CC BY 4.0 · TH Open 2019; 03(01): e50-e57
DOI: 10.1055/s-0039-1681020
Original Article
Georg Thieme Verlag KG Stuttgart · New York

The Role of Stroke as a Trigger for Incident Venous Thromboembolism: Results from a Population-based Case-Crossover Study

Vânia M. Morelli
1   K. G. Jebsen Thrombosis Research and Expertise Center (TREC), Department of Clinical Medicine, UiT - The Arctic University of Norway, Tromsø, Norway
,
Joakim K. Sejrup
1   K. G. Jebsen Thrombosis Research and Expertise Center (TREC), Department of Clinical Medicine, UiT - The Arctic University of Norway, Tromsø, Norway
,
Birgit Småbrekke
1   K. G. Jebsen Thrombosis Research and Expertise Center (TREC), Department of Clinical Medicine, UiT - The Arctic University of Norway, Tromsø, Norway
,
Ludvig B. Rinde
1   K. G. Jebsen Thrombosis Research and Expertise Center (TREC), Department of Clinical Medicine, UiT - The Arctic University of Norway, Tromsø, Norway
,
Gro Grimnes
1   K. G. Jebsen Thrombosis Research and Expertise Center (TREC), Department of Clinical Medicine, UiT - The Arctic University of Norway, Tromsø, Norway
2   Division of Internal Medicine, University Hospital of North Norway, Tromsø, Norway
,
Trond Isaksen
1   K. G. Jebsen Thrombosis Research and Expertise Center (TREC), Department of Clinical Medicine, UiT - The Arctic University of Norway, Tromsø, Norway
2   Division of Internal Medicine, University Hospital of North Norway, Tromsø, Norway
,
John-Bjarne Hansen
1   K. G. Jebsen Thrombosis Research and Expertise Center (TREC), Department of Clinical Medicine, UiT - The Arctic University of Norway, Tromsø, Norway
2   Division of Internal Medicine, University Hospital of North Norway, Tromsø, Norway
,
Kristian Hindberg
1   K. G. Jebsen Thrombosis Research and Expertise Center (TREC), Department of Clinical Medicine, UiT - The Arctic University of Norway, Tromsø, Norway
2   Division of Internal Medicine, University Hospital of North Norway, Tromsø, Norway
,
Sigrid K. Brækkan
1   K. G. Jebsen Thrombosis Research and Expertise Center (TREC), Department of Clinical Medicine, UiT - The Arctic University of Norway, Tromsø, Norway
2   Division of Internal Medicine, University Hospital of North Norway, Tromsø, Norway
› Author Affiliations
Further Information

Publication History

22 August 2018

21 January 2019

Publication Date:
22 February 2019 (online)

Abstract

Stroke is associated with a short-term increased risk of subsequent venous thromboembolism (VTE). It is unclear to what extent this association is mediated by stroke-related complications that are potential triggers for VTE, such as immobilization and infection. We aimed to investigate the role of acute stroke as a trigger for incident VTE while taking other concomitant VTE triggers into account. We conducted a population-based case-crossover study with 707 VTE patients. Triggers were registered during the 90 days before a VTE event (hazard period) and in four preceding 90-day control periods. Conditional logistic regression was used to estimate odds ratios with 95% confidence intervals (CIs) for VTE according to triggers. Stroke was registered in 30 of the 707 (4.2%) hazard periods and in 6 of the 2,828 (0.2%) control periods, resulting in a high risk of VTE, with odds ratios of 20.0 (95% CI: 8.3–48.1). After adjustments for immobilization and infection, odds ratios for VTE conferred by stroke were attenuated to 6.0 (95% CI: 1.6–22.1), and further to 4.0 (95% CI: 1.1–14.2) when other triggers (major surgery, red blood cell transfusion, trauma, and central venous catheter) were added to the regression model. A mediation analysis revealed that 67.8% of the total effect of stroke on VTE risk could be mediated through immobilization and infection. Analyses restricted to ischemic stroke yielded similar results. In conclusion, acute stroke was a trigger for VTE, and the association between stroke and VTE risk appeared to be largely mediated by immobilization and infection.

Authors' Contributions

V.M. Morelli contributed to statistical analysis and data interpretation, and drafted the manuscript. J.K. Sejrup contributed to data interpretation and draft of the manuscript. L.B. Rinde and B. Småbrekke contributed to data interpretation, and revision of the manuscript. G. Grimnes and T. Isaksen contributed to data collection, data interpretation, and revision of the manuscript. K. Hindberg contributed to statistical analysis, data interpretation, and revision of the manuscript. J.B. Hansen contributed to the conception and design of the study, data interpretation, and revision of the manuscript. S. K. Brækkan contributed to the conception and design of the study, data collection, statistical analysis, data interpretation, and revision of the manuscript. All authors reviewed and approved the final version of the manuscript.


Supplementary Material

 
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