ORCID Profile
0000-0002-1621-1756
Current Organisations
UiT The Arctic University of Norway
,
University Hospital of North Norway
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Publisher: Public Library of Science (PLoS)
Date: 16-09-2016
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: 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: 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.
No related grants have been discovered for Ludvig Rinde.