| 51. |
- Sharashova, E., et al.
(författare)
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Sex-specific time trends in incident atrial fibrillation and the contribution of risk factors: the Tromso Study 1994-2016
- 2023
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Ingår i: European Journal of Preventive Cardiology. - : Oxford University Press (OUP). - 2047-4873 .- 2047-4881. ; 30:1, s. 72-81
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Tidskriftsartikel (refereegranskat)abstract
- Aims To explore sex-specific time trends in atrial fibrillation (AF) incidence and to estimate the impact of changes in risk factor levels using individual participant-level data from the population-based Tromso Study 1994-2016. Methods and results A total of 14 818 women and 13 225 men aged 25 years or older without AF were enrolled in the Tromso Study between 1994 and 2008 and followed up for incident AF throughout 2016. Poisson regression was used for statistical analyses. During follow-up, age-adjusted AF incidence rates in women decreased from 1.19 to 0.71 per 1000 person-years. In men, AF incidence increased from 1.18 to 2.82 per 1000 person-years in 2004, and then declined to 1.94 per 1000 person-years in 2016. Changes in systolic blood pressure (SBP) and diastolic blood pressure (DBP), body mass index (BMI), physical activity, smoking and alcohol consumption together accounted for 10.9% [95% confidence interval (CI): -2.4 to 28.6] of the AF incidence decline in women and for 44.7% (95% CI: 19.2; 100.0) of the AF incidence increase in men. Reduction in SBP and DBP had the largest contribution to the decrease in AF incidence in women. Increase in BMI had the largest contribution to the increase in AF incidence in men. Conclusion In the population-based Tromso Study 1994-2016, AF incidence decreased in women and increased following a reverse U-shape in men. Individual changes in SBP and DBP in women and individual changes in BMI in men were the most important risk factors contributing to the AF incidence trends.
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| 52. |
- Sternby Eilard, Malin, 1974, et al.
(författare)
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Quality of life as a prognostic factor for survival in hepatocellular carcinoma
- 2018
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Ingår i: Liver International. - : Wiley. - 1478-3223. ; 38:5, s. 885-894
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Tidskriftsartikel (refereegranskat)abstract
- Background & Aims: Prognostication in hepatocellular carcinoma (HCC) is demanding. Not only tumour extent and performance status are to be considered, but also liver function, which is often limiting for both survival itself and for treatment possibilities. This study was conducted to assess whether patient-reported questionnaires containing general and liver-specific questions could improve prognostication of survival. Methods: 185 patients with hepatocellular carcinoma in Norway and Sweden were prospectively included. Patients completed the quality-of-life questionnaires EORTC QLQ C30 and HCC18, and clinical, radiological and laboratory parameters were registered. Multivariate Cox regression and Harrell's C-statistics were used to identify the model that best predicted mortality. Results: Quality-of-life data were prognostic for overall survival. Fatigue and nutrition scales were prognostic in the multivariable analyses alone and in combination with clinical parameters. The prognostic value of established scoring systems was increased by the addition of QoL data. The best prognostic power was achieved by combining HCC18 nutrition scale with selected background parameters. Conclusion: Quality-of-life questionnaires can prognosticate mortality in HCC patients. When combined with established scoring systems, both the general cancer questionnaire EORTC QLQ C30, and the additional liver cancer-specific HCC18 increased the prognostic accuracy slightly.
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| 53. |
- Svatun, A. L., et al.
(författare)
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Association between espresso coffee and serum total cholesterol: the Tromso Study 2015-2016
- 2022
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Ingår i: Open Heart. - : BMJ. - 2053-3624. ; 9:1
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Tidskriftsartikel (refereegranskat)abstract
- Background Coffee raises serum cholesterol because of its diterpenes, cafestol and kahweol, and the effect varies by brewing method. Population-based research on espresso coffee's impact on serum cholesterol is scarce. Our aim was to examine how various brewing methods, in particular espresso, were associated with serum total cholesterol (S-TC). Methods We used cross-sectional population data from the seventh survey of the Tromso Study in Northern Norway (N=21 083, age >= 40 years). Multivariable linear regression was used to assess the association between S-TC as the dependent variable and each level of coffee consumption using 0 cups as the reference level, adjusting for relevant covariates and testing for sex differences. Results Consumption of 3-5 cups of espresso daily was significantly associated with increased S-TC (0.09 mmol/L, 95% CI 0.01 to 0.17 for women and 0.16 mmol/L, 95% CI 0.07 to 0.24 for men), compared with participants drinking 0 cups of espresso per day. Consumption of >= 6 cups of boiled/plunger coffee daily was also associated with increased S-TC (0.30 mmol/L, 95% CI 0.13 to 0.48 for women and 0.23 mmol/L, 95% CI 0.08 to 0.38 for men), compared with participants drinking 0 cups of boiled/plunger coffee. Consumption of cups of filtered coffee daily was associated with 0.11 mmol/L (95% CI 0.03 to 0.19) higher S-TC levels for women but not for men. Instant coffee consumption had a significant linear trend but showed no dose-response relationship when excluding participants not drinking instant coffee. There were significant sex differences for all coffee types except boiled/plunger coffee. Conclusion Espresso coffee consumption was associated with increased S-TC with significantly stronger association for men compared with women. Boiled/plunger coffee was associated with increased S-TC in both sexes and with similar magnitude as shown in previous research. Filtered coffee was associated with a small increase in S-TC in women. Further research on espresso and S-TC is warranted.
