scholarly journals Clinical characteristics and role of early cardiac magnetic resonance imaging in patients with suspected ST-elevation myocardial infarction and normal coronary arteries

2010 ◽  
Vol 27 (3) ◽  
pp. 355-365 ◽  
Author(s):  
K. H. Stensaeth ◽  
E. Fossum ◽  
P. Hoffmann ◽  
A. Mangschau ◽  
N. E. Klow
Keyword(s):  
Magnetic Resonance Imaging ◽  
Myocardial Infarction ◽  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Cardiac Magnetic Resonance Imaging ◽  
Coronary Arteries ◽  
Clinical Characteristics ◽  
Resonance Imaging ◽  
St Elevation

scholarly journals Using proximity extension proteomics assay to identify biomarkers associated with infarct size and ejection fraction after ST-elevation myocardial infarction

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Moman A. Mohammad ◽  
Sasha Koul ◽  
Anna Egerstedt ◽  
J. Gustav Smith ◽  
Marko Noc ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Myocardial Infarction ◽  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Ejection Fraction ◽  
Infarct Size ◽  
Cardiac Magnetic Resonance Imaging ◽  
Resonance Imaging ◽  
St Elevation ◽  
Inflammatory Proteins

Abstract Plasma concentrations of many cardiovascular and inflammatory proteins are altered after ST-elevation myocardial infarction (STEMI) and may provide prognostic information. We conducted a large-scale proteomic analysis in patients with STEMI, correlating protein levels to infarct size and left ventricular ejection fraction (LVEF) determined with cardiac magnetic resonance imaging. We analysed 131 cardiovascular and inflammatory proteins using a multiplex proximity extension assay and blood samples obtained at baseline, 6, 24, and 96 h from the randomised clinical trial CHILL-MI. Cardiac magnetic resonance imaging data at 4 ± 2 days and 6 months were available as per trial protocol. Using a linear regression model with bootstrap resampling and false discovery rate adjustment we identified five proteins (ST2, interleukin-6, pentraxin-3, interleukin-10, renin, and myoglobin) with elevated values corresponding to larger infarct size or worse LVEF and four proteins (TNF-related apoptosis-inducing ligand, TNF-related activation induced cytokine, interleukin-16, and cystatin B) with values inversely related to LVEF and infarct size, concluding that among 131 circulating inflammatory and cardiovascular proteins in the acute and sub-acute phase of STEMI, nine showed a relationship with infarct size and LVEF post-STEMI, with IL-6 and ST2 exhibiting the strongest association.

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