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.
Highlights
Stroke is a major cause of death and disability worldwide.[1]
Under the assumption that immobilization and infection were a consequence of acute stroke, we further examined to what extent both factors could mediate the association between stroke and venous thromboembolism (VTE) using the method developed by Karlson, Holm, and Breen (KHB method).[24]
In this population-based case-crossover study of 707 patients with incident VTE, we investigated the role of acute stroke as a VTE trigger, and found that stroke was associated with a substantial increased risk of subsequent VTE, with an odds ratios (ORs) of 20.0
Summary
Stroke is a major cause of death and disability worldwide.[1] patients with acute stroke are at risk of developing venous thromboembolism (VTE).[2,3,4,5] In a meta-analysis involving patients with acute ischemic stroke from several randomized controlled trials, the incidence of VTE among stroke patients who did not receive antithrombotic therapy during follow-up was 17% for asymptomatic and symptomatic deep vein thrombosis (DVT).[3] clinically overt pulmonary embolism (PE) occurs in only 1% of patients during the first 14 days after an acute stroke,[2,3,6] PE may account for up to 25 to 50% of deaths after acute stroke.[2,7,8] In population-based studies, the risk of VTE has been shown to received August 22, 2018 accepted after revision January 21, 2019.
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