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Laugsand, L. E., Asvold, B. O., Vatten, L. J., Romundstad, P. R., Wiseth, R., Hveem, K., et al. (2012). Metabolic factors and high-sensitivity C-reactive protein: the HUNT study. Eur J Prev Cardiol, 19(5), 1101–1110.
Abstract: BACKGROUND: The association of high-sensitivity C-reactive protein (hsCRP) with metabolic syndrome in younger age groups has not been studied extensively and few population-based studies have included both sexes. Therefore we estimated the association of high-sensitivity C-reactive protein (hsCRP) with the metabolic factors at different ages in men and women in a large population-based study. METHODS AND OBJECTIVES: In this cross-sectional study, clinical information and non-fasting blood samples including measurement of hsCRP from 4587 men and 5408 women 20 years and older in the HUNT study in Norway were used to study the association of components of the metabolic syndrome with levels of hsCRP, by sex and age group. RESULTS: All measured metabolic factors were associated with hsCRP. Among these factors, body mass index appeared to be the most strongly associated, and the strong positive association persisted also after adjustment for the other metabolic factors, with similar associations in women and men. The associations were generally somewhat stronger in younger than in older age groups. CONCLUSION: Metabolic factors, especially body mass index, have a relatively strong association with high-sensitivity C-reactive protein at all ages both in men and women.
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Skaug, E. - A., Aspenes, S. T., Oldervoll, L., Morkedal, B., Vatten, L., Wisloff, U., et al. (2013). Age and gender differences of endothelial function in 4739 healthy adults: the HUNT3 Fitness Study. Eur J Prev Cardiol, 20(4), 531–540.
Abstract: AIMS: Endothelial dysfunction is an important marker for prognosis in patients with coronary heart disease. However, there are no reference values for endothelial function in a healthy population. Our aim was to determine the distribution of flow-mediated dilation (FMD) values by gender and age in healthy adults. METHODS: FMD was measured by ultrasound during reactive hyperaemia in the brachial artery of 4739 adults aged 20-89 years, who were free from self-reported cardiovascular or pulmonary disease. Differences in FMD across age and gender were analysed by multiple linear regression. RESULTS: Total mean +/- SD FMD was 4.8 +/- 4.2%, with corresponding estimates of 4.3 +/- 3.9% for men and 5.3 +/- 4.5% for women (p < 0.001). In total, 17% had FMD </=0%, indicating endothelial dysfunction. FMD decreased with increasing age in both genders up to 70 years for men and 80 for women (p < 0.001). In women, age-related decline in FMD was steepest after age 45; in men, a steady decline after age 30. In men 80 years and older, FMD was higher than in men aged 50-79 years. CONCLUSIONS: The distribution of FMD in this study is representative of the respective age and gender groups of a healthy population and may be a useful reference for future studies. The high proportion of endothelial dysfunction came as a surprise. Its age and gender distribution suggest that FMD </=0% precedes cardiovascular disease and that it may be a powerful non-invasive biomarker for identifying high-risk individuals.
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Ueland, T., Laugsand, L. E., Vatten, L. J., Janszky, I., Platou, C., Michelsen, A. E., et al. (2017). Extracellular matrix markers and risk of myocardial infarction: The HUNT Study in Norway. Eur J Prev Cardiol, 24(11), 1161–1167.
Abstract: Aims Extracellular matrix remodelling may influence atherosclerotic progression and plaque stability. We hypothesized that evaluation of extracellular matrix markers, with potentially different roles during atherogenesis, could provide information on underlying mechanisms and risk of myocardial infarction (MI) in apparently healthy individuals. Methods We conducted a case-control study nested within the population-based HUNT2 cohort in Norway. A total of 58,761 men and women, free of known cardiovascular disease, were followed for a first MI. During 11.3 years of follow-up, 1587 incident MIs were registered, and these cases were compared with 3959 age- and sex-matched controls. Circulating levels of the ECM proteins CD147 (ECM metalloproteinase inducer; EMMPRIN), cartilage oligomeric matrix protein (COMP: thrombospondin-5) and YKL-40 (chitinase-3-like-1) were measured by enzyme immunoassays. Results We found an inverse association