Abstract 14527: Temporal Changes in Cardiac Troponin I and Risk ofCardiovascular Events in the General Population: The Nord-Trøndelag Health Study
Introduction: Concentrations of cardiac troponin are strongly associated with risk of heart failure (HF), myocardial infarction (MI), and cardiovascular death (CVD) in the general population. Temporal changes in cardiac troponin T have also been associated with increased cardiovascular risk, but the corresponding association for cardiac troponin I (cTnI) remains unclear.
Hypothesis: Temporal changes in cTnI are associated with risk of HF, MI, and CVD in the general population.
Methods: We measured cTnI with a high-sensitivity assay in 4803 participants of the prospective observational HUNT Study, at study visit 2 (1995-97) and visit 3 (2006-2008). All subjects were free from known cardiovascular disease at baseline. Change in cTnI was modeled as change of <50%, increase of ≥50%, or decrease of ≥50% from concentrations at visit 2. A composite endpoint of first admission for MI or HF, or CVD was generated.
Results: Participants with relative decrease in cTnI were more frequently younger and female, and had lower blood pressure, body mass index, blood lipids and glucose. Participant with relative increase in cTnI were more frequently older and male, with higher systolic blood pressure and blood lipids. After a median follow-up time of 1326 days, 70 events for the composite endpoint were registered. The incidence rate was 21.0/1000 patient-years for study participants with relative increase in cTnI, and 1.8/1000 patient-years for participants with relative decrease in cTnI (p<0.001). This finding was reflected in Kaplan-Meier survival curves according to relative changes in cTnI (Figure). The adjusted hazard ratio (HR) associated with relative decrease in cTnI was 1.60 (0.78-3.25). The corresponding adjusted HR for relative increase in cTnI was 2.43 (1.28-4.58).
Conclusions: Relative increase in cTnI is independently associated with risk of HF, MI, and CVD. Serial measurements of cardiac troponin could provide guidance in individual risk prediction.
Author Disclosures: M.N. Lyngbakken: None. H. Røsjø: Honoraria; Modest; Personal fee from Novartis. O.L. Holmen: None. H. Dalen: None. K. Hveem: None. T. Omland: Research Grant; Modest; Grants from Abbott Diagnostics and Astra Zeneca,. Other Research Support; Modest; Non-financial support from Astra Zeneca, Thermo Fisher, and Biomedica. Honoraria; Modest; Personal fees from Abbott Diagnostics, Roche Diagnostics, and Novartis.
- © 2017 by American Heart Association, Inc.