Assessment of myocardial necrosis biomarker release after acute myocardial infarction determined by kinetic modeling and correlation with infarct size determined by magnetic resonance imaging

2019 
Introduction Infarct size (IS) is a key determinant of cardiovascular events and is ideally assessed by cardiac MRI. MRI availability is limited and many studies used necrosis biomarkers (CK, troponin) as a surrogate marker of IS by determination of their peak concentration and/or their area under the concentration versus time curve (AUC). These biological methods, excluding biomarkers kinetic data may provide inaccurate results. We recently developed a compartmental kinetic model allowing estimation of the total amount of necrosis biomarker released during ST-segment elevation myocardial infarction (STEMI), noted A0. Objective The aim of this study was to determine the correlation level between the amount of biomarkers released in STEMI patients obtained with this kinetic modeling and cardiac MRI measurements of IS. Methods We retrospectively included all patients admitted for STEMI in Tours University Hospital (France) from February 2015 to September 2017, that were treated by primary percutaneous coronary intervention and who had had a cardiac MRI in the days following their admission. CK, troponin I (cTnI) and troponin T (cTnT) concentrations data were collected and kinetics of these biomarkers were described by our kinetic model. For each biomarker, we compared the maximum concentration (Cmax), AUC and A0 determined by the model to cardiac MRI measurements of IS. Results Among the 41 patients included, all had CK assays available, 16 had cTnI assays (cTnI subgroup) and 25 hadcTnT assays (cTnT subgroup) available. The model described satisfactorily biomarker kinetic data with only 3 values of each biomarker. IS was correlated with all CK and cTnT parameters, particularly with CK Cmax (R2 = 64,8%) and cTnT A0 (R2 = 67,1%). For cTnI, there was no correlation between IS and cTnI Cmax (R2 = 2%). Furthermore, in cTnI subgroup, IS correlation was stronger with CK parameters than with cTnI parameters. Conclusion This model allows an accurate description of necrosis biomarkers kinetics following STEMI, which only few measurements. Estimated parameters, particularly CK peak concentration and the total amount of cTnT released by the injured myocardium, were highly correlated to IS measured by cardiac MRI. This method may be used in future clinical trials on the assessment of therapies aiming to reduce IS, such as conditioning therapies.
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