Logan T Cowan1, Pamela L Lutsey2, James S Pankow2, Mary Cushman3, Aaron R Folsom2. 1. Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN, United States. Electronic address: cowan046@umn.edu. 2. Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN, United States. 3. Department of Medicine, Division of Hematology/Oncology, Larner College of Medicine at the University of Vermont, Burlington, VT, United States.
Abstract
BACKGROUND AND OBJECTIVES: Acute triggers for VTE, which may include infection, are understudied, as is the timing and duration of VTE risk after infection. We hypothesized that there is an association between hospitalization with infection and short-term VTE risk that exceeds the known association between hospitalization and VTE. METHODS: VTE cases and infections were identified in the Atherosclerosis Risk in Communities (ARIC) cohort. A case-crossover design and conditional logistic regression were used to compare hospitalized infections among VTE cases (14, 30, 42, and 90days before VTE) with corresponding control periods 1year and 2years prior. Since hospitalization is a known VTE trigger, study design and analytical techniques were used to isolate the impact of infection. RESULTS: There were 845 adjudicated incident VTE cases. Hospitalization with infection was more common in all case periods compared to equivalent control periods: 14day OR (95% CI)=1.7 (0.5, 5.8), 30day OR (95% CI)=2.7 (1.1, 6.4), 42day OR (95% CI)=2.2 (1.1, 4.7), and 90day OR (95% CI)=1.2 (0.7, 2.0). The association was generally strongest in exposure periods closest to the VTE event and decreased as the time window before VTE increased. CONCLUSIONS: These results support the hypothesis that hospitalized infection is a trigger of VTE. VTE preventive measures may prevent VTE events if used in the peri-infection period but clinical trials are needed.
BACKGROUND AND OBJECTIVES: Acute triggers for VTE, which may include infection, are understudied, as is the timing and duration of VTE risk after infection. We hypothesized that there is an association between hospitalization with infection and short-term VTE risk that exceeds the known association between hospitalization and VTE. METHODS:VTE cases and infections were identified in the Atherosclerosis Risk in Communities (ARIC) cohort. A case-crossover design and conditional logistic regression were used to compare hospitalized infections among VTE cases (14, 30, 42, and 90days before VTE) with corresponding control periods 1year and 2years prior. Since hospitalization is a known VTE trigger, study design and analytical techniques were used to isolate the impact of infection. RESULTS: There were 845 adjudicated incident VTE cases. Hospitalization with infection was more common in all case periods compared to equivalent control periods: 14day OR (95% CI)=1.7 (0.5, 5.8), 30day OR (95% CI)=2.7 (1.1, 6.4), 42day OR (95% CI)=2.2 (1.1, 4.7), and 90day OR (95% CI)=1.2 (0.7, 2.0). The association was generally strongest in exposure periods closest to the VTE event and decreased as the time window before VTE increased. CONCLUSIONS: These results support the hypothesis that hospitalized infection is a trigger of VTE. VTE preventive measures may prevent VTE events if used in the peri-infection period but clinical trials are needed.
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