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dc.contributor.author
Manka, Robert
dc.contributor.author
Kozerke, Sebastian
dc.contributor.author
Rutz, Andrea K.
dc.contributor.author
Stöck, Christian T.
dc.contributor.author
Bösiger, Peter
dc.contributor.author
Schwitter, Jürg
dc.date.accessioned
2019-03-13T11:14:25Z
dc.date.available
2017-06-10T08:34:43Z
dc.date.available
2019-03-13T11:14:25Z
dc.date.issued
2012-07
dc.identifier.issn
1097-6647
dc.identifier.issn
1532-429X
dc.identifier.other
10.1186/1532-429X-14-47
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/55216
dc.identifier.doi
10.3929/ethz-b-000055216
dc.description.abstract
Background In acute myocardial infarction (AMI), both tissue necrosis and edema are present and both might be implicated in the development of intraventricular dyssynchrony. However, their relative contribution to transient dyssynchrony is not known. Cardiovascular magnetic resonance (CMR) can detect necrosis and edema with high spatial resolution and it can quantify dyssynchrony by tagging techniques. Methods Patients with a first AMI underwent percutaneous coronary interventions (PCI) of the infarct-related artery within 24 h of onset of chest pain. Within 5–7 days after the event and at 4 months, CMR was performed. The CMR protocol included the evaluation of intraventricular dyssynchrony by applying a novel 3D-tagging sequence to the left ventricle (LV) yielding the CURE index (circumferential uniformity ratio estimate; 1 = complete synchrony). On T2-weighted images, edema was measured as high-signal (>2 SD above remote tissue) along the LV mid-myocardial circumference on 3 short-axis images (% of circumference corresponding to the area-at-risk). In analogy, on late-gadolinium enhancement (LGE) images, necrosis was quantified manually as percentage of LV mid-myocardial circumference on 3 short-axis images. Necrosis was also quantified on LGE images covering the entire LV (expressed as %LV mass). Finally, salvaged myocardium was calculated as the area-at-risk minus necrosis (expressed as % of LV circumference). Results After successful PCI (n = 22, 2 female, mean age: 57 ± 12y), peak troponin T was 20 ± 36ug/l and the LV ejection fraction on CMR was 41 ± 8%. Necrosis mass was 30 ± 10% and CURE was 0.91 ± 0.05. Edema was measured as 58 ± 14% of the LV circumference. In the acute phase, the extent of edema correlated with dyssynchrony (r2 = −0.63, p < 0.01), while extent of necrosis showed borderline correlation (r2 = −0.19, p = 0.05). PCI resulted in salvaged myocardium of 27 ± 14%. LV dyssynchrony (=CURE) decreased at 4 months from 0.91 ± 0.05 to 0.94 ± 0.03 (p < 0.004, paired t-test). At 4 months, edema was absent and scar %LV slightly shrunk to 23.7 ± 10.0% (p < 0.002 vs baseline). Regression of LV dyssynchrony during the 4 months follow-up period was predicted by both, the extent of edema and its necrosis component in the acute phase. Conclusions In the acute phase of infarction, LV dyssynchrony is closely related to the extent of edema, while necrosis is a poor predictor of acute LV dyssynchrony. Conversely, regression of intraventricular LV dyssynchrony during infarct healing is predicted by the extent of necrosis in the acute phase.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
BioMed Central
en_US
dc.rights.uri
http://creativecommons.org/licenses/by/2.0/
dc.subject
Cardiovascular magnetic resonance
en_US
dc.subject
Tagging
en_US
dc.subject
Myocardial infarction
en_US
dc.subject
Dyssynchrony
en_US
dc.title
A CMR study of the effects of tissue edema and necrosis on left ventricular dyssynchrony in acute myocardial infarction: implications for cardiac resynchronization therapy
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 2.0 Generic
dc.date.published
2012-07-17
ethz.journal.title
Journal of Cardiovascular Magnetic Resonance
ethz.journal.volume
14
en_US
ethz.journal.abbreviated
J Cardiovasc Magn Reson
ethz.pages.start
47
en_US
ethz.size
10 p.
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.publication.place
London
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02140 - Dep. Inf.technologie und Elektrotechnik / Dep. of Inform.Technol. Electrical Eng.::02631 - Institut für Biomedizinische Technik / Institute for Biomedical Engineering::09548 - Kozerke, Sebastian / Kozerke, Sebastian
en_US
ethz.leitzahl
03656 - Bösiger, Peter
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02140 - Dep. Inf.technologie und Elektrotechnik / Dep. of Inform.Technol. Electrical Eng.::02631 - Institut für Biomedizinische Technik / Institute for Biomedical Engineering::03628 - Prüssmann, Klaas P. / Prüssmann, Klaas P.
en_US
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02140 - Dep. Inf.technologie und Elektrotechnik / Dep. of Inform.Technol. Electrical Eng.::02631 - Institut für Biomedizinische Technik / Institute for Biomedical Engineering::09548 - Kozerke, Sebastian / Kozerke, Sebastian
ethz.leitzahl.certified
03656 - Bösiger, Peter
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02140 - Dep. Inf.technologie und Elektrotechnik / Dep. of Inform.Technol. Electrical Eng.::02631 - Institut für Biomedizinische Technik / Institute for Biomedical Engineering::03628 - Prüssmann, Klaas P. / Prüssmann, Klaas P.
ethz.date.deposited
2017-06-10T08:37:42Z
ethz.source
ECIT
ethz.identifier.importid
imp59364fb90273424244
ethz.ecitpid
pub:89007
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-19T09:02:48Z
ethz.rosetta.lastUpdated
2019-03-13T11:14:44Z
ethz.rosetta.exportRequired
true
ethz.rosetta.versionExported
true
ethz.COinS
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