High-sensitivity troponin I in persistent atrial fibrillation – relation to NT-proBNP and markers of inflammation and haemostasis

Abstract

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 r_s).

Results: Baseline levels of hs-TnI correlated significantly, although weakly, with interleukin-6 (r_s = 0.260, p = .003), N-terminal pro-B-type natriuretic peptide (r_s = 0.251, p = .004), tissue-plasminogen activator antigen (r_s = 0.233, p = .008), D-dimer (r_s = 0.220, p = .013), E-selectin (r_s = 0.207, p = .019), high-sensitivity C-reactive protein (r_s = 0.202, p = .022) and vascular cell adhesion molecule-1 (r_s = 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
• biomarkers
• CHA2DS2-VASc score
• cardiac troponins
• cardiology
• endothelial activation
• high-sensitivity troponin I
• haemostasis
• inflammation

Acknowledgements

We thank CAPRAF co-investigator Irene Grundvold, MD, PhD, study nurse Anne Kari Brun, RN, and study nurse Mona Olufsen, RN, Baerum Hospital, for excellent study conduct. We thank Vibeke Bratseth for laboratory analyses at Center for Clinical Heart Research at Department of Cardiology, Oslo University Hospital Ullevål.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This derivation of the CAPRAF study, including the cost of hs-TnI analyses, was supported by Vestre Viken Hospital Trust. The original CAPRAF study was supported by the Regional Health Corporation of Eastern Norway and the Medical Research Foundation, Baerum Hospital, Norway. AstraZeneca, Molndal, Sweden provided the study medication, and AstraZeneca, Oslo, Norway supported the study with a grant to cover for the previous laboratory analyses.