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

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Paana ◽  
S Jaakkola ◽  
E Tuunainen ◽  
S Wittfooth ◽  
K Bamberg ◽  
...  

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.

Author(s):  
Mary McLaurin ◽  
Fred S Apple ◽  
Timothy D Henry ◽  
Scott W Sharkey

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.


2016 ◽  
Vol 49 (6) ◽  
pp. 421-432 ◽  
Author(s):  
Seoung Mann Sou ◽  
Christian Puelacher ◽  
Raphael Twerenbold ◽  
Max Wagener ◽  
Ursina Honegger ◽  
...  

2007 ◽  
Vol 40 (5-6) ◽  
pp. 423-426 ◽  
Author(s):  
Salim Fredericks ◽  
Hans Degens ◽  
Godfrina McKoy ◽  
Katie Bainbridge ◽  
Paul O. Collinson ◽  
...  

2021 ◽  
Author(s):  
Prima Hapsari Wulandari

Abstract The severe and acute manifestation of coronary artery disease (CAD) is acute coronary syndrome (ACS); therefore, prompt diagnosis can save lives. Cardiac biomarkers that are accepted to use in evaluating ACS are creatine kinase muscle/brain subtype (CK-MB), cardiac troponin I (CTnI), or cardiac troponin T (CTnT). However, these markers have several drawbacks, such as prolonged time to rise for prompt diagnosis and elevation in patients with chronic kidney diseases (CKD). Lately, potential, novel candidates for cardiac ischemia biomarkers have been developed, one of which is micro-ribonucleic acids (miRNAs). miRNAs are potential due to their remarkable reproducibility and stability. Several miRNAs, such as, miR-1, miR-133a, miR-133b, miR-208a, miR-208b, and miR-499a, greatly rise in concentration in the plasma or serum of patients with acute cardiac ischemia, signifying their cardiac specificity and promising biomarkers in patients with ACS. This systematic review aims to elucidate the role of cardio-specific miRNA in acute myocardial ischemia (AMI) and its relationship with other cardiac biomarkers.


2000 ◽  
Vol 46 (9) ◽  
pp. 1338-1344 ◽  
Author(s):  
Hugo Stiegler ◽  
Yuriko Fischer ◽  
Jaime F Vazquez-Jimenez ◽  
Jürgen Graf ◽  
Karsten Filzmaier ◽  
...  

Abstract Background: The use of plasma rather than serum for determination of cardiac troponins can improve turnaround time and potentially avoid incomplete serum separation that may produce falsely increased results. We investigated the influence of incomplete serum separation and the effect of heparin-plasma on cardiac troponin concentrations. Methods: Serum and heparin-plasma samples were drawn simultaneously from 100 patients (50 patients with acute coronary syndrome and 50 patients after open heart surgery) and measured on three different analytical systems, two for determination of cardiac troponin I (cTnI; Abbott AxSYM and Bayer ACS:Centaur) and one for cardiac troponin T (cTnT; Roche Elecsys cTnT STAT). Serum samples were reanalyzed after a second centrifugation to assess the influence of incomplete serum separation. Results: Mean results (± 95% confidence interval) in heparin-plasma compared with serum were 101% ± 2% (AxSYM cTnI), 94% ± 3% (ACS:Centaur cTnI), and 99% ± 3% (Elecsys cTnT). Differences &gt;20% were seen in 11% of results on the ACS:Centaur, 9% of results on Elecsys cTnT, and 2% of results on the AxSYM. For the Elecsys cTnT assay, the magnitude of the difference between serum and plasma was independent of the absolute concentration and confined to individual samples, and was reversed by treatment with heparinase. A second centrifugation had no effect on serum results by any of the assays. Conclusion: The concentrations of troponins measured in heparin-plasma are markedly lower than in serum in some cases.


2020 ◽  
Vol 27 (4) ◽  
pp. e72-e79 ◽  
Author(s):  
Congcong Fu ◽  
Yu Xia ◽  
Fan Meng ◽  
Fei Li ◽  
Qiang Liu ◽  
...  

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