{"id":{"repo_id":"bielefeld","oai_identifier":"oai:pub.uni-bielefeld.de:2994479"},"canonical_url":"https://search.dev.ndltd.org/etd/bielefeld/oai:pub.uni-bielefeld.de:2994479","repository":{"repo_id":"bielefeld","name":"Universität Bielefeld","base_url":"https://pub.uni-bielefeld.de/oai"},"display":{"title":"Erhöhung des hochsensitiven kardialen Troponin T bei Erkrankungen mit nicht-atherothrombotischer Myokardischämie","abstract":"#### Background: Elevated levels of high-sensitivity troponin T (hsTnT) indicate myocardial damage and can establish the diagnosis of acute coronary syndrome (ACS). However, also diseases without coronary artery occlusion can cause an elevated hsTnT, such as bradycardia, atrial fibrillation (AF), cerebral ischemia (CI), pulmonary embolism (PE), heart failure (HF), impaired kidney function and other disease states. This raises the question whether a hsTnT threshold level can be determined, above which an ACS is likely, and appropriate therapeutic steps should be undertaken, while a non-atherothrombotic cause is unlikely. To answer this question, we measured the hsTnT in patients with one of the diseases that can cause elevated hsTnT as outlined above in whom an ACS was excluded. We compared hsTnT values in different diseases and subgroups and evaluated if hsTnT unrelated to an ACS was associated with intrahospital death. #### Methods: Data from patients treated in a single center between 2019 and 2022 were retrospectively analyzed. Of 4302 initially screened patients, 1850 patients were considered for analysis after exclusion of patients without hsTnT measurements or with an ACS or heart surgery. Using SPSS, parametric tests (t-tests), non-parametric tests (Mann-Whitney-U-Test), and the Chi-Square test were applied for statistical analysis, and regression, correlation analysis, and ROC curve analysis were applied. A p-value < 0.05 was considered as significant. #### Results: We analyzed 425 patients with HF, 360 patients with bradycardia, 411 patients with AF, 325 patients with PE and 329 patients with CI. Of these 1850 patients without an ACS, 1410 (76%) had elevated hsTnT levels. In 95% of patients with severe HF at rest hsTnT were elevated, while only 65% of patients with AF showed elevated hsTnT. The highest mean hsTnT was found in patients with PE (92 pg/ml; median 41 pg/ml), and the lowest average and median hsTnT level was found in patients with AF (22 pg/ml; median 16 pg/ml). In 78% with bradycardia, an elevated hsTnT value was present (mean 32 pg/ml; median 25 pg/ml). The heart rate in bradycardia as well as in AF, and the duration of AF (days, weeks, months, or years) did not affect the level of hsTnT. The level of renal impairment correlated with hsTnT results. In patients with reduced eGFR (< 60 (ml/min)/1.73 m2), an increase in hsTnT ≥ 14 pg/ml was found in 747 of 816 patients (92%) and ≥ 100 pg/ml in 108/816 (13%) patients. In patients with PE and CI, hsTnT predicted in-hospital mortality with an AUC of 0,79 (p<0.001, 95% CI 0.73-0.84); and 0.712 (p<0.001; 95% CI 0.63-0.79). #### Conclusions: Elevated hsTnT levels are common in patients with AF, CI, PE, bradycardia and HF without an atherothrombotic ACS but rarely reach values < 100 pg/ml. In >90% of patients with highly impaired kidney function, hsTnT levels are elevated, frequently even >100pg/ml. Bradycardia and tachyarrhythmia lead to mild hsTnT elevations, unrelated to the heart rate and persistence of the arrhythmia. In patients with PE and CI, hsTnT predicted-in-hospital mortality.","abstract_html":"#### Background: Elevated levels of high-sensitivity troponin T (hsTnT) indicate myocardial damage and can establish the diagnosis of acute coronary syndrome (ACS). However, also diseases without coronary artery occlusion can cause an elevated hsTnT, such as bradycardia, atrial fibrillation (AF), cerebral ischemia (CI), pulmonary embolism (PE), heart failure (HF), impaired kidney function and other disease states. This raises the question whether a hsTnT threshold level can be determined, above which an ACS is likely, and appropriate therapeutic steps should be undertaken, while a non-atherothrombotic cause is unlikely. To answer this question, we measured the hsTnT in patients with one of the diseases that can cause elevated hsTnT as outlined above in whom an ACS was excluded. We compared hsTnT values in different diseases and subgroups and evaluated if hsTnT unrelated to an ACS was associated with intrahospital death. #### Methods: Data from patients treated in a single center between 2019 and 2022 were retrospectively analyzed. Of 4302 initially screened patients, 1850 patients were considered for analysis after exclusion of patients without hsTnT measurements or with an ACS or heart surgery. Using SPSS, parametric tests (t-tests), non-parametric tests (Mann-Whitney-U-Test), and