Relationship between CMR-derived parameters of ischemia/reperfusion injury and the timing of CMR after reperfused ST-segment elevation myocardial infarction.
Details
Serval ID
serval:BIB_F184A0673B26
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Relationship between CMR-derived parameters of ischemia/reperfusion injury and the timing of CMR after reperfused ST-segment elevation myocardial infarction.
Journal
Journal of cardiovascular magnetic resonance
ISSN
1532-429X (Electronic)
ISSN-L
1097-6647
Publication state
Published
Issued date
23/07/2018
Peer-reviewed
Oui
Volume
20
Number
1
Pages
50
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: epublish
Publication Status: epublish
Abstract
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 (T <sub>revasc-CMR</sub> : 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 T <sub>revasc-CMR</sub> tertiles. T2 values of infarct and remote regions increased with increasing T <sub>revasc-CMR</sub> 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 T <sub>revasc-CMR</sub> 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 T <sub>revasc-CMR</sub> . LGE-derived IS and MVO were not influenced by T <sub>revasc-CMR</sub> (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 T <sub>revasc-CMR</sub> 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).
The study included 163 reperfused STEMI patients undergoing CMR during the index hospitalization. Patients were divided according to the time between revascularization and CMR (T <sub>revasc-CMR</sub> : 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 T <sub>revasc-CMR</sub> tertiles. T2 values of infarct and remote regions increased with increasing T <sub>revasc-CMR</sub> 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 T <sub>revasc-CMR</sub> 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 T <sub>revasc-CMR</sub> . LGE-derived IS and MVO were not influenced by T <sub>revasc-CMR</sub> (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 T <sub>revasc-CMR</sub> 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).
Keywords
Adult, Aged, Contrast Media/administration & dosage, Edema, Cardiac/diagnostic imaging, Edema, Cardiac/etiology, Edema, Cardiac/physiopathology, Female, Humans, Magnetic Resonance Imaging, Cine, Male, Middle Aged, Myocardial Reperfusion/adverse effects, Myocardial Reperfusion Injury/diagnostic imaging, Myocardial Reperfusion Injury/etiology, Myocardial Reperfusion Injury/physiopathology, Organometallic Compounds/administration & dosage, Predictive Value of Tests, Registries, ST Elevation Myocardial Infarction/diagnostic imaging, ST Elevation Myocardial Infarction/physiopathology, ST Elevation Myocardial Infarction/surgery, Time Factors, Treatment Outcome, Cardiovascular magnetic resonance, Extracellular volume, Myocardial edema, Myocardial infarction, T1-mapping, T2-mapping
Pubmed
Web of science
Open Access
Yes
Create date
31/07/2018 11:03
Last modification date
20/08/2019 16:19
Usage data
