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1 ll percentage (21%) despite normalization of cardiac enzymes.
2 l echocardiography, electrocardiography, and cardiac enzymes.
3 placing linoleic acid with DHA lowers select cardiac enzyme activities by potentially targeting domai
4 ostprocedural ECGs and measurement of serial cardiac enzymes after revascularization are recommended.
5 dial infarction, ST depression, and elevated cardiac enzymes (all P<.001).
6 s, chest pain, relatively minor elevation of cardiac enzyme and biomarker levels, and transient apica
7        The patient was asymptomatic, and the cardiac enzymes and echocardiogram were normal; therefor
8 istic ECG changes in association with normal cardiac enzymes and echocardiogram.
9                           Absolute levels of cardiac enzymes and inflammatory markers at baseline did
10       This is the first study reporting that cardiac enzymes and inflammatory parameters do not suffi
11 rged in less than 24 h after negative serial cardiac enzymes and stable electrocardiograms and 17 wer
12 ts, as shown by cardiac function, release of cardiac enzymes, and metabolic preservation.
13 dmission to ICU, new electrocardiographic or cardiac enzyme changes suggestive of cardiac ischemia or
14  Typically an algorithm includes chest pain, cardiac enzymes, electrocardiographic findings, and auto
15 , the incidence and prognostic importance of cardiac enzyme elevation after coronary stenting have no
16    Several small studies have suggested that cardiac enzyme elevation in the 24 hours following coron
17 jection of cells or saline did not result in cardiac enzyme elevation, perforation, or pericardial ef
18 iograms, computed tomography angiography, or cardiac enzyme elevation, some argue for the use of thro
19 ization and collection, 4.6% of patients had cardiac enzyme elevations consistent with non-ST segment
20  -collection procedures were associated with cardiac enzyme elevations, which will be addressed in fu
21                                Elevations in cardiac enzymes, including small increases (between one
22 are diagnostic tests to expedite testing for cardiac enzymes indicative of acute myocardial infarctio
23     However, postoperative surveillance with cardiac enzymes is not routinely performed in these pati
24 ms data repository using MI diagnoses and/or cardiac enzyme laboratory results (1995-2012).
25 served coronary flow, reduced release of the cardiac enzyme lactic dehydrogenase, and reduced myocard
26                    The detection of elevated cardiac enzyme levels and the occurrence of electrocardi
27 levels, chest radiograph, electrocardiogram, cardiac enzyme levels, and magnetic resonance imaging or
28   'Routine cardiac investigations' (ECGs and cardiac enzymes obtained 2 weeks after injections of MVA
29                                 Elevation of cardiac enzymes often occurs after PCI, but its clinical
30 nd systemic vascular resistances, ECG, serum cardiac enzymes, plasma catecholamines and atrial natriu
31 inee first operators (15.3% vs 12.5%), lower cardiac enzyme rise, shorter length of stay, and fewer c
32                                     Although cardiac enzymes such as troponin I and CKMB are reliable
33 iochemical markers (natriuretic peptides and cardiac enzymes) that indicate that a new genetic progra
34 stment accounted for change from reliance on cardiac enzymes to widespread use of troponin measuremen
35 t was myocardial infarct size as assessed by cardiac enzymes, troponin I, and creatine kinase.
36        Efficacy end points and postprocedure cardiac enzyme were similar, but there was a nonsignific
37 sia, fluid requirements, cardiac output, and cardiac enzymes were generally similar or lower in HBOC
38 n admission was 11.3+/- 22.7 ng/dl, and peak cardiac enzymes were noted within 8 h of presentation.

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