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Background: Obesity is a major risk factor for venous thromboembolism (VTE), but it is unknown to what extent weight change over time affects VTE risk., Aims: To investigate the association between weight change and risk of incident VTE in a population-based cohort with repeated measurements., Methods: Participant data were collected from the Tromsø 3 (1986-87), 4 (1994-95), 5 (2000-01) and 6 (2007-08) surveys. Subjects who attended two subsequent or more surveys were included (n = 17802), and weight change between the surveys was calculated. Person-time at risk was accrued from the second of two subsequent vists until the next survey, the date of an incident VTE, migration, death or study end (December 31st 2012), whichever came first. Cox regression models were used to calculate risk of VTE according to change in body weight., Results: There were 302 incident VTE events during a median of 6.0 years of follow-up. Subjects who gained most weight (7.5-40.0 kg weight gain) had a 1.9-fold higher risk of VTE compared to those with no or a moderate (0-7.4 kg) weight gain (HR 1.92; 95% CI 1.38-2.68). The VTE risk by ≥7.5 kgs over no or moderate (0-7.4 kg) weight gain was highest (HR 3.75; 95% 1.83-7.68) in subjects with baseline body mass index (BMI) ≥30 kg/m2. There was a joint effect of weight gain and baseline BMI on VTE risk. Those with BMI ≥30 who gained ≥7.5 kgs had a 6.6-fold increased risk (HR 6.64; 95% CI 3.61-12.22) compared to subjects with BMI <25 and no or moderate (0-7.4 kg) weight gain., Conclusions: Our findings imply that further weight gain is a considerable risk factor for VTE, particularly in obese individuals., Competing Interests: The authors have declared that no competing interests exist.

Obesity is a risk factor for arterial and venous thromboembolism. However, it is not known whether obesity mediates risk through shared mechanisms. In a population-based cohort, we aimed to compare the impact of obesity measures on risk of venous thromboembolism (VTE) and myocardial infarction (MI), and explore how obesity-related atherosclerotic risk factors influenced these relationships. Measures of body composition including body mass index , waist circumference (WC), hip circumference (HC), waist-hip ratio (WHR) and waist-to-height ratio (WHtR) were registered in 6,708 subjects aged 25-84 years, who participated in the Tromsø Study (1994-1995). Incident VTE- and MI-events were registered until January 1, 2011. There were 288 VTEs and 925 MIs during a median of 15.7 years of follow-up. All obesity measures were related to risk of VTE. In linear models, WC showed the highest risk estimates in both genders. In categorized models (highest versus lowest quintile), WC showed highest risk in men (HR 3.59; 95 % CI 1.82-7.06) and HC in women (HR 2.27; 95 % CI 1.54-4.92). Contrary, WHR and WHtR yielded the highest risk estimates for MI. The HR of MI (highest vs. lowest quintile) for WHR was 2.11 (95 % CI 1.59-2.81) in men and 1.62 (95 % CI 1.13-2.31) in women. The risk estimates for MI were substantially attenuated after adjustment for atherosclerotic risk factors, whereas the estimates for VTE remained unchanged. Our findings suggest that the impact of body fat distribution, and the causal pathway, differs for the association between obesity and arterial and venous thrombosis.

The number of overweight and obese individuals in the population has increased dramatically in the past few decades, and the rising prevalence of obesity is a major public health concern. Growing evidence has accrued for obesity as a risk factor for venous thrombosis. The risk of venous thrombosis increases in a dose-dependent manner with increasing body mass index and is also associated with the majority of other anthropometric measures of overweight and obesity, such as waist circumference, hip circumference, and waist-to-hip ratio. An increased relative risk of both unprovoked and provoked venous thrombosis has been shown in obese compared with normal-weight subjects. However, encountering obesity as a causal factor for venous thrombosis is problematic due to the ill-defined concept of obesity. In this review, we will examine the current epidemiological evidence for an association between obesity and venous thrombosis. We will comment on the problem of causal interpretation of obesity per se and discuss how individual components that define obesity can serve as potential biological mechanisms for the observed association between obesity and venous thrombosis., (Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.)

Objective: The purpose of this study was to assess the impact of various obesity measures on identification of subjects at risk and their respective risk estimates for VTE in a prospective population-based study., Methods and Results: Measures of body composition such as body mass index (BMI), waist circumference (WC), hip circumference (HC), and waist-hip ratio (WHR) were registered in 6708 subjects aged 25 to 84 years, who participated in the Tromsø Study (1994-1995). Incident VTE-events were registered during follow-up until September 1, 2007. There were 222 VTE-events during a median of 12.3 years of follow-up. All measures of obesity exhibited significantly increased HR for VTE in multivariable models with highest risk estimates for WC in both genders. The risk of VTE increased across quartiles of BMI, WC, and HC in both genders, but not for WHR. WC identified more subjects at risk using established criteria for obesity. WC had the highest area under the curve in both genders in ROC analysis, and WC above ROC-derived cut-off values (WC > or =85 cm in women and > or =95 cm in men) were associated with HRs of 1.92 (95% CI: 1.05 to 3.48) in women and 2.78 (95% CI: 1.47 to 5.27) in men., Conclusions: Our findings indicate that WC is the preferable anthropometric measure of obesity to identify subjects at risk and to predict risk of VTE.

