High-sensitivity C-reactive protein is not a risk factor for venous thromboembolism: the Tromsø study

High-sensitivity C-reactive protein is associated with risk of arterial cardiovascular disease but conflicting results have been reported on its role in venous thromboembolic disease. The objective of our study was to investigate the association between high-sensitivity C-reactive protein levels and risk of future venous thromboembolism in a prospective cohort recruited from a general population. High-sensitivity C-reactive protein was measured in serum samples from 6,426 men and women, aged 25-84 years, recruited from the Tromsø Study in the period 1994-1995. Incident venous thromboembolism events (n=209) were registered during a median of 12.5 years of follow up. Cox’s proportional hazards regression models were used to estimate age- and genderand multivariable-adjusted hazard ratios with 95% confidence intervals for total venous thromboembolism, and for provoked and unprovoked venous thromboembolism by increasing levels of high-sensitivity C-reactive protein. There was no increased risk of venous thromboembolism per 1 standard deviation increase in high-sensitivity C-reactive protein (hazard ratio 1.08; 95% confidence interval 0.95-1.23) or across quartiles of high-sensitivity C-reactive protein (P for trend 0.6) in analyses adjusted for age and gender. Further adjustment for body mass index, smoking and diabetes did not alter the risk estimates. Moreover, high-sensitivity C-reactive protein was not associated with venous thromboembolism in either gender specific analysis or in separate analyses of provoked and unprovoked venous thromboembolism events. In this prospective study, serum levels of high-sensitivity C-reactive protein were not associated with future development of venous thromboembolism. Our findings do not suggest a causal role for C-reactive protein in the pathogenesis of venous thromboembolism

Atrial fibrillation and future risk of venous thromboembolism: The Tromsø study

Aims: Whether atrial fibrillation is related to risk of venous thromboembolism (VTE) has not been extensively studied. Therefore, we investigated the association between atrial fibrillation and future risk of VTE in a population-based cohort. Methods: In total, 29 975 subjects were recruited from three surveys of the Tromsø study and followed from enrollment (1994–1995, 2001–2002 and 2007–2008) up to 2010. Incident events of atrial fibrillation and VTE during follow-up were recorded. Information on potential confounders was obtained at baseline. Cox-regression models with atrial fibrillation as time-dependent variable were used to calculate hazard ratios (HRs) for VTE with 95% confidence intervals (CIs). Results: During 16 years of median follow-up, 1604 subjects were diagnosed with atrial fibrillation and 614 with incident VTE. The risk of VTE was substantially increased during the first 6 months after diagnosis of atrial fibrillation (HR, 8.44; 95% CI, 5.61–12.69), and remained increased throughout the study period (HR, 1.43; 95% CI, 1.43–1.99) compared with those without atrial fibrillation. Atrial fibrillation displayed higher risk estimates for pulmonary embolism (HR, 11.84; 95% CI, 6.80–20.63) than for deep vein thrombosis (HR, 6.20; 95% CI, 3.37–11.39) during the first 6 months, and was still associated with pulmonary embolism (HR, 1.96; 95% CI, 1.24–3.10) but not with deep vein thrombosis (HR, 1.08; 95% CI, 0.66–1.75) more than 6 months after diagnosis. Conclusion: Atrial fibrillation was associated with increased risk of VTE, and pulmonary embolism in particular. Our findings support the concept that isolated pulmonary embolism may originate from right atrial thrombi due to atrial fibrillation

Repeated measurements of carotid atherosclerosis and future risk of venous thromboembolism: the Tromsø Study

Background: Whether a relationship between atherosclerosis and subsequent venous thromboembolism (VTE) exists is controversial. Objective: To investigate the association between carotid atherosclerosis and VTE by using repeated measurements of intima media thickness (IMT) and total plaque area (TPA) in participants recruited from the general population. Methods: Participants were recruited from the fourth (1994–1995), fifth (2001–2002) and sixth (2007–2008) surveys of the Tromsø Study. In total, 10 426 participants attended, for whom measurements of carotid IMT and TPA and potential confounders were updated at each available survey. Time‐varying Cox regression models were used to calculate hazard ratios (HRs) of VTE across various levels of IMT and TPA adjusted for age, sex, and body mass index. Results: There were 368 incident VTE events during a median follow‐up of 10.8 years. Participants with increasing IMT were, on average, older and had a less favorable cardiovascular risk profile. There was no association between tertiles of increasing TPA and the risk of VTE in the time‐varying model, and increasing IMT was not associated with an increased risk of VTE (HR 0.96, 95% confidence interval [CI] 0.86–1.07). Neither plaque formation nor plaque progression was associated with the risk of VTE (respectively: HR 1.00, 95% CI 0.98–1.02; and HR 0.96, 95% CI 0.84–1.11). Conclusion: Carotid IMT and TPA were not associated with an increased risk of VTE in time‐varying analyses. Furthermore, there was no association between plaque initiation or plaque progression and subsequent VTE

Carotid atherosclerosis predicts future myocardial infarction but not venous thromboembolism: The Tromsø Study

Objective: Recent studies have suggested that arterial and venous thrombosis share common risk factors. Although carotid atherosclerosis is associated with arterial cardiovascular events, its role in venous thromboembolic disease is unclear. We wanted to investigate and compare the effect of carotid atherosclerosis on the risk of myocardial infarction (MI) and venous thromboembolism (VTE) in a general population, taking into account competing risks. Approach and Results: Mean intima-media thickness and total plaque area in the right carotid artery were measured with ultrasound in 6257 people aged 25 to 84 years who participated in a population-based health study, the Tromsø Study, from 1994 to 1995. Incident MI and VTE events were registered from date of enrollment to end of follow-up on December 31, 2010. Cox proportional hazards regression models using age as time scale were used to estimate cause-specific hazard ratios with 95% confidence intervals for MI and VTE by increasing levels of intima-media thickness and total plaque area. There were 894 incident MI cases and 256 VTE events during a median of 15.4 years of follow-up. The risk of MI increased significantly across quartiles of mean intima-media thickness (P for trend < 0.001) and with increasing total plaque area (P for trend < 0.001), but neither intima-media thickness (P for trend=0.94) nor total plaque area (P for trend=0.45) was associated with VTE risk in multivariable-adjusted analysis. Conclusions: In this study, carotid atherosclerosis was strongly associated with future MI but not with VTE. Our findings suggest that carotid atherosclerosis does not represent a link between arterial and venous thrombosis

Calima culture artefacts, Museo del Oro, Bogota, Colombia, 1977, [4] [picture] /

Condition: Good.; Title devised by cataloguer based on inscription on reverse.; Part of Wolfgang Sievers photographic archive.; Sievers number: V4560-add4 (devised number).; Inscriptions: "Calima-5202".; Also available in an electronic version via the Internet at: http://nla.gov.au/nla.pic-vn4193267

A sequence variant in ZFHX3 on 16q22 associates with atrial fibrillation and ischemic stroke

We expanded our genome-wide association study on atrial fibrillation (AF) in Iceland, which previously identified risk variants on 4q25, and tested the most significant associations in samples from Iceland, Norway and the United States. A variant in the ZFHX3 gene on chromosome 16q22, rs7193343-T, associated significantly with AF (odds ratio OR = 1.21, P = 1.4 x 10(-10)). This variant also associated with ischemic stroke (OR = 1.11, P = 0.00054) and cardioembolic stroke (OR = 1.22, P = 0.00021) in a combined analysis of five stroke samples