C-reactive protein, obesity, and the risk of arterial and venous thrombosis

L D Horvei; G Grimnes; K Hindberg; E B Mathiesen; I Njølstad; T Wilsgaard; J Brox; S K Braekkan; J-B Hansen

doi:10.1111/jth.13369

C-reactive protein, obesity, and the risk of arterial and venous thrombosis

J Thromb Haemost. 2016 Aug;14(8):1561-71. doi: 10.1111/jth.13369. Epub 2016 Jun 22.

Authors

L D Horvei^{1

2

3}, G Grimnes^{1

2

3}, K Hindberg^{1

2}, E B Mathiesen^{1

4}, I Njølstad^{1

5}, T Wilsgaard⁵, J Brox^{1

6}, S K Braekkan^{1

2

3}, J-B Hansen^{1

2

3}

Affiliations

¹ K. G. Jebsen Thrombosis Research and Expertise Center, Department of Clinical Medicine, UiT The Arctic University of Norway, Tromsø, Norway.
² Hematologic Research Group, Department of Clinical Medicine, UiT The Arctic University of Norway, Tromsø, Norway.
³ Division of Internal Medicine, University Hospital of North Norway, Tromsø, Norway.
⁴ Brain and Circulation Research Group, Department of Clinical Medicine, UiT The Arctic University of Norway, Tromsø, Norway.
⁵ Department of Community Medicine, UiT The Arctic University of Norway, Tromsø, Norway.
⁶ Department of Laboratory Medicine, University Hospital of North Norway, Tromsø, Norway.

PMID: 27208592
DOI: 10.1111/jth.13369

Abstract

Essentials We performed repeated measurements of C-reactive protein (CRP) and obesity in a cohort study. CRP was associated with risk of myocardial infarction and venous thromboembolism. CRP was a mediator for risk of myocardial infarction in obese men and women. CRP was a partial mediator for risk of venous thromboembolism in obese women, but not in men.

Summary: Background Low-grade inflammation in obesity may be a shared pathway for the risk of venous thromboembolism (VTE) and myocardial infarction (MI). Objectives To investigate the associations between repeated measurements of C-reactive protein (CRP) and the risks of MI and VTE, and to explore whether CRP mediated these risks in obese subjects. Methods CRP and obesity measures were collected from 15 134 subjects who participated in one or more surveys of the Tromsø study in 1994-1995, 2001-2002, or 2007-2008. Incident VTEs and MIs were registered until 1 January 2011. Time-varying Cox regression models were used to calculate hazard ratios of MI and VTE according to categories of CRP and obesity measures. Results There were 291 VTEs and 920 MIs during follow-up. High levels of CRP (≥ 3 mg L(-1) versus < 1 mg L(-1) ) were associated with increased risks of MI (hazard ratio [HR] 1.73; 95% confidence interval [CI] 1.32-2.26) and VTE (HR 1.84; 95% CI 1.22-2.78) in women, but only with MI in men (HR 1.93; 95% CI 1.53-2.44). All obesity measures showed stronger associations with CRP in women than in men. In obese women (body mass index [BMI] of ≥ 30 kg m(-2) versus < 25 kg m(-2) ), adjustment for CRP attenuated the risk estimate for VTE by 22%, whereas the incidence rates of VTE increased with combined categories of higher BMI and CRP. No association was found in men. Conclusions Our findings suggest that low-grade inflammation, assessed by measurement of CRP, is associated with the risks of MI and VTE, and may be a shared pathway for MI and VTE in obesity.

Keywords: cardiovascular diseases; inflammation; obesity; risk factors; venous thrombosis.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Adult
Aged
Aged, 80 and over
Arteries / pathology*
Body Mass Index
C-Reactive Protein / analysis*
Female
Humans
Incidence
Male
Middle Aged
Myocardial Infarction / blood*
Myocardial Infarction / pathology
Norway
Obesity / blood*
Proportional Hazards Models
Prospective Studies
Regression Analysis
Risk Factors
Treatment Outcome
Venous Thromboembolism / blood*
Venous Thromboembolism / pathology
Venous Thrombosis / blood*

Substances

C-Reactive Protein