ORCID Profile
0000-0002-9678-9696
Current Organisation
UiT Norges arktiske universitet
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Publisher: Elsevier BV
Date: 06-2016
DOI: 10.1111/JTH.13329
Abstract: Essentials Registry-based studies indicate a link between arterial- and venous thromboembolism (VTE). We studied this association in a cohort with confounder information and validated outcomes. Myocardial infarction (MI) was associated with a 4.8-fold increased short-term risk of VTE. MI was associated with a transient increased risk of VTE, and pulmonary embolism in particular. Background Recent studies have demonstrated an association between venous thromboembolism (VTE) and arterial thrombotic diseases. Objectives To study the association between incident myocardial infarction (MI) and VTE in a prospective population-based cohort. Methods Study participants (n = 29 506) were recruited from three surveys of the Tromsø Study (conducted in 1994-1995, 2001-2002, and 2007-2008) and followed up to 2010. All incident MI and VTE events during follow-up were recorded. Cox regression models with age as the time scale and MI as a time-dependent variable were used to calculate hazard ratios (HRs) of VTE adjusted for sex, body mass index, blood pressure, diabetes mellitus, HDL cholesterol, smoking, physical activity, and education level. Results During a median follow-up of 15.7 years, 1853 participants experienced an MI and 699 experienced a VTE. MI was associated with a 51% increased risk of VTE (HR 1.51 95% confidence interval [CI] 1.08-2.10) and a 72% increased risk of pulmonary embolism (PE) (HR 1.72 95% CI 1.07-2.75), but not significantly associated with the risk of deep vein thrombosis (DVT) (HR 1.36 95% CI 0.86-2.15). The highest risk estimates for PE were observed during the first 6 months after the MI (HR 8.49 95% CI 4.00-18.77). MI explained 6.2% of the PEs in the population (population attributable risk) and 78.5% of the PE risk in MI patients (attributable risk). Conclusions Our findings indicate that MI is associated with a transient increased VTE risk, independently of traditional atherosclerotic risk factors. The risk estimates were particularly high for PE.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 27-01-2014
Abstract: Pulmonary embolism (PE) may trigger atrial fibrillation through increased right atrial pressure and subsequent atrial strain, but the degree of evidence is low. In this study, we wanted to investigate the impact of incident venous thromboembolism ( VTE ) on future risk of atrial fibrillation in a prospective population‐based study. The study included 29 974 subjects recruited from the T romsø study (1994–1995, 2001–2002, 2007–2008). Incident VTE and atrial fibrillation events were registered from date of enrolment to end of follow‐up, December 31, 2010. C ox proportional hazard regression models using age as time‐scale and VTE as a time‐dependent variable were used to estimate crude and multivariable hazard ratios ( HR s) for atrial fibrillation with 95% confidence intervals ( CI s). During 16 years of follow up, 540 (1.8%) subjects had an incident VTE event, and 1662 (5.54%) were diagnosed with atrial fibrillation. Among those with VTE , 50 (9.3%) developed subsequent atrial fibrillation. Patients with VTE had 63% higher risk of atrial fibrillation compared to subjects without VTE (multivariable‐adjusted HR : 1.63, 95% CI : 1.22 to 2.17). The risk of atrial fibrillation was particularly high during the first 6 months after the VTE event ( HR 4.00, 95% CI : 2.21 to 7.25) and among those with PE ( HR 1.78, 95% CI : 1.13 to 2.80). We found that incident VTE was associated with future risk of atrial fibrillation. Our findings support the hypothesis that PE may lead to cardiac dysfunctions that, in turn, could trigger atrial fibrillation.
