Purpose: As cardiac troponins emerge as prognostic markers in atrial fibrillation (AF), it is important to identify mechanisms initiating and perpetuating cardiac troponin release, including its relations to other circulating biomarkers, in AF populations. We studied associations between high-sensitivity troponin I (hs-TnI) and markers representing myocardial wall tension, inflammation and haemostasis in persistent AF.
Methods: In a double blind, placebo-controlled study, 171 patients referred for electrical cardioversion for persistent AF were randomised to receive candesartan or placebo for 3-6 weeks before and 6 months after cardioversion. Associations between baseline levels of hs-TnI and other biomarkers were investigated by bivariate non-parametric correlations (Spearman's correlation coefficient denoted rs).
Results: Baseline levels of hs-TnI correlated significantly, although weakly, with interleukin-6 (rs = 0.260, p = .003), N-terminal pro-B-type natriuretic peptide (rs = 0.251, p = .004), tissue-plasminogen activator antigen (rs = 0.233, p = .008), D-dimer (rs = 0.220, p = .013), E-selectin (rs = 0.207, p = .019), high-sensitivity C-reactive protein (rs = 0.202, p = .022) and vascular cell adhesion molecule-1 (rs = 0.189, p = .032).
Conclusions: Hs-TnI correlated weakly with biomarkers representing myocardial wall tension, inflammation and haemostasis in persistent AF. The lack of any strong correlation between hs-TnI and the investigated biomarkers is in concert with the idea that hs-TnI release is an independent process parallel to other pathophysiological mechanisms associated with AF.
Keywords: Atrial fibrillation; CHA2DS2-VASc score; biomarkers; cardiac troponins; cardiology; endothelial activation; haemostasis; high-sensitivity troponin I; inflammation.