Key result
In STEMI patients, T2-mapping-derived area-at-risk size and other CMR-based parameters of ischemia/reperfusion injury did not vary significantly with the timing of CMR after revascularization.
Why the study?
Does the timing of CMR after revascularization influence CMR-derived parameters of ischemia/reperfusion injury in patients with STEMI?
Observational (n=163)
No
Does the timing of CMR after revascularization influence CMR-derived parameters of ischemia/reperfusion injury in patients with STEMI?
p-value: p=0.385
In reperfused STEMI patients, T2-mapping-derived area-at-risk and LGE-derived infarct size are independent of the timing of CMR after revascularization, despite dynamic changes in absolute T2 values.
Supports flexible post-revascularization CMR timing for T2-mapping AAR in STEMI; leaves open prospective validation across broader cohorts.
To investigate the influence of cardiovascular magnetic resonance (CMR) timing after reperfusion on CMR-derived parameters of ischemia/reperfusion (I/R) injury in patients with ST-segment elevation myocardial infarction (STEMI). The study included 163 reperfused STEMI patients undergoing CMR during the index hospitalization. Patients were divided according to the time between revascularization and CMR (Trevasc-CMR: Tertile-1 ≤ 43; 43 < Tertile-2 ≤ 93; Tertile-3 > 93 h). T2-mapping derived area-at-risk (AAR) and intramyocardial-hemorrhage (IMH), and late gadolinium enhancement (LGE)-derived infarct size (IS) and microvascular obstruction (MVO) were quantified. T1-mapping was performed before and > 15 min after Gd-based contrast-agent administration yielding extracellular volume (ECV) of infarct. Main factors influencing I/R injury were homogenously balanced across Trevasc-CMR tertiles. T2 values of infarct and remote regions increased with increasing Trevasc-CMR tertiles (infarct: 60.0 ± 4.9 vs 63.5 ± 5.6 vs 64.8 ± 7.5 ms; P < 0.001; remote: 44.3 ± 2.8 vs 46.1 ± 2.8 vs ± 46.1 ± 3.0; P = 0.001). However, T2 value of infarct largely and significantly exceeded that of remote myocardium in each tertile yielding comparable T2-mapping-derived AAR extent throughout Trevasc-CMR tertiles (17 ± 9% vs 19 ± 9% vs 18 ± 8% of LV, respectively, P = 0.385). Similarly, T2-mapping-based IMH detection and quantification were independent of Trevasc-CMR. LGE-derived IS and MVO were not influenced by Trevasc-CMR (IS: 12 ± 9% vs 12 ± 9% vs 14 ± 9% of LV, respectively, P = 0.646). In 68 patients without MVO, T1-mapping based ECV of infarct region was comparable across Trevasc-CMR tertiles (P = 0.470). In STEMI patients, T2 values of infarct and remote myocardium increase with increasing CMR time after revascularization. However, these changes do not give rise to substantial variation of T2-mapping-derived AAR size nor of other CMR-based parameters of I/R. ISRCTN03522116 . Registered 30.4.2018 (retrospectively registered).
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Masci et al. (2018) conducted an observational in ST-segment elevation myocardial infarction (STEMI) (n=163). Timing of Cardiovascular Magnetic Resonance (CMR) vs. Different time intervals (tertiles) after revascularization was evaluated on T2-mapping-derived area-at-risk (AAR) extent (% of LV) (p=0.385). In STEMI patients, T2-mapping-derived area-at-risk size and other CMR-based parameters of ischemia/reperfusion injury did not vary significantly with the timing of CMR after revascularization.
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