Publisher: Elsevier BV
Date: 05-2019
DOI: 10.1111/JTH.14410
Abstract: Essentials Prothrombotic genotypes may agument the risk of venous thromboembolism (VTE) after ischemic stroke. We studied this effect in a case-cohort study using a genetic risk score. In stroke patients, a one-category increase in the genetic risk score was associated with a 50% higher relative risk of VTE. The risk of VTE in stroke patients increased with an increasing number of risk alleles. SUMMARY: Background Patients with ischemic stroke have a transiently increased risk of subsequent venous thromboembolism (VTE). Prothrombotic genotypes may augment VTE risk under conditions of high thrombosis risk related to stroke. Aims To investigate the effect of prothrombotic genotypes in patients with ischemic stroke on the risk of VTE in a population-based case-cohort study. Methods Cases with incident VTE (n = 664) and a randomly selected age-weighted subcohort (n = 1817) were s led from three surveys of the Tromsø Study (1994-2008). Participants were genotyped for ABO (rs8176719), F5 (rs6025), F2 (rs1799963), FGG (rs2066865) and F11 (rs2036914) single-nucleotide polymorphisms (SNPs). Cox regression models were used to calculate hazard ratios (HRs) for incident VTE according to in idual SNPs and categories of risk alleles (5-SNP score 0-1, 2, 3-4 and ≥ 5) in participants with and without ischemic stroke. Results There were 192 patients with incident stroke, of whom 43 developed VTE during a median of 15.2 years of follow-up. The risk alleles of in idual SNPs augmented the elevated VTE risk brought about by ischemic stroke. In stroke patients, a one-category increase in the genetic risk score was associated with a 50% higher relative risk of overall VTE (HR 1.5, 95% confidence interval [CI] 1.3-1.8) and an 80% higher relative risk of provoked VTE (HR 1.8, 95% CI 1.5-2.1). Stroke patients with ≥ 5 risk alleles had a 12-fold (HR 11.7, 95% CI 4.1-33.3) higher relative risk of VTE than stroke-free participants with 0-1 risk alleles. Conclusions Prothrombotic genotypes increased the risk of VTE in stroke patients, and the risk increased with an increasing number of risk alleles.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 15-08-2014
Abstract: Red cell distribution width (RDW), a measure of the variability in size of circulating erythrocytes, is associated with mortality and adverse outcome in selected populations with cardiovascular disease. It is scarcely known whether RDW is associated with incident myocardial infarction (MI). We aimed to investigate whether RDW was associated with risk of first‐ever MI in a large cohort study with participants recruited from a general population. Baseline characteristics, including RDW, were collected for 25 612 participants in the Tromsø Study in 1994–1995. Incident MI during follow‐up was registered from inclusion through December 31, 2010. Cox regression models were used to calculate hazard ratios with 95% confidence intervals for MI, adjusted for age, sex, body mass index, smoking, hemoglobin, white blood cells, platelets, and other traditional cardiovascular risk factors. A total of 1779 participants experienced a first‐ever MI during a median follow‐up time of 15.8 years. There was a linear association between RDW and risk of MI, for which a 1% increment in RDW was associated with a 13% increased risk (hazard ratio 1.13 95% CI, 1.07 to 1.19). Participants with RDW above the 95th percentile had 71% higher risk of MI compared with those with RDW in the lowest quintile (hazard ratio 1.71 95% CI, 1.34 to 2.20). All effect estimates were essentially similar after exclusion of participants with anemia (n=1297) from the analyses. RDW is associated with incident MI in a general population independent of anemia and cardiovascular risk factors.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 26-10-2016
Abstract: Even though clinical data support a relation between ischemic stroke and venous thromboembolism ( VTE ), the strength and time dependence of the association remain to be settled at the population level. We therefore aimed to investigate the association between ischemic stroke and VTE in a prospective population‐based cohort. Participants (n=30 002) were recruited from 3 surveys of the Tromsø study (conducted in 1994–1995, 2001, and 2007–2008) and followed through 2010. All incident events of ischemic stroke and VTE during follow‐up were recorded. Cox‐regression models with age as time scale and ischemic stroke as a time‐dependent variable were used to calculate hazard ratios ( HR ) of VTE adjusted for cardiovascular risk factors. During a median follow‐up time of 15.7 years, 1360 participants developed ischemic stroke and 722 had a VTE . The risk of VTE was highest the first month ( HR 19.7 95% CI , 10.1–38.5) and from 1 to 3 months after the stroke ( HR 10.6 95% CI 5.0–22.5), but declined rapidly thereafter. The risk estimates were approximately the same for deep vein thrombosis ( HR 19.1 95% CI , 7.8–38.5), and pulmonary embolism ( HR 20.2 95% CI , 7.4–55.1). Stroke was associated with higher risk for provoked ( HR 22.6 95% CI , 12.5–40.9) than unprovoked VTE ( HR 7.4 95% CI , 2.7–20.1) the first 3 months. The risk of VTE increased during the first 3 months after an ischemic stroke. The particularly high risk of provoked VTE suggests that additional predisposing factors, such as immobilization, potentiate the VTE risk in patients with ischemic stroke.
Publisher: Public Library of Science (PLoS)
Date: 16-09-2016
Publisher: Elsevier BV
Date: 2015
DOI: 10.1111/JTH.12762
Abstract: 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. 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). 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. 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.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 2014
DOI: 10.1161/ATVBAHA.113.302162
Abstract: 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. 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 .001) and with increasing total plaque area ( P for trend .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. 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.