the Chi-Square test were applied for statistical analysis, and regression, correlation analysis, and ROC curve analysis were applied. A p-value &lt; 0.05 was considered as significant. #### Results: We analyzed 425 patients with HF, 360 patients with bradycardia, 411 patients with AF, 325 patients with PE and 329 patients with CI. Of these 1850 patients without an ACS, 1410 (76%) had elevated hsTnT levels. In 95% of patients with severe HF at rest hsTnT were elevated, while only 65% of patients with AF showed elevated hsTnT. The highest mean hsTnT was found in patients with PE (92 pg/ml; median 41 pg/ml), and the lowest average and median hsTnT level was found in patients with AF (22 pg/ml; median 16 pg/ml). In 78% with bradycardia, an elevated hsTnT value was present (mean 32 pg/ml; median 25 pg/ml). The heart rate in bradycardia as well as in AF, and the duration of AF (days, weeks, months, or years) did not affect the level of hsTnT. The level of renal impairment correlated with hsTnT results. In patients with reduced eGFR (&lt; 60 (ml/min)/1.73 m2), an increase in hsTnT ≥ 14 pg/ml was found in 747 of 816 patients (92%) and ≥ 100 pg/ml in 108/816 (13%) patients. In patients with PE and CI, hsTnT predicted in-hospital mortality with an AUC of 0,79 (p&lt;0.001, 95% CI 0.73-0.84); and 0.712 (p&lt;0.001; 95% CI 0.63-0.79). #### Conclusions: Elevated hsTnT levels are common in patients with AF, CI, PE, bradycardia and HF without an atherothrombotic ACS but rarely reach values &lt; 100 pg/ml. In &gt;90% of patients with highly impaired kidney function, hsTnT levels are elevated, frequently even &gt;100pg/ml. Bradycardia and tachyarrhythmia lead to mild hsTnT elevations, unrelated to the heart rate and persistence of the arrhythmia. In patients with PE and CI, hsTnT predicted-in-hospital mortality.","abstract_has_math":false,"creators":["Angleitner, Alexander Casimir"],"institution":"Universität Bielefeld","degree_name":null,"degree_level":"thesis.doctoral","degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2024,"date_issued":"2024-11-05","date_published":"2024-11-05","updated_at":"2026-07-27T18:50:01Z","subjects":[],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://pub.uni-bielefeld.de/record/2994479","outbound_label":"Repository record","outbound_source":"source_url"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Angleitner, Alexander Casimir"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:publisher","label":"Institution","values":["Universitätsbibliothek Bielefeld"]},{"key":"dc:type","label":"Dc Type","values":["doctoralThesis"]},{"key":"thesis:degree_level","label":"Degree Level","values":["thesis.doctoral"]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["Universität Bielefeld"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["#### Background: Elevated levels of high-sensitivity troponin T (hsTnT) indicate myocardial damage and can establish the diagnosis of acute coronary syndrome (ACS). However, also diseases without coronary artery occlusion can cause an elevated hsTnT, such as bradycardia, atrial fibrillation (AF), cerebral ischemia (CI), pulmonary embolism (PE), heart failure (HF), impaired kidney function and other disease states. This raises the question whether a hsTnT threshold level can be determined, above which an ACS is likely, and appropriate therapeutic steps should be undertaken, while a non-atherothrombotic cause is unlikely. To answer this question, we measured the hsTnT in patients with one of the diseases that can cause elevated hsTnT as outlined above in whom an ACS was excluded. We compared hsTnT values in different diseases and subgroups and evaluated if hsTnT unrelated to an ACS was associated with intrahospital death. #### Methods: Data from patients treated in a single center between 2019 and 2022 were retrospectively analyzed. Of 4302 initially screened patients, 1850 patients were considered for analysis after exclusion of patients without hsTnT measurements or with an ACS or heart surgery. Using SPSS, parametric tests (t-tests), non-parametric tests (Mann-Whitney-U-Test), and the Chi-Square test were applied for statistical analysis, and regression, correlation analysis, and ROC curve analysis were applied. A p-value < 0.05 was considered as significant. #### Results: We analyzed 425 patients with HF, 360 patients with bradycardia, 411 patients with AF, 325 patients with PE and 329 patients with CI. Of these 1850 patients without an ACS, 1410 (76%) had elevated hsTnT levels. In 95% of patients with severe HF at rest hsTnT were elevated, while only 65% of patients with AF showed elevated hsTnT. The highest mean hsTnT was found in patients with PE (92 pg/ml; median 41 pg/ml), and the lowest average and median hsTnT level was found in patients with AF (22 pg/ml; median 16 pg/ml). In 78% with bradycardia, an elevated