OBJECTIVE: The aim of the study was to find out if single time point and estimated cumulative release of cardiac troponin T (cTnT) and creatine kinase (CK) correlate with early infarct size and left ventricular function measured by cardiac magnetic resonance (CMR). METHODS: CMR and serial CK and cTnT measurements were performed in 103 patients (85 male, mean age 55.8 ± 12.1 years) within at least 8 days (3.1 ± 1.5 days) after first acute myocardial infarction and successful primary percutaneous coronary interventions. Infarct size was determined on delayed gadolinium-enhanced phase-sensitive IR-SSFP CMR sequences. Single time point, peak and cumulative cardiac protein release were correlated with infarct size. RESULTS: All single time point, peak and estimated cumulative release of CK and cTnT values except on admission showed significant correlations with infarct size. Among single time point values, cTnT after 96 h (cTnT(96); r = 0.680, p < 0.001) and CK after 24 h (CK(24); r = 0.699, p < 0.001) showed the closest correlations with infarct size. Peak CK and cTnT levels correlated only slightly better than single time point values (r = 0.703 and 0.688, p < 0.001), whereas cumulative release values did not show closer correlations than single point values. Receiver-operator characteristics analysis showed that cTnT(96) and CK(24) detected large infarct areas (>16.8 g) and decreased left ventricular function (EF < 40%) with high sensitivity and specificity. CONCLUSION: Both single time point cTnT concentrations and CK activities correlate well with infarct size early after primary PCI for STEMI. Cardiac TnT levels determined 3-4 days after revascularization for acute myocardial infarction allow for a good estimation of acute infarct size as well as an approximation of LV function and morphology.
OBJECTIVE: The aim of the study was to find out if single time point and estimated cumulative release of cardiac troponin T (cTnT) and creatine kinase (CK) correlate with early infarct size and left ventricular function measured by cardiac magnetic resonance (CMR). METHODS: CMR and serial CK and cTnT measurements were performed in 103 patients (85 male, mean age 55.8 ± 12.1 years) within at least 8 days (3.1 ± 1.5 days) after first acute myocardial infarction and successful primary percutaneous coronary interventions. Infarct size was determined on delayed gadolinium-enhanced phase-sensitive IR-SSFP CMR sequences. Single time point, peak and cumulative cardiac protein release were correlated with infarct size. RESULTS: All single time point, peak and estimated cumulative release of CK and cTnT values except on admission showed significant correlations with infarct size. Among single time point values, cTnT after 96 h (cTnT(96); r = 0.680, p < 0.001) and CK after 24 h (CK(24); r = 0.699, p < 0.001) showed the closest correlations with infarct size. Peak CK and cTnT levels correlated only slightly better than single time point values (r = 0.703 and 0.688, p < 0.001), whereas cumulative release values did not show closer correlations than single point values. Receiver-operator characteristics analysis showed that cTnT(96) and CK(24) detected large infarct areas (>16.8 g) and decreased left ventricular function (EF < 40%) with high sensitivity and specificity. CONCLUSION: Both single time point cTnT concentrations and CK activities correlate well with infarct size early after primary PCI for STEMI. Cardiac TnT levels determined 3-4 days after revascularization for acute myocardial infarction allow for a good estimation of acute infarct size as well as an approximation of LV function and morphology.
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