Publisher: Springer Science and Business Media LLC
Date: 07-02-2017
DOI: 10.1007/S10654-017-0231-5
Abstract: The association between myocardial infarction (MI) and future risk of incident cancer is scarcely investigated. Therefore, we aimed to study the risk of cancer after a first time MI in a large cohort recruited from a general population. Participants in a large population-based study without a previous history of MI or cancer (n = 28,763) were included and followed from baseline to date of cancer, death, migration or study end. Crude incidence rates (IRs) and hazard ratios (HRs) for cancer after MI were calculated. During a median follow-up of 15.7 years, 1747 subjects developed incident MI, and of these, 146 suffered from a subsequent cancer. In the multivariable-adjusted model (adjusted for age, sex, BMI, systolic blood pressure, diabetes mellitus, HDL cholesterol, smoking, physical activity and education level), MI patients had 46% (HR 1.46 95% CI: 1.21-1.77) higher hazard ratio of cancer compared to those without MI. The increased cancer incidence was highest during the first 6 months after the MI, with a 2.2-fold higher HR (2.15 95% CI: 1.29-3.58) compared with subjects without MI. After a 2-year period without higher incidence rate, MI patients displayed 60% (HR 1.60 95% CI: 1.27-2.03) higher HR of future cancer more than 3 years after the event. The increased IRs were higher in women than men. Patients with MI had a higher short- and long-term incidence rate of cancer compared to subjects without MI. Our findings suggest that occult cancer and shared risk factors of MI and cancer may partly explain the association.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 06-02-2018
Abstract: Atrial fibrillation ( AF ) is a well‐established risk factor for ischemic stroke ( IS ). Emerging evidence also indicates an association between AF and pulmonary embolism ( PE ). Because IS may potentially mediate the observed risk of PE in AF , we aimed to assess the impact of AF on the cause‐specific risks of PE and IS in a large cohort recruited from the general population. We observed 29 842 participants from 3 surveys of the Tromsø study (inclusion in 1994–1995, 2001–2002, and 2007–2008) to the end of 2012. Incident events of AF , IS, and PE during follow‐up were recorded, and information on potential confounders was obtained at baseline. Cox regression models, with AF as a time‐dependent variable, were used to calculate cause‐specific hazard ratios ( HR s) with 95% confidence intervals ( CI s) for PE and IS . There were 2067 participants diagnosed as having AF , 296 with PE and 1164 with IS, during a median of 17.6 years of follow‐up. The risks of PE ( HR, 10.88 95% CI , 6.23–18.89) and IS ( HR, 6.16 95% CI , 4.47–8.48) were substantially increased during the first 6 months after AF diagnosis, with crude incidence rates of 18.5 per 1000 person‐years for PE and 52.8 per 1000 person‐years for IS . The risk estimates remained elevated for both PE ( HR , 1.72 95% CI, 1.10–2.71) and IS ( HR, 2.45 95% CI, 2.05–2.92) throughout the study period. AF was associated with increased cause‐specific risks of both PE and IS . Our findings infer that the risk of PE in AF is not explained by intermediate IS .
Publisher: Elsevier BV
Date: 10-2022
DOI: 10.1111/JTH.15812
Abstract: Myocardial infarction (MI) is associated with an increased risk of venous thromboembolism (VTE). Obesity is a recognized risk factor for both MI and VTE. Whether obesity further increases the risk of VTE in MI patients is scarcely investigated. To study the joint effect of MI and obesity on the risk of VTE. Study participants (n = 29 410) were recruited from three surveys of the Tromsø Study (conducted in 1994-1995, 2001, and 2007-2008) and followed up through 2014. All incident MI and VTE cases during follow-up were recorded. Cox regression models with MI as a time-dependent variable were used to estimate hazard ratios (HRs) of VTE (adjusted for age and sex) by combinations of MI exposure and obesity status. Joint effects were assessed by calculating relative excess risk and attributable proportion (AP) due to interaction. During a median of 19.6 years of follow-up, 2090 study participants experienced an MI and 784 experienced a VTE. Among those with MI, 55 developed a subsequent VTE, yielding an overall incidence rate (IR) of VTE of 5.3 per 1000 person-years (95% confidence interval [CI]: 4.1-6.9). In the combined exposure group (MI+/Obesity+), the IR was 11.3 per 1000 person-years, and the adjusted HR indicated a 3-fold increased risk of VTE (HR 3.16, 95% CI: 1.99-4.99) compared to the reference group (MI-/Obesity-). The corresponding AP was 0.46 (95% CI: 0.17-0.74). The combination of MI and obesity yielded a supra-additive effect on VTE risk of which 46% of the VTE events were attributed to the interaction.
No related grants have been discovered for Sigrid Braekkan.