The Experts below are selected from a list of 249 Experts worldwide ranked by ideXlab platform
Paul O. Collinson - One of the best experts on this subject based on the ideXlab platform.
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Cardiac troponin T and Creatine Kinase MB content in skeletal muscle of the uremic rat
Clinical Chemistry, 2002Co-Authors: Salim Fredericks, Joanne F. Murray, Nicholas D. Carter, Alistair Chesser, Stavroula Papachristou, Magdi Yaqoob, Paul O. Collinson, David Gaze, David W. HoltAbstract:Background: The assertion that Creatine Kinase MB (CK-MB) and the developmental isoforms of cardiac troponin T (cTnT) are expressed by skeletal muscle in some clinical settings is an extrapolation from nonuremic rodent studies. We studied the content of CK-MB and cTnT in skeletal muscle of the renal-insufficient rat. Methods: Skeletal muscles (gastrocnemius) were collected from both five-sixths nephrectomized rats (n = 11) and sham-operated controls (n = 11). cTnT content was analyzed by Elecsys (Roche), immunoblotting, and immunohistochemistry with antibodies M7 and M11-7 (Roche). CK isoenzymes were analyzed electrophoretically. Results: Trace concentrations of cTnT were detected in some of the skeletal muscle samples [controls (3 of 11) and uremic rats (1 of 11)] at concentrations Conclusion: The detection of cTnT and CK-MB in skeletal muscle does not differ for uremic rats compared with sham-operated controls. cTnT isoforms detected by qualitative methods are not detected with the cTnT immunoassay. Observations with rodents should not necessarily be extrapolated to humans.
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measurement of serum troponin t Creatine Kinase MB isoenzyme and total Creatine Kinase following arduous physical training
Annals of Clinical Biochemistry, 1995Co-Authors: Paul O. Collinson, Henry A Chandler, Peter J Stubbs, David Moseley, David Lewis, Michael D SimmonsAbstract:SUMMARY. We have compared measurement of cardiac troponin T by enzyme linked immunosorbent assay with Creatine Kinase MB isoenzyme (CK-MB) concentration measurement in 219 Royal Marine commandos with no evidence of cardiovascular disease who have elevated Creatine Kinase (CK) produced by arduous physical training. CK was elevated up to 22.6 times and CK-MB mass up to 6.6 times the upper reference limit. Only two commandos had detectable cardiac troponin T, with neither exceeding the upper reference limit of 0.2 /lg/L. At decision thresholds optimized for diagnosis of acute myocardial infarction in previous published work, 58.3070 of the total CK activity, 13.8% of the CK-MB concentration/CK activity ratio and 1.6% of CK-MB concentration measurements showed elevated values but no elevations in cardiac troponin T occurred. Cardiac troponin T is currently the investigation of choice for the differential diagnosis of patients with an elevated CK due to skeletal muscle trauma to exclude myocardial damage.
David W. Holt - One of the best experts on this subject based on the ideXlab platform.
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Cardiac troponin T and Creatine Kinase MB content in skeletal muscle of the uremic rat
Clinical Chemistry, 2002Co-Authors: Salim Fredericks, Joanne F. Murray, Nicholas D. Carter, Alistair Chesser, Stavroula Papachristou, Magdi Yaqoob, Paul O. Collinson, David Gaze, David W. HoltAbstract:Background: The assertion that Creatine Kinase MB (CK-MB) and the developmental isoforms of cardiac troponin T (cTnT) are expressed by skeletal muscle in some clinical settings is an extrapolation from nonuremic rodent studies. We studied the content of CK-MB and cTnT in skeletal muscle of the renal-insufficient rat. Methods: Skeletal muscles (gastrocnemius) were collected from both five-sixths nephrectomized rats (n = 11) and sham-operated controls (n = 11). cTnT content was analyzed by Elecsys (Roche), immunoblotting, and immunohistochemistry with antibodies M7 and M11-7 (Roche). CK isoenzymes were analyzed electrophoretically. Results: Trace concentrations of cTnT were detected in some of the skeletal muscle samples [controls (3 of 11) and uremic rats (1 of 11)] at concentrations Conclusion: The detection of cTnT and CK-MB in skeletal muscle does not differ for uremic rats compared with sham-operated controls. cTnT isoforms detected by qualitative methods are not detected with the cTnT immunoassay. Observations with rodents should not necessarily be extrapolated to humans.
