%) patients and absent in 11 (46%) patients. Mean T2 was increased in the infarct region (84.9+/-23.7 ms) compared with in the remote myocardium (62.8+/-10.3 ms, p=0.0001) and in control subjects (55.7+/-4.6 ms, p<0.0001), but also in the remote myocardium compared with control subjects (p<0.02). In patients with no-reflow, T2 was further increased within the infarcted subendocardium compared with in patients without no-reflow (97.9+/-24.8 ms vs 76.3+/-24.7 ms, p<0.03). Peak troponin correlated with T2 (r=0.47, p<0.02) and was higher in patients with no-reflow (297.9+/-249.7 microg/L) than in patients without no-reflow (42.4+/-43.1 microg/L, p=0.003).


T2 was lengthened in both infarcted and remote myocardium and was influenced by the occurrence of no-reflow.

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