To cite this article: Naess IA, Christiansen SC, Romundstad P, Cannegieter SC, Rosendaal FR, Hammerstrøm J. Incidence and mortality of venous thrombosis: a population-based study. J Thromb Haemost 2007; 5: 692-9.See also Sørensen HT. Venous thromboembolism and the concepts of the incidence and mortality. This issue, pp 690-1.Summary. Background: Estimates of the incidence of venous thrombosis (VT) vary, and data on mortality are limited. Objectives: We estimated the incidence and mortality of a first VT event in a general population. Methods: From the residents of Nord-Trøndelag county in Norway aged 20 years and older (n = 94 194), we identified all cases with an objectively verified diagnosis of VT that occurred between 1995 and 2001. Patients and diagnosis characteristics were retrieved from medical records. Results: Seven hundred and forty patients were identified with a first diagnosis of VT during 516 405 personyears of follow-up. The incidence rate for all first VT events was 1.43 per 1000 person-years [95% confidence interval (CI): 1.33-1.54], that for deep-vein thrombosis (DVT) was 0.93 per 1000 person-years (95% CI: 0.85-1.02), and that for pulmonary embolism (PE) was 0.50 per 1000 person-years (95% CI: 0.44-0.56). The incidence rates increased exponentially with age, and were slightly higher in women than in men. The 30-day casefatality rate was higher in patients with PE than in those with DVT [9.7% vs. 4.6%, risk ratio 2.1 (95% CI: 1.2-3.7)]; it was also higher in patients with cancer than in patients without cancer [19.1% vs. 3.6%, risk ratio 3.8 (95% CI 1.6-9.2)]. The risk of dying was highest in the first months subsequent to the VT, after which it gradually approached the mortality rate in the general population. Conclusions: This study provides estimates of incidence and mortality of a first VT event in the general population.

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Background There is much controversy surrounding the association of traditional cardiovascular disease (CVD) risk factors with venous thromboembolism (VTE). Methods We performed an individual level random-effect meta-analysis including 9 prospective studies with measured baseline CVD risk factors and validated VTE events. Definitions were harmonized across studies. Traditional CVD risk factors were modeled categorically, as well as continuously using restricted cubic splines. Estimates were obtained for overall VTE, provoked (i.e., VTE occurring in the presence of one or more established VTE risk factors) and unprovoked VTE, pulmonary embolism (PE) and deep-vein thrombosis (DVT). Results The studies included 244,865 participants with 4,910 VTE events occurring during a mean follow-up 4.7–19.7 years per study. Age, sex, and body-mass index adjusted hazard ratios for overall VTE were 0.98 (95%CI, 0.89–1.07) for hypertension, 0.97 (0.88–1.08) for hyperlipidemia, 1.01 (0.89–1.15) for diabetes and 1.19 (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 (HR=0.79 [95% CI, 0.68–0.92] at systolic blood pressure 160 vs. 110 mmHg), 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 with 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 (0.90–1.29), respectively. Conclusions Except the association of cigarette smoking with provoked VTE, which is potentially mediated through comorbid conditions such as cancer, the modifiable traditional CVD risk factors are not associated with increased VTE risk. Higher systolic blood pressure showed inverse association with VTE.

Key Points Bendamustine-rituximab therapy results in high overall and CR rates with sustained remissions in CAD. Bendamustine plus rituximab may be considered in first line for most patients with CAD requiring therapy.

BackgroundIn case-control studies, elevated levels of interleukins 6 and 8 have been found to be associated with an increased risk of venous thrombosis (VT). Because of the design of these studies, it remained uncertain whether these alterations were a cause or a result of the VT. In order to distinguish between the two, we set out to measure the levels of six inflammatory markers prior to thrombosis in a population-based cohort using a nested case-cohort design.Methods and FindingsBetween August 1995 and June 1997, blood was collected from 66,140 people in the second Norwegian Health Study of Nord-Trøndelag (HUNT2). We identified venous thrombotic events occurring between entry and 1 January 2002. By this date we had registered 506 cases with a first VT; an age- and sex-stratified random sample of 1,464 controls without previous VT was drawn from the original cohort. Levels of interleukins 1β, 6, 8, 10, 12p70, and tumour necrosis factor-α were measured in the baseline sample that was taken 2 d to 75 mo before the event (median 33 mo). Cut-off points for levels were the 80th, 90th, and 95th percentile in the control group. With odds ratios ranging from 0.9 (95% CI: 0.6–1.5) to 1.1 (95% CI: 0.7–1.8), we did not find evidence for a relationship between VT and an altered inflammatory profile.ConclusionsThe results from this population sample show that an altered inflammatory profile is more likely to be a result rather than a cause of VT, although short-term effects of transiently elevated levels cannot be ruled out.