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| 54. |
- Tiwari, S., et al.
(författare)
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Lifestyle factors as mediators of area-level socio-economic differentials in cardiovascular disease risk factors. The Troms? Study
- 2022
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Ingår i: Ssm-Population Health. - : Elsevier BV. - 2352-8273. ; 19
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Cardiovascular disease (CVD) is a leading cause of death and disability and living in areas with low socio-economic status (SES) is associated with increased risk of CVD. Lifestyle factors such as smoking, physical inactivity, an unhealthy diet and harmful alcohol use are main risk factors that contribute to other modifiable risk factors, such as hypertension, raised blood cholesterol, obesity, and diabetes. The potential impact of area -level socio-economic status (ASES) on metabolic CVD risk factors via lifestyle behaviors independent of indi-vidual SES has not been investigated previously.Aims: To estimate associations of ASES with CVD risk factors and the mediating role of lifestyle behaviors in-dependent of individual-level SES.Methods: In this cross-sectional study, we included 19,415 participants (52% women) from the seventh survey of the Tromso Study (2015-2016) (Tromso7). The exposure variable ASES was created by aggregating individual -level SES variables (education, income, housing ownership) at the geographical subdivision level. Individual -level SES data and geographical subdivision of Tromso municipality (36 areas) were obtained from Statistics Norway. Variables from questionnaires and clinical examinations obtained from Tromso7 were used as mediators (smoking, snuff, alcohol, and physical activity), while the outcome variables were body mass index (BMI), total/ high-density lipoprotein (HDL) cholesterol ratio, waist circumference, hypertension, diabetes. Mediation and mediated moderation analysis were performed with age as a moderator, stratified by sex.Results: ASES was significantly associated with all outcome variables. CVD risk factor level declined with an increase in ASES. These associations were mediated by differences in smoking habits, alcohol use and physical activity. The associations of ASES with total/HDL cholesterol ratio and waist circumference (women) were moderated by age, and the moderating effects were mediated by smoking and physical activity in both sexes. The largest mediated effects were seen in the associations of ASES with total/HDL cholesterol ratio, with the me-diators accounting for 43% of the observed effects.Conclusions: Living in lower SES areas is associated with increased CVD risk due to unhealthy lifestyle behaviors, such as smoking, alcohol use and physical inactivity. These associations were stronger in women and among older participants.
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| 55. |
- van der Laan, Sander W., et al.
(författare)
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Cystatin C and Cardiovascular Disease : A Mendelian Randomization Study
- 2016
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Ingår i: Journal of the American College of Cardiology. - : Elsevier BV. - 0735-1097 .- 1558-3597. ; 68:9, s. 934-945
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND Epidemiological studies show that high circulating cystatin C is associated with risk of cardiovascular disease (CVD), independent of creatinine-based renal function measurements. It is unclear whether this relationship is causal, arises from residual confounding, and/or is a consequence of reverse causation. OBJECTIVES The aim of this study was to use Mendelian randomization to investigate whether cystatin C is causally related to CVD in the general population. METHODS We incorporated participant data from 16 prospective cohorts (n = 76,481) with 37,126 measures of cystatin C and added genetic data from 43 studies (n = 252,216) with 63,292 CVD events. We used the common variant rs911119 in CST3 as an instrumental variable to investigate the causal role of cystatin C in CVD, including coronary heart disease, ischemic stroke, and heart failure. RESULTS Cystatin C concentrations were associated with CVD risk after adjusting for age, sex, and traditional risk factors (relative risk: 1.82 per doubling of cystatin C; 95% confidence interval [CI]: 1.56 to 2.13; p = 2.12 x 10(-14)). The minor allele of rs911119 was associated with decreased serum cystatin C (6.13% per allele; 95% CI: 5.75 to 6.50; p = 5.95 x 10(-211)), explaining 2.8% of the observed variation in cystatin C. Mendelian randomization analysis did not provide evidence fora causal role of cystatin C, with a causal relative risk for CVD of 1.00 per doubling cystatin C (95% CI: 0.82 to 1.22; p = 0,994), which was statistically different from the observational estimate (p = 1.6 x 10(-5)). A causal effect of cystatin C was not detected for any individual component of CVD. CONCLUSIONS Mendelian randomization analyses did not support a causal role of cystatin C in the etiology of CVD. As such, therapeutics targeted at lowering circulating cystatin C are unlikely to be effective in preventing CVD.
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