Public Defence: Sjur Hansen Tveit
Cand.med Sjur Hansen Tveit at Institute of Clinical Medicine will be defending the thesis “Cardiac Troponin I and T: Comparison of the Diagnostic and Prognostic Performance in Coronary Artery Disease” for the degree of PhD (Philosophiae Doctor).
Photo: Felix Haidl.
An electronic copy of the thesis may be ordered from the faculty up to 2 days prior to the public defence. Inquiries regarding the thesis after the public defence must be addressed to the candidate.
Trial Lecture – time and place
See Trial Lecture.
- First opponent: Associate Professor Ziad Hijazi, Uppsala University and Uppsala Clinical Research Center
- Second opponent: Clinical Lecturer Andrew R. Chapman, Center for Cardiovascular Science, University of Edinburgh
- Third member and chair of the evaluation committee: Professor Mathis Korseberg Stokke, University of Oslo
Chair of the Defence
Professor Vidar Søyseth, Faculty of Medicine, University of Oslo
Associate Professor Peder L. Myhre, Faculty of Medicine, University of Oslo
Cardiac specific troponin I and T (cTnI, cTnT) are well established biomarkers in patients presenting with suspected myocardial infarction. However, the clinical implementation of biochemical assays with superior analytical sensitivity might enable the utilization of both isotypes in novel diagnostic and prognostic pathways. Further, mounting evidence suggests differential association between the two isotypes and patient and disease characteristics. In this thesis we demonstrate the differential diagnostic and prognostic efficacy of cTnI and cTnT, measured with high sensitivity assays, in patients with acute and chronic coronary syndromes.
In patients with chronic coronary syndrome, elevated concentrations of cTnI and cTnT were associated with traditional risk factors for cardiovascular disease, such as old age, high blood pressure and diabetes, and there was a graded relationship between increased concentrations of cardiac troponins and the degree of coronary artery disease. However, the diagnostic power of troponin was dependent on the patients’ baseline cardiovascular risk profile, with an attenuation of efficacy in higher risk patients. Further, although considered diagnostically equivalent in patients with acute coronary syndrome, baseline cTnI concentrations appeared to be a better diagnostic marker of coronary artery disease than cTnT. In contrast, we found cTnT to be a superior predictor of long-term all-cause mortality in patients with acute coronary syndromes without myocardial infarction, despite the superior analytical sensitivity of the cTnI assay.
Although both isoforms provide useful clinical information, our research suggests differential associations with patient and disease characteristics and support the use of cTn in certain settings of acute and chronic coronary syndromes. It further highlights the importance of a nuanced interpretation of troponin concentrations in any clinical context.