BackgroundMuch controversy surrounds the association of traditional cardiovascular disease risk factors with venous thromboembolism (VTE).MethodsWe performed an individual level random-effect meta-analysis including 9 prospective studies with measured baseline cardiovascular disease risk factors and validated VTE events. Definitions were harmonized across studies. Traditional cardiovascular disease risk factors were modeled categorically and continuously using restricted cubic splines. Estimates were obtained for overall VTE, provoked VTE (ie, VTE occurring in the presence of 1 or more established VTE risk factors), and unprovoked VTE, pulmonary embolism, and deep-vein thrombosis.ResultsThe studies included 244 865 participants with 4910 VTE events occurring during a mean follow-up of 4.7 to 19.7 years per study. Age, sex, and body mass index-adjusted hazard ratios for overall VTE were 0.98 (95% confidence interval [CI]: 0.89-1.07) for hypertension, 0.97 (95% CI: 0.88-1.08) for hyperlipidemia, 1.01 (95% CI: 0.89-1.15) for diabetes mellitus, and 1.19 (95% CI: 1.08-1.32) for current smoking. After full adjustment, these estimates were numerically similar. When modeled continuously, an inverse association was observed for systolic blood pressure (hazard ratio=0.79 [95% CI: 0.68-0.92] at systolic blood pressure 160 vs 110 mm Hg) but not for diastolic blood pressure or lipid measures with VTE. An important finding from VTE subtype analyses was that cigarette smoking was associated with provoked but not unprovoked VTE. Fully adjusted hazard ratios for the associations of current smoking with provoked and unprovoked VTE were 1.36 (95% CI: 1.22-1.52) and 1.08 (95% CI: 0.90-1.29), respectively.ConclusionsExcept for the association between cigarette smoking and provoked VTE, which is potentially mediated through comorbid conditions such as cancer, the modifiable traditional cardiovascular disease risk factors are not associated with increased VTE risk. Higher systolic blood pressure showed an inverse association with VTE.

Current knowledge of the effect of fish consumption on risk of venous thromboembolism (VTE) is scarce and diverging. Therefore, the purpose of the present study was to investigate the impact of fish consumption and fish oil supplements on the risk of VTE in a population-based cohort. Weekly intake of fish for dinner and intake of fish oil supplements during the previous year were registered in 23,621 persons aged 25-97 y who participated in the Tromsø Study from 1994 to 1995. Incident VTE events were registered throughout follow-up (31 December 2010). Cox-regression models were used to calculate HRs for VTE, adjusted for age, body mass index, sex, triglycerides, HDL cholesterol, physical activity, and education level. During a median of 15.8 y of follow-up there were 536 incident VTE events. High fish consumption was associated with a slightly reduced risk of VTE. Participants who ate fish ≥3 times/wk had 22% lower risk of VTE than those who consumed fish 1-1.9 times/wk (multivariable HR: 0.78; 95% CI: 0.60, 1.01; P = 0.06). The addition of fish oil supplements strengthened the inverse association with risk of VTE. Participants who consumed fish ≥3 times/wk who additionally used fish oil supplements had 48% lower risk than those who consumed fish 1-1.9 times/wk but did not use fish oil supplements (HR: 0.52; 95% CI: 0.34, 0.79; P = 0.002). In conclusion, a high weekly intake (≥3 times/wk) of fish was associated with a slightly reduced risk of VTE, and the addition of fish oil supplements strengthened the inverse effect. [ABSTRACT FROM AUTHOR]

D-dimer, a global biomarker for activation of the coagulation and fibrinolysis systems, is useful in assessing individual risk of venous thromboembolism (VTE) recurrence. However, there is limited information on the association between D-dimer and risk of a first lifetime VTE event. To investigate the association between plasma D-dimer levels and risk of future incident VTE. A population-based nested case-control study, comprising 414 VTE patients and 843 randomly selected age- and sex-matched controls, was derived from the Tromsø Study (1994–2007). D-dimer was measured in plasma samples collected at cohort baseline (1994–95). Odds ratios (ORs) for VTE with 95% confidence intervals (CIs) were estimated according to quartile cut-offs of D-dimer levels determined in controls. The risk of VTE increased across quartiles of D-dimer levels (P trend = 0.014) in the age- and sex-adjusted model. Participants with plasma D-dimer levels in the highest quartile (≥152 ng/mL) had an OR for VTE of 1.65 (95% CI 1.14–2.40) compared with those in the lowest quartile (<94 ng/mL). The ORs were marginally attenuated after additional adjustment for body mass index (BMI) (OR 1.51, 95% CI 1.04–2.20) and C-reactive protein (CRP) (OR 1.34, 95% CI 0.90–1.98). Similar results were obtained for VTE subgroups, i.e. deep vein thrombosis, pulmonary embolism, and provoked/unprovoked events. Our results indicate that elevated plasma D-dimer levels are associated with increased risk of incident VTE. However, the attenuation of risk estimates upon additional adjustment for BMI and CRP suggests that D-dimer partly reflects underlying conditions associated with obesity and an inflammatory state. • Data on the association of D-dimer with incident venous thrombosis (VT) is scarce. • This association was investigated in a population-based nested case-control study. • Elevated D-dimer plasma levels were associated with increased risk of VT. • Inflammation (reflected by C-reactive protein) partially explained the association. [ABSTRACT FROM AUTHOR]