hsTnT value was present (mean 32 pg/ml; median 25 pg/ml). The heart rate in bradycardia as well as in AF, and the duration of AF (days, weeks, months, or years) did not affect the level of hsTnT. The level of renal impairment correlated with hsTnT results. In patients with reduced eGFR (< 60 (ml/min)/1.73 m2), an increase in hsTnT ≥ 14 pg/ml was found in 747 of 816 patients (92%) and ≥ 100 pg/ml in 108/816 (13%) patients. In patients with PE and CI, hsTnT predicted in-hospital mortality with an AUC of 0,79 (p<0.001, 95% CI 0.73-0.84); and 0.712 (p<0.001; 95% CI 0.63-0.79). #### Conclusions: Elevated hsTnT levels are common in patients with AF, CI, PE, bradycardia and HF without an atherothrombotic ACS but rarely reach values < 100 pg/ml. In >90% of patients with highly impaired kidney function, hsTnT levels are elevated, frequently even >100pg/ml. Bradycardia and tachyarrhythmia lead to mild hsTnT elevations, unrelated to the heart rate and persistence of the arrhythmia. In patients with PE and CI, hsTnT predicted-in-hospital mortality."]},{"key":"dc:format.medium","label":"Dc Format Medium","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Erhöhung des hochsensitiven kardialen Troponin T bei Erkrankungen mit nicht-atherothrombotischer Myokardischämie"]}]}],"canonical_facts":{"dc:creator":["Angleitner, Alexander Casimir"],"dc:description.abstract":["#### Background: Elevated levels of high-sensitivity troponin T (hsTnT) indicate myocardial damage and can establish the diagnosis of acute coronary syndrome (ACS). However, also diseases without coronary artery occlusion can cause an elevated hsTnT, such as bradycardia, atrial fibrillation (AF), cerebral ischemia (CI), pulmonary embolism (PE), heart failure (HF), impaired kidney function and other disease states. This raises the question whether a hsTnT threshold level can be determined, above which an ACS is likely, and appropriate therapeutic steps should be undertaken, while a non-atherothrombotic cause is unlikely. To answer this question, we measured the hsTnT in patients with one of the diseases that can cause elevated hsTnT as outlined above in whom an ACS was excluded. We compared hsTnT values in different diseases and subgroups and evaluated if hsTnT unrelated to an ACS was associated with intrahospital death. #### Methods: Data from patients treated in a single center between 2019 and 2022 were retrospectively analyzed. Of 4302 initially screened patients, 1850 patients were considered for analysis after exclusion of patients without hsTnT measurements or with an ACS or heart surgery. Using SPSS, parametric tests (t-tests), non-parametric tests (Mann-Whitney-U-Test), and the Chi-Square test were applied for statistical analysis, and regression, correlation analysis, and ROC curve analysis were applied. A p-value < 0.05 was considered as significant. #### Results: We analyzed 425 patients with HF, 360 patients with bradycardia, 411 patients with AF, 325 patients with PE and 329 patients with CI. Of these 1850 patients without an ACS, 1410 (76%) had elevated hsTnT levels. In 95% of patients with severe HF at rest hsTnT were elevated, while only 65% of patients with AF showed elevated hsTnT. The highest mean hsTnT was found in patients with PE (92 pg/ml; median 41 pg/ml), and the lowest average and median hsTnT level was found in patients with AF (22 pg/ml; median 16 pg/ml). In 78% with bradycardia, an elevated hsTnT value was present (mean 32 pg/ml; median 25 pg/ml). The heart rate in bradycardia as well as in AF, and the duration of AF (days, weeks, months, or years) did not affect the level of hsTnT. The level of renal impairment correlated with hsTnT results. In patients with reduced eGFR (< 60 (ml/min)/1.73 m2), an increase in hsTnT ≥ 14 pg/ml was found in 747 of 816 patients (92%) and ≥ 100 pg/ml in 108/816 (13%) patients. In patients with PE and CI, hsTnT predicted in-hospital mortality with an AUC of 0,79 (p<0.001, 95% CI 0.73-0.84); and 0.712 (p<0.001; 95% CI 0.63-0.79). #### Conclusions: Elevated hsTnT levels are common in patients with AF, CI, PE, bradycardia and HF without an atherothrombotic ACS but rarely reach values < 100 pg/ml. In >90% of patients with highly impaired kidney function, hsTnT levels are elevated, frequently even >100pg/ml. Bradycardia and tachyarrhythmia lead to mild hsTnT elevations, unrelated to the heart rate and persistence of the arrhythmia. In patients with PE and CI, hsTnT predicted-in-hospital mortality."],"dc:format.medium":["application/pdf"],"dc:publisher":["Universitätsbibliothek Bielefeld"],"dc:title":["Erhöhung des hochsensitiven kardialen Troponin T bei Erkrankungen mit nicht-atherothrombotischer Myokardischämie"],"dc:type":["doctoralThesis"],"thesis:degree_level":["thesis.doctoral"],"thesis:institution_name":["Universität Bielefeld"]},"updated_at":"2026-07-27T18:50:01Z"}