Dynamic changes in injured myocardium, very early after acute myocardial infarction, quantified using T1 mapping cardiovascular magnetic resonance

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: Area at risk; STEMI; T1-mapping.

Fig. 1

Study flow chart. Patients presenting with ST elevation myocardial infarction (STEMI) and occluded vessel were prospectively recruited to either temporal changes cohort or single scan cohort, depending on CMR feasibility within 3 h post stent implantation

Fig. 2

Bimodal changes of T1 relaxation time. Panel a short-axis T1 maps in a patient with inferior ischaemic injury (black arrow) acquired at three time points post STEMI presentation. The magnitude of change in native T1 value within the area at risk (AAR) (contoured in black) is illustrated against a colour scale map. Panel b T1 relaxation time showed significant attenuation of oedematous reaction in the injured myocardium after 24 h and returns to previous level at 6 days (blue lines representing mean +/− 2 standard error). Changes within remote myocardium over time are illustrated in black lines (mean +/− 2 standard error). Panel c excluding central area with low T1 values (T1-core), T1 relaxation time was compared serially. The deferred wave of oedematous reaction was more prominent with significant difference between 24 h and 6 days (blue lines representing mean +/− 2 standard error)

Fig. 3

Changes in extent of oedema. Panel a AAR, quantified using T1 mapping sequence, did not undergo significant changes within 24 h. There was significant increase in extent of oedema at 6 days mirroring increase in T1 relaxation time (mean +/− 2 standard error). Panel b pairwise comparison between injured myocardium in T2-weighted and T1 mapping (mean +/− 2 standard error)

Fig. 4

Changes in T1 core, LGE, MVO and IMH. Development of T1 core (yellow arrow), area of low T1 value within injured myocardium that progressed over time. The extent of late gadolinium enhancement (LGE) was comparable across time points with early peak of microvascular obstruction (MVO) (red arrows) compared to more lagged peak of intramyocardial haemorrhage (IMH) (contoured in black)