Combined analyses of creatine kinase MB, cardiac troponin I and myoglobin in pericardial and cerebrospinal fluids to investigate myocardial and skeletal muscle injury in medicolegal autopsy cases

Patients with cocaine-related chest pain with electrocardiographic (ECG) abnormalities are often admitted to rule out acute myocardial infarction (AMI). Cardiac troponin I and T should be superior to measurement of creatine kinase (CK)—MB for detecting cardiac injury in patients with coexisting skeletal muscle injury. We prospectively evaluated 19 consecutive patients with acute chest pain related to cocaine use who were hospitalized to rule out AMI. The admission ECG was abnormal in 16 of 19 patients. Total CK and CK—MB were elevated during the hospital course in 14 and 3 patients, respectively. Cardiac troponin I and cardiac troponin T levels were within normal limits in all patients demonstrating that recent myocardial injury did not occur. Clinically, no patient had an AMI. Cocaine-induced thoracic skeletal muscle injury or transient cocaine-induced coronary vasospasm should be considered as alternative sources of chest pain in these patients.

Download Full-text

Postmortem cardiac troponin I and creatine kinase MB levels in the blood and pericardial fluid as markers of myocardial damage in medicolegal autopsy

Legal Medicine ◽

10.1016/j.legalmed.2007.01.010 ◽

2007 ◽

Vol 9 (5) ◽

pp. 241-250 ◽

Cited By ~ 57

Author(s):

Bao-Li Zhu ◽

Takaki Ishikawa ◽

Tomomi Michiue ◽

Dong-Ri Li ◽

Dong Zhao ◽

...

Keyword(s):

Creatine Kinase ◽

Cardiac Troponin ◽

Troponin I ◽

Myocardial Damage ◽

Pericardial Fluid ◽

Cardiac Troponin I ◽

Creatine Kinase Mb ◽

Medicolegal Autopsy

Download Full-text

Frontal QRS-T angle as a predictive marker for myocardial damage in acute carbon monoxide poisoning

Human & Experimental Toxicology ◽

10.1177/09603271211043477 ◽

2021 ◽

pp. 096032712110434

Author(s):

Yusuf K Tekin ◽

Gülaçan Tekin ◽

Naim Nur ◽

İlhan Korkmaz ◽

Sefa Yurtbay

Keyword(s):

Carbon Monoxide ◽

Creatine Kinase ◽

Cardiac Troponin ◽

Troponin I ◽

Myocardial Damage ◽

Cardiac Troponin I ◽

Arterial Oxygen ◽

Co Poisoning ◽

Arterial Blood ◽

Creatine Kinase Mb

Introduction The present study was undertaken to investigate the prognostic value of the frontal QRS-T angle associated with adverse cardiac outcomes in patients with carbon monoxide (CO) poisoning in early stages in the emergency department. Materials and methods The data of 212 patients with CO poisoning who were admitted to the ED between January 2010 and May 2020 were retrospectively analyzed. The frontal QRS-T angle was obtained from the automatic reports of the EKG device. Results Compared to patients without myocardial damage, among patients with myocardial damage, statistically high creatinine, creatine kinase MB, cardiac troponin I, and frontal QRS-T angle values were found ( p < 0.001 for all parameters), while the saturation of arterial blood pH and arterial oxygen values were found to be lower ( p = 0.002 and p < 0.001, respectively). The frontal QRS-T angle values were correlated with creatine kinase, creatine kinase-MB, cardiac troponin I, and oxygen saturation (SpO2) in arterial blood (r = 0. 232, p = 0.001; r = 0. 253, p = < 0.001; r = 0. 389, p = < 0.001; r = −0. 198, p = 0.004, respectively). The optimum cut-off value of the frontal QRS-T angle was found to be 44.5 (area under the curve: 0.901, 95% confidence interval: 0.814–0.988, sensitivity: 87%, specificity: 84%). Conclusions The frontal QRS-T angle, a simple and inexpensive parameter that can be easily obtained from 12-lead surface electrocardiography, can be used as an early indicator in the detection of myocardial damage in patients with CO poisoning.

Download Full-text

Impact of Antibody Specificity and Calibration Material on the Measure of Agreement between Methods for Cardiac Troponin I

Clinical Chemistry ◽

10.1093/clinchem/45.6.822 ◽

1999 ◽

Vol 45 (6) ◽

pp. 822-828 ◽

Cited By ~ 20

Author(s):

David J Newman ◽

Yemi Olabiran ◽

William D Bedzyk ◽

Suzette Chance ◽

Eileen G Gorman ◽

...

Keyword(s):

