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Dynamic changes in injured myocardium,very early after acute myocardial infarction,quantified using T1 mapping cardiovascular magnetic resonance
Authors:" target="_blank">Mohammad Alkhalil  Alessandra Borlotti  Giovanni Luigi De Maria  Lisa Gaughran  Jeremy Langrish  Andrew Lucking  Vanessa Ferreira  Rajesh K Kharbanda  Adrian P Banning  Keith M Channon  Erica Dall’Armellina  Robin P Choudhury
Institution:1.Acute Vascular Imaging Centre, Radcliffe Department of Medicine,University of Oxford,Oxford,UK;2.Oxford Heart Centre, NIHR Biomedical Research Centre,Oxford University Hospitals,Oxford,UK;3.Division of Cardiovascular Medicine, BHF Centre of Research Excellence,University of Oxford,Oxford,UK;4.Division of Cardiovascular Medicine,University of Oxford Centre for Clinical Magnetic Resonance Research (OCMR),Oxford,UK
Abstract:

Background

It has recently been suggested that myocardial oedema follows a bimodal pattern early post ST-segment elevation myocardial infarction (STEMI). Yet, water content, quantified using tissue desiccation, did not return to normal values unlike oedema quantified by cardiovascular magnetic resonance (CMR) imaging. We studied the temporal changes in the extent and intensity of injured myocardium using T1-mapping technique within the first week after STEMI.

Methods

A first group (n?=?31) underwent 3 acute 3?T CMR scans (time-point (TP) <?3?h, 24?h and 6?days), including cine, native shortened modified look-locker inversion recovery T1 mapping, T2* mapping and late gadolinium enhancement (LGE). A second group (n?=?17) had a single scan at 24?h with an additional T2-weighted sequence to assess the difference in the extent of area-at-risk (AAR) compared to T1-mapping.

Results

The mean T1 relaxation time value within the AAR of the first group was reduced after 24?h (P?<?0.001 for TP1 vs.TP2) and subsequently increased at 6?days (P?=?0.041 for TP2 vs.TP3). However, the extent of AAR quantified using T1-mapping did not follow the same course, and no change was detected between TP1&TP2 (P?=?1.0) but was between TP2 &TP3 (P?=?0.019). In the second group, the extent of AAR was significantly larger on T1-mapping compared to T2-weighted (42?±?15% vs. 39?±?15%, P?=?0.025). No change in LGE was detected while microvascular obstruction and intra-myocardial haemorrhage peaked at different time points within the first week of reperfusion.

Conclusion

The intensity of oedema post-STEMI followed a bimodal pattern; while the extent of AAR did not track the same course. This discrepancy has implications for use of CMR in this context and may explain the previously reported disagreement between oedema quantified by imaging and tissue desiccation.
Keywords:
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