Background Recent findings suggest that chronic kidney disease (CKD) may be associated with increased risk of venous thromboembolism (VTE). Given the high prevalence of mild-to-moderate CKD in the general population, in depth analysis of this association is warranted. Methods and Results We pooled individual participant data from five community-based cohorts from Europe (HUNT2, PREVEND and Tromsø study) and United States (ARIC and CHS study) to assess the association of estimated glomerular filtration rate (eGFR), albuminuria and CKD with objectively verified VTE. To estimate adjusted hazard ratios (HRs) for VTE, categorical and continuous spline models were fit using Cox regression with shared-frailty or random-effect meta-analysis. A total of 1,178 VTE events occurred over 599,453 person-years follow-up. Relative to eGFR 100 mL/min/1.73m2, HRs for VTE were 1.29 (95%CI, 1.04-1.59) for eGFR 75, 1.31 (1.00-1.71) for 60, 1.82 (1.27-2.60) for 45 and 1.95 (1.26-3.01) for 30 mL/min/1.73m2. Compared with albumin-creatinine ratio (ACR) of 5.0 mg/g, the HRs for VTE were 1.34 (1.04-1.72) for 30 mg/g, 1.60 (1.08-2.36) for 300 mg/g and 1.92 (1.19-3.09) for 1000 mg/g. There was no interaction between clinical categories of eGFR and ACR (P=0.20). The adjusted HR for CKD defined as eGFR <60 mL/min/1.73m2 or albuminuria ≥30 mg/g (vs. no CKD) was 1.54 (95%CI, 1.15-2.06). Associations were consistent in subgroups according to age, gender, and comorbidities as well as for unprovoked versus provoked VTE. Conclusions Both eGFR and ACR are independently associated with increased risk of VTE in the general population, even across the normal eGFR and ACR ranges.

Conclusion: Infection is a risk factor for venous thromboembolism (VTE).Summary: Rates of acute infections and acute venous thromboembolism (VTE) are both high; therefore, any relationship between infection and VTE has potential major clinical importance. Evidence is emerging of a possible relationship between deep venous thrombosis, pulmonary embo-

To cite this article: Naess IA, Christiansen SC, Cannegieter SC, Rosendaal FR, Hammerstroem J. A prospective study of anticardiolipin antibodies as a risk factor for venous thrombosis in a general population (the HUNT study). J Thromb Haemost 2006; 4: 44-9.See also de Groot PG, Derksen RHWM. The importance of measuring anticardiolipin antibodies. This issue, pp 41-3.Summary. We prospectively examined whether there is an association between elevated anticardiolipin antibody levels and the risk for a future first venous thrombosis (VT) in a general population. We studied this in a large population-based nested case-cohort study of 508 VT cases and 1464 matched control subjects from a cohort of 66 140 participants in the Health Study of Nord-Trøndelag in Norway. Venous thrombosis was validated using standardized criteria for venous thrombosis and pulmonary embolism. Prethrombotic serum anticardiolipin antibodies were measured by an enzyme-linked immunoassay. There was no association between elevated anticardiolipin antibody levels and subsequent venous thrombosis, overall or after stratification by sex, different age groups or idiopathic vs. secondary thrombosis. The overall odds ratio was 1.11 (95% CI: 0.71-1.74) for greater than vs. less than the 95th percentile of anticardiolipin antibody levels. In conclusion, in this general population sample elevated anticardiolipin antibody levels was not a risk factor for subsequent venous thrombosis.