Creatine Kinase ◽

Regression Analysis ◽

Cardiac Troponin ◽

Troponin I ◽

Cardiac Troponin I ◽

Antibody Specificity ◽

Serum Pool ◽

Creatine Kinase Mb ◽

Patient Values ◽

Calibration Material

Abstract Background: Available assays for cardiac troponin I (cTnI) yield numerically different results. The aim of this study was to compare patient values obtained from four cTnI immunoassays. Methods: We studied the Stratus® II assay, the Opus® II assay, the Access® assay, and a research-only cTnI heterogeneous immunoassay that uses the Dade Behring aca® plus immunoassay system equipped with two new noncommercial monoclonal antibodies. Because the aca plus cTnI assay is for research only, we first evaluated and analytically validated it for serum and citrated plasma. Initially, each method was calibrated using the method-specific calibrator supplied by each manufacturer; however, the aca plus cTnI assay was calibrated using patient serum pools containing cTnI and selected on the basis of increased creatine kinase MB isoenzyme and with values assigned by use of the Stratus cTnI assay. For method comparisons, individual patient sample cTnI values were determined and compared with the Stratus II assay. Results: Passing and Bablock regression analysis yielded slopes of 1.44 (r = 0.96; n = 72) for the Opus II vs Stratus II assays; 0.07 (r = 0.91; n = 72) for the Access vs Stratus II assays; and 0.90 (r = 0.91, n = 72) for the aca plus vs Stratus II assays. The recalibration of each method with a Stratus II-assigned serum pool improved, but did not entirely eliminate, the slope differences between the different assays (range, 1.00–1.16). The observed scatter in the correlation curves remained. Conclusion: There is a need to further explore the specificities of these assays with respect to the different circulating forms of cTnI.

Download Full-text

Comparable detection of acute myocardial infarction by creatine kinase MB isoenzyme and cardiac troponin I

Clinical Chemistry ◽

10.1093/clinchem/40.7.1291 ◽

1994 ◽

Vol 40 (7) ◽

pp. 1291-1295 ◽

Cited By ~ 197

Author(s):

J E Adams ◽

K B Schechtman ◽

Y Landt ◽

J H Ladenson ◽

A S Jaffe

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Creatine Kinase ◽

Cardiac Troponin ◽

Troponin I ◽

Characteristic Curve ◽

Cardiac Injury ◽

Cardiac Troponin I ◽

Creatine Kinase Mb ◽

Coronary Care

Abstract Although measurement of cardiac troponin I (cTnI) is, in some situations, more specific for detection of cardiac injury than is measurement of the MB isoenzyme of creatine kinase (MBCK), its sensitivity and specificity relative to MBCK for detection of myocardial infarction has not been established. Accordingly, we studied prospectively 199 consecutive patients admitted to the coronary care unit. Values of MBCK and cTnI mass were determined in all samples. Of the 188 patients admitted with a suspicion of acute myocardial ischemia, 89 were diagnosed as having an acute myocardial infarction on the basis of the patterns of MBCK values. Eighty-six of these patients also had increased cTnI (concordance, 96.6%); three did not. Of the patients diagnosed as without infarction, five with unstable angina and symptoms in the day(s) prior to admission had increased cTnI, for a cTnI specificity of 94.9%. Receiver operating characteristic curve analysis indicated that cTnI and MBCK had statistically indistinguishable diagnostic accuracies for the detection of acute myocardial infarction.

Download Full-text

P4420Is exercise-induced cardiac troponin release caused by skeletal muscle injury?

European Heart Journal ◽

10.1093/eurheartj/ehz745.0822 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

T Paana ◽

S Jaakkola ◽

E Tuunainen ◽

S Wittfooth ◽

K Bamberg ◽

...

Keyword(s):

Skeletal Muscle ◽

Cardiac Troponin ◽

Muscle Injury ◽

Troponin I ◽

Troponin T ◽

Skeletal Muscle Injury ◽

Coronary Syndrome ◽

Marathon Race ◽

Recreational Runners ◽

Exercise Induced

Abstract Background Cardiac troponins (cTn) are highly sensitive and specific markers for cardiac injury and a key element in the diagnosis of acute coronary syndrome. Strenuous exercise is known to induce increases in cTn, but the causative factors remain ambiguous. It is also equivocal whether exercise induced skeletal muscle injury is associated with cTn elevation. Purpose The aim of this study was to identify independent predictors for the rise in cardiac troponin T (cTnT) and I (cTnI) concentration and to focus on the relationship between skeletal muscle injury measured by skeletal troponin I (skTnI) and cTn elevations after a marathon race in a large group of male recreational runners. Methods A total of 40 recreational runners participating in the marathon in our city were recruited. The study included baseline visit (prerace) and immediate post-race sampling. Results The post-marathon cTnT concentration rose above the reference limit in 38 (95%) participants and the detection limit for cTnI was exceeded in 34 (85%) participants. Similarly, a 10-fold increase in skTnI concentration was observed and elevated post-race values were seen in all participants. There was no significant correlation between the post-race cTnT or cTnT change and post-race skTnI (Spearman's rho = 0.249, p=0.122, rho = 0.285, p=0.074). However, post-race cTnI and change in cTnI were associated with post-race skTnI (rho = 0.404, p=0.01, rho = 0.460, p=0.003) and creatine kinase (r=0.368, p=0.019) concentration. Subjective exertion or self-reported muscle symptoms did not correlate with post-race cTnT, cTnI or skTnI levels. Post-Race cTnT <40 Post-Race cTnT ≥40 p-value n=18 n=22 Age, years 53.3±12.2 44.0±11.9 0.002 Active training, years 12.0 (9.3) 17.0 (15.8) 0.190 Muscle symptoms 7 (38.9) 11 (52.4) 0.523 Creatinine kinase, ug/l 406 (137) 399 (319) 0.163 N-terminal proBNP ng/l 137±168 158±277 0.783 Skeletal Troponin I, ng/ml 28.6 (41) 56.7 (143) 0.199 Figure 1 Conclusions Cardiac troponin became abnormal in almost all runners after marathon race. The exercise-induced rise in cardiac troponin I is related to simultaneous release of skeletal troponin I. The mechanism of this association remains uncertain, but clinicians should be cautious when interpreting post-exercise troponin levels without clinical symptoms and signs of myocardial ischemia.

Download Full-text