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Longitudinal increases in blood biomarkers of inflammation or cardiovascular disease and the incidence of venous thromboembolism
Author(s): ,
A. R. Folsom
Affiliations:
Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, USA
Correspondence: Aaron R. Folsom, Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, 1300 South 2nd Street, Suite 300, Minneapolis, MN 55454, USA|Tel.: +1 612 626 8862|E‐mail: folso001@umn.edu
,
P. L. Lutsey
Affiliations:
Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, USA
,
S. R. Heckbert
Affiliations:
Department of Epidemiology, University of Washington, Seattle, USA
,
K. Poudel
Affiliations:
Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, USA
,
S. Basu
Affiliations:
Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, USA
,
R. C. Hoogeveen
Affiliations:
Department of Medicine, Baylor College of Medicine and Methodist DeBakey Heart and Vascular Center, Houston, USA
,
M. Cushman
Affiliations:
Department of Medicine, University of Vermont, Burlington, USA. Department of Pathology, University of Vermont, Burlington, USA
C. M. Ballantyne
Affiliations:
Department of Medicine, Baylor College of Medicine and Methodist DeBakey Heart and Vascular Center, Houston, USA
ISTH Academy. R. Folsom A. Oct 4, 2018; 234160
Aaron R. Folsom
Aaron  R. Folsom

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Background
We previously showed that participants in the population‐based Atherosclerosis Risk in Communities (ARIC) cohort with elevated levels of blood biomarkers of inflammation or cardiac disease were at increased risk of venous thromboembolism (VTE).
Objective
We hypothesized that ARIC participants with larger 6‐year increases in the levels of three biomarkers – C‐reactive protein (CRP), N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP), and troponin T – would also have an increased subsequent risk of VTE.
Methods
We measured changes in the levels of these biomarkers in 9844 participants from 1990–1992 to 1996–1998, and then identified VTEs through 2015.
Results
A greater 6‐year rise in the level of NT‐proBNP, but not in that of CRP or troponin T, was significantly associated with increased VTE incidence over a median of 17.6 years of follow‐up. After adjustment for other VTE risk factors, those whose NT‐proBNP level rose from < 100 pg mL to ≥ 100 pg mL had a hazard ratio for VTE of 1.44 (95% confidence interval [CI] 1.15–1.80), as compared with the reference group with an NT‐proBNP level of < 100 pg mL at both times. This hazard ratio was slightly higher (1.66, 95% CI 1.19–2.31) during the first 10 years of follow‐up, but was attenuated (1.24, 95% CI 0.99–1.56) after adjustment for prevalent and incident coronary heart disease, heart failure, and atrial fibrillation.
Conclusions
The two most likely explanations for our results are that: (i) an increasing NT‐proBNP level reflects increasing subclinical volume overload and potentially increased venous stasis or subclinical PE that had gone unrecognized over time; or (ii) an increasing NT‐proBNP level is a risk marker for impending cardiac disease that places patients at risk of VTE.
Keyword(s)
Atherosclerosis Risk in Communities Study, C‐reactive protein, NT‐proBNP, troponin, venous thromboembolism
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