Key result
In patients with STEMI, the intensity of myocardial edema assessed by T1 mapping followed a bimodal pattern, with mean T1 relaxation time significantly decreasing from 1404 ms at <3 hours to 1345 ms at 24 hours.
Why the study?
Does serial T1 mapping CMR detect dynamic changes in myocardial edema in STEMI patients post-PCI?
Cohort (n=48)
Single-blind
No
Does serial T1 mapping CMR detect dynamic changes in myocardial edema in STEMI patients post-PCI?
T1 mapping CMR reveals that the intensity of myocardial edema follows a bimodal pattern early after STEMI, whereas the anatomical extent of the area at risk remains stable initially, highlighting the dynamic nature of tissue water content post-reperfusion.
Answers are grounded in this paper and cite their sources.
Serial T1 mapping may refine edema assessment timing in STEMI; leaves open its impact on risk stratification or trial endpoints.
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.
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Alkhalil et al. (2018) conducted a cohort in ST-segment elevation myocardial infarction (STEMI) (n=48). T1 mapping cardiovascular magnetic resonance vs. Serial time points (<3 h, 24 h, 6 days) was evaluated on Mean T1 relaxation time within the area at risk (AAR) at 24 hours compared to <3 hours (ms) (p=<0.001). In patients with STEMI, the intensity of myocardial edema assessed by T1 mapping followed a bimodal pattern, with mean T1 relaxation time significantly decreasing from 1404 ms at <3 hours to 1345 ms at 24 hours.
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