ArticlesRisk of deep vein thrombosis and pulmonary embolism after acute infection in a community setting
Introduction
Deep vein thrombosis (DVT) and pulmonary embolism (PE) are major causes of morbidity and mortality.1 A systematic review of published studies, mostly undertaken in the USA and Sweden, estimated the overall population incidence of DVT to be 0·5 per 1000 person-years.2 Although several studies have focused on the mechanisms and causes of atherothrombosis and acute cardiovascular events, less is known about venous thromboembolic disease. In 1856, Virchow proposed three precipitants for venous thrombosis: venous stasis; increased coagulability of the blood; and damage to the vessel wall.3 Infection could affect venous stasis or increase coagulability of the blood. Furthermore, parallels with the arterial system suggest that damage to the vessel wall might not be limited to physical damage but could also affect endothelial function. Inflammation is a key determinant of endothelial function in both arteries and veins,4, 5 and a link between infection and venous thrombosis via endothelial activation has been suggested.6, 7 Thus, there are several mechanisms by which acute infections could increase the risk of venous thromboembolism. Acute infections have been associated with a transient increase in the risk of myocardial infarction and stroke.8, 9 Using a similar approach, we tested the hypothesis that acute infections trigger a transient increase in the risk of venous thromboembolic disease.
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Participants
The Health Improvement Network is an electronic database of medical records from general practice, and includes complete prescribing and diagnostic information. Recorded rates of consultations and drug prescriptions as well as pregnancy and death rates are equivalent to UK national data.10 The database information is anonymous.
Patients were derived from the population for whom data was available in the database between 1987 and 2004—this comprised more than 20 million person-years of
Results
10 284 people with a first DVT were identified from the database, of whom 7278 people were included in the analysis. The median age at the time of diagnosis of DVT was 67·6 years (IQR 53·4–77·5), 41·6% were male, and the mean observation period was 10·2 years. 5574 people with a first PE were identified, of whom 3755 were included in our analysis. The median age at the time of diagnosis of PE was 67·9 years (IQR 54·9–77·6), 42·6% were male, and the mean observation period was 9·6 years.
During
Discussion
Our results show that in a community setting, acute infection is linked to a transient increase in the risk of venous thromboembolism—both DVT and PE—suggesting a role for acute infections in triggering such events. Using a large data set we were able to identify the magnitude of the association and its temporal resolution. The effect we observed was similar for respiratory and urinary tract infections, suggesting the effect of infections on risk of venous thromboembolism might be generic and
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