Anja Wiedswang Horjen has looked at the impact of atrial fibrillation on high-sensitivity troponin I levels in the elderly.
- Atrial fibrillation is not independently associated with increased high-sensitivity troponin I in elderly.
- Rate control drugs reduce troponin I in patients with permanent atrial fibrillation.
- High-sensitivity troponin I levels do not predict recurrence of atrial fibrillation after cardioversion.
Thesis: High-Sensitivity Troponin I in Atrial Fibrillation – Impact of rate and rhythm control and associations with biomarkers related to atrial fibrillation pathophysiology
Candidate: Anja Wiedswang Horjen
Time: October 19, 2018 at 12:15
Place: University of Oslo, Domus Academica: Gamle festsal
Link to university website (in Norwegian)
(1) 75-year-olds with atrial fibrillation have higher levels of troponin I, a marker of cardiac damage, compared to peers without atrial fibrillation. However, the difference is explained by other cardiovascular diseases. Horjen and co-workers measured high-sensitivity troponin I in 62 elderly with and 126 without atrial fibrillation. After adjustments for heart failure, coronary heart disease and stroke, the levels did not differ between the two groups.
(2) Beta blockers and calcium channel blockers reduce troponin I levels in patients with permanent atrial fibrillation. The 60 participants received four drugs in random order, and all of them lowered troponin I during rest and hard exercise.
(3/4) The levels of troponin I are unchanged six months after cardioversion for permanent atrial fibrillation. Baseline levels did not predict recurrence of atrial fibrillation after electrical cardioversion. 171 patients referred to cardioversion were randomized to receive either candesartan or placebo during the study period, but the drug did not affect the levels of troponin I. Furthermore, sustained sinus rhythm for six months following cardioversion had no impact on markers of thrombin generation.
(5) High-sensitive troponin I is weakly associated with several inflammatory markers in patients with persistent atrial fibrillation. The weak associations indicate that troponin I-release is a process parallel to other pathophysiological mechanisms associated with atrial fibrillation.
(1) Horjen, A. W., Ulimoen, S. R., Enger, S., Berge, T., Ihle-Hansen, H., Norseth, J., & Tveit, A. (2015). Impact of atrial fibrillation on levels of high-sensitivity troponin I in a 75-year-old population. Scandinavian journal of clinical and laboratory investigation, 75(4), 308-313.
(2) Horjen, A. W., Ulimoen, S. R., Enger, S., Norseth, J., Seljeflot, I., Arnesen, H., & Tveit, A. (2016). Troponin I levels in permanent atrial fibrillation—impact of rate control and exercise testing. BMC cardiovascular disorders, 16(1), 79.
(3) Horjen, A. W., Ulimoen, S. R., Seljeflot, I., Smith, P., Arnesen, H., Norseth, J., & Tveit, A. (2016). High-sensitivity troponin I and rhythm outcome after electrical cardioversion for persistent atrial fibrillation. Cardiology, 133(4), 233-238.
(4) Horjen, A. W., Seljeflot, I., Berge, T., Smith, P., Arnesen, H., & Tveit, A. (2017). Effect of sinus rhythm restoration on markers of thrombin generation in atrial fibrillation. Thrombosis journal, 15(1), 30.
(5) Horjen, A. W., Ulimoen, S. R., Norseth, J., Svendsen, J. H., Smith, P., Arnesen, H., Seljeflot, I., & Tveit, A. (2018). High-sensitivity troponin I in persistent atrial fibrillation–relation to NT-proBNP and markers of inflammation and haemostasis. Scandinavian Journal of Clinical and Laboratory Investigation, 1-7.