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

Summary Background 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. Aim To assess the spatial distribution of T2 in patients wit...

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Published inArchives of cardiovascular diseases Vol. 102; no. 8; pp. 633 - 639
Main Authors Manrique, Alain, Gerbaud, Edouard, Derumeaux, Geneviève, Cribier, Alain, Bertrand, David, Lebon, Alain, Dacher, Jean-Nicolas
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier Masson SAS 01.08.2009
Elsevier
Elsevier/French Society of Cardiology
Subjects
IRM
MRI
MRI
IRM
NS
TE
T1
T2
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Summary:Summary Background 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. Aim To assess the spatial distribution of T2 in patients with recent acute myocardial infarction. Methods 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). Results 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 μg/L) than in patients without no-reflow (42.4 ± 43.1 μg/L, p = 0.003). Conclusion T2 was lengthened in both infarcted and remote myocardium and was influenced by the occurrence of no-reflow.
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ISSN:1875-2136
1875-2128
DOI:10.1016/j.acvd.2009.05.006