Nancy A Nussmeier - One of the best experts on this subject based on the ideXlab platform.
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increased Creatine Kinase MB level predicts postoperative mortality after cardiac surgery independent of new q waves
The Journal of Thoracic and Cardiovascular Surgery, 2005Co-Authors: James Ramsay, Stanton K Shernan, Jane C K Fitch, Paul Finnegan, Thomas G Todaro, Thomas G Filloon, Nancy A NussmeierAbstract:BACKGROUND: Recent consensus statements recommend cardiac enzyme release as the essential criterion for diagnosing myocardial infarction. However, the outcome implications of cardiac enzyme release in patients undergoing coronary artery bypass grafting are controversial. METHODS: Eight hundred patients were followed for 30 days after elective on-pump coronary artery bypass grafting in a multicenter, prospective, randomized trial of the anti-C5 complement antibody pexelizumab. Data from centralized electrocardiography and Creatine Kinase MB analyses were examined for any association with death or severe left ventricular dysfunction. RESULTS: More than half of the 800 patients had peak Creatine Kinase MB levels of more than 5 times the upper limit of 5 ng/mL set by the core laboratory. The median peak value was 29 ng/mL. The incidence of the coMBined outcome (death or severe left ventricular dysfunction) was 1.7% if the peak Creatine Kinase MB level was less than 25 ng/mL and 18.0% if 100 ng/mL or greater (P < .01). Similarly, the incidence of new Q-wave myocardial infarction was 3.9% if the peak Creatine Kinase MB level was less than 25 ng/mL and 30.6% if 100 ng/mL or greater (P < .01). In a multivariate analysis that included preoperative and intraoperative factors, as well as peak enzyme release and Q-wave myocardial infarction, the strongest predictor of the coMBined outcome was a peak Creatine Kinase MB level of 100 ng/mL or greater. New Q-wave myocardial infarction did not significantly predict the coMBined outcome. CONCLUSIONS: Increased postoperative peak Creatine Kinase MB level, especially when 20 times or more of the upper limit of normal, indicates increased risk of severe postoperative left ventricular dysfunction and mortality within 30 days of coronary artery bypass grafting. High peak enzyme level is a stronger predictor of adverse outcomes than is postoperative Q-wave myocardial infarction in this population.
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Increased Creatine Kinase MB level predicts postoperative mortality after cardiac surgery independent of new Q waves.
The Journal of thoracic and cardiovascular surgery, 2005Co-Authors: James Ramsay, Stanton K Shernan, Jane C K Fitch, Paul Finnegan, Thomas G Todaro, Thomas G Filloon, Nancy A NussmeierAbstract:Background Recent consensus statements recommend cardiac enzyme release as the essential criterion for diagnosing myocardial infarction. However, the outcome implications of cardiac enzyme release in patients undergoing coronary artery bypass grafting are controversial. Methods Eight hundred patients were followed for 30 days after elective on-pump coronary artery bypass grafting in a multicenter, prospective, randomized trial of the anti-C5 complement antibody pexelizumab. Data from centralized electrocardiography and Creatine Kinase MB analyses were examined for any association with death or severe left ventricular dysfunction. Results More than half of the 800 patients had peak Creatine Kinase MB levels of more than 5 times the upper limit of 5 ng/mL set by the core laboratory. The median peak value was 29 ng/mL. The incidence of the coMBined outcome (death or severe left ventricular dysfunction) was 1.7% if the peak Creatine Kinase MB level was less than 25 ng/mL and 18.0% if 100 ng/mL or greater (P Conclusions Increased postoperative peak Creatine Kinase MB level, especially when 20 times or more of the upper limit of normal, indicates increased risk of severe postoperative left ventricular dysfunction and mortality within 30 days of coronary artery bypass grafting. High peak enzyme level is a stronger predictor of adverse outcomes than is postoperative Q-wave myocardial infarction in this population.
Michael D Simmons - One of the best experts on this subject based on the ideXlab platform.
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measurement of serum troponin t Creatine Kinase MB isoenzyme and total Creatine Kinase following arduous physical training
Annals of Clinical Biochemistry, 1995Co-Authors: Paul O. Collinson, Henry A Chandler, Peter J Stubbs, David Moseley, David Lewis, Michael D SimmonsAbstract:SUMMARY. We have compared measurement of cardiac troponin T by enzyme linked immunosorbent assay with Creatine Kinase MB isoenzyme (CK-MB) concentration measurement in 219 Royal Marine commandos with no evidence of cardiovascular disease who have elevated Creatine Kinase (CK) produced by arduous physical training. CK was elevated up to 22.6 times and CK-MB mass up to 6.6 times the upper reference limit. Only two commandos had detectable cardiac troponin T, with neither exceeding the upper reference limit of 0.2 /lg/L. At decision thresholds optimized for diagnosis of acute myocardial infarction in previous published work, 58.3070 of the total CK activity, 13.8% of the CK-MB concentration/CK activity ratio and 1.6% of CK-MB concentration measurements showed elevated values but no elevations in cardiac troponin T occurred. Cardiac troponin T is currently the investigation of choice for the differential diagnosis of patients with an elevated CK due to skeletal muscle trauma to exclude myocardial damage.
Allan S Jaffe - One of the best experts on this subject based on the ideXlab platform.
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requiem for a heavyweight the demise of Creatine Kinase MB
Circulation, 2008Co-Authors: Amy K Saenger, Allan S JaffeAbstract:The development of rapid, automated, and accurate laboratory testing for Creatine Kinase MB (CK-MB) revolutionized the treatment of patients with acute cardiac events in the 1970s and 1980s.1 To clinicians, CK-MB values augmented a thorough history, physical, and ECG findings, and elevations rapidly became the gold standard for identifying cardiac injury.1 CK-MB allowed earlier diagnosis of acute myocardial infarction (AMI), and detection of reinfarction, and measurements could be used to provide a facile clinical estimate of infarct size. Elevations of CK-MB were never intended to be synonymous with myocardial infarction, only indicative of cardiac injury.1 However, because of the relative insensitivity of measurements, increased concentrations occurred predominantly with larger insults such those associated with acute ischemic heart disease. For that reason, AMI was rarely diagnosed, assuming appropriate timing of the samples, in the absence of a CK-MB elevation.2,3 CK-MB assays initially relied on the measurement of enzyme activity, but over time, improved accuracy and ease of use were established by the use of mass assays. Mass assays allowed earlier detection of abnormal values and improved both clinical sensitivity and specificity. However, mass assays unmasked an increased frequency of CK-MB elevations due primarily to skeletal muscle injury because of their increased sensitivity.4–6 Clinical use of the percent relative index was then initiated. This approach improved the specificity of elevations for cardiac muscle injury but was insensitive when concurrent cardiac injury and skeletal muscle injury were present because elevations from skeletal muscle often are of a large magnitude.7–10 A large nuMBer of analytical confounds such as macroKinases and interfering substances also were substantial problems with these assays.10,11 Attempts to standardize assays12 have been partially successful, but differences still exist between manufacturers and even between the same testing antibodies used on different analytical platforms (ie, …
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bedside multimarker testing for risk stratification in chest pain units the chest pain evaluation by Creatine Kinase MB myoglobin and troponin i checkmate study
Circulation, 2001Co-Authors: Fred S. Apple, Allan S JaffeAbstract:Background—Earlier, rapid evaluation in chest pain units may make patient care more efficient. A multimarker strategy (MMS) testing for several markers of myocardial necrosis with different time-to-positivity profiles also may offer clinical advantages. Methods and Results—We prospectively compared bedside quantitative multimarker testing versus local laboratory results (LL) in 1005 patients in 6 chest pain units. Myoglobin, Creatine Kinase-MB, and troponin I were measured at 0, 3, 6, 9 to 12, and 16 to 24 hours after admission. Two MMS were defined: MMS-1 (all 3 markers) and MMS-2 (Creatine Kinase-MB and troponin I only). The primary assessment was to relate marker status with 30-day death or infarction. More patients were positive by 24 hours with MMS than with LL (MMS-1, 23.9%; MMS-2, 18.8%; LL, 8.8%; P=0.001, all comparisons), and they became positive sooner with MMS-1 (2.5 hours, P=0.023 versus LL) versus MMS-2 (2.8 hours, P=0.026 versus LL) or LL (3.4 hours). The relation between baseline MMS status...