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1 n the activity of creatine phosphokinase and creatine kinase-MB.
2 measured by ECG, echocardiography and plasma creatine kinase-MB.
3 models and included haptoglobin, IL-10, and creatine kinase-MB.
4 utcome information as a cutoff of 5x ULN for creatine kinase-MB.
5 43; P=0.003 and hazard ratio per doubling of creatine kinase-MB, 1.30; 95% confidence interval, 1.05-
6 ocardial infarction defined by enzymes (peak creatine kinase-MB 173+/-119 U/L) were scanned twice by
10 function, and perfusion), injury biomarkers (creatine-kinase-MB and troponin I), and histopathologic
14 rocedural MI, the primary MI definition used creatine kinase-MB as the preferred biomarker, whereas t
15 rocedural MI, the primary MI definition used creatine kinase-MB as the preferred biomarker, whereas t
16 activity but reduced neither infarct size by creatine kinase-MB assessment nor adverse clinical outco
17 similar or lower in HBOC than HEX pigs, but creatine kinase-MB (but not creatine kinase-MB/creatine
18 of serum levels of cardiac troponin T, serum creatine kinase MB (CK-MB) levels, and electrocardiograp
19 cell count (WBC), C-reactive protein (CRP), creatine kinase MB (CK-MB), and troponin I levels were m
23 cally evident complications to elevations of creatine kinase-MB (CK-MB) enzyme levels during percutan
25 nts with unstable angina were determined for creatine kinase-MB (CK-MB) subforms, myoglobin, total CK
26 ditis Treatment Trial and were compared with creatine kinase-MB (CK-MB) values measured in the same p
28 (TnI), B-type natriuretic peptide (BNP), and creatine kinase-MB (CK-MB), and TnI and BNP by CART.
29 MI (PMI(Prot)) required a large elevation of creatine kinase-MB (CK-MB), with identical threshold for
30 e diagnostic performance of serum myoglobin, creatine-kinase-MB (CK-MB) and cardiac troponin-I (cTnI)
31 an HEX pigs, but creatine kinase-MB (but not creatine kinase-MB/creatine kinase ratio) was higher wit
33 l-resistant patients had higher incidence of creatine kinase-MB elevation than the respective sensiti
34 revious 24 hours and ischemic ECG changes or creatine kinase-MB elevation were eligible for enrollmen
36 ity C-reactive protein (hs-CRP), Troponin-T, creatine kinase-MB, fibrinogen, and D-Dimer concentratio
39 ons, with no deaths, myocardial infarctions (creatine kinase, MB fraction > 50 IU/liter) or emergent
40 rdial infarction were identified by elevated creatine kinase, MB fraction (CK-MB) and one of the foll
42 d the predictive properties of P-selectin to creatine kinase, MB fraction (CK-MB) for detecting acute
43 easurements of cardiac troponin I (cTnI) and creatine kinase, MB fraction (CK-MB) levels before, imme
45 were triaged to a chest pain unit, cTnT and creatine kinase, MB fraction (CK-MB) were evaluated > or
49 ungstate significantly decreased circulating creatine kinase-MB fraction activity after hepatoenteric
51 injury, manifested by increased circulating creatine kinase-MB fraction activity, was significantly
53 integrated into clinical algorithms such as creatine kinase-MB fraction or troponin testing for acut
54 e cardiac events, post-PCI peak troponin and creatine kinase-MB fraction, and a longer length of stay
56 dural non-Q-wave myocardial infarction (MI) (creatine kinase-MB > or =5 times normal) was notably hig
57 graft surgery [2.8% versus 3.3%]), although creatine kinase-MB >3X normal was more common with DCA (
58 similar information as a value of 5x ULN for creatine kinase-MB (hazard ratio, 4.31; 99% confidence i
62 ved hemodynamics and decreased the levels of creatine kinase, MB isoenzyme of creatine kinase, blood
63 dy evaluated the incidence and predictors of creatine kinase-MB isoenzyme (CK-MB) elevation after suc
64 the impact of aggressive stent expansion on creatine kinase-MB isoenzyme (CK-MB) release and clinica
67 re hemodynamic deterioration, preangiography creatine kinase-MB isoenzyme rise >2 x normal, and time
70 eroxidase levels, in contrast to troponin T, creatine kinase MB isoform, and C-reactive protein level
71 study was to assess the long-term impact of creatine kinase-MB isoform (CK-MB) elevation after percu
73 (cardiac troponin I level > or =0.7 ng/mL or creatine kinase-MB level > or =5.0 ng/mL and/or diagnost
74 rdial infarction was classified according to creatine kinase-MB level as type 1 (>1 but <3 times norm
75 images provided equal performance, and peak creatine kinase-MB levels correlated with MRI infarct si
77 combined with select clinical variables and creatine kinase-MB levels, enhances the noninvasive pred
80 tive model containing clinical variables and creatine kinase-MB measures, its contribution remained s
83 thickening score, was not predicted by peak creatine kinase-MB (P=0.66) or by total infarct size, as
85 re was a 40% reduction in myocardial injury (creatine kinase-MB release, P=0.05) in patients who rece
87 and serial myocardial marker measurements of creatine kinase-MB, total creatine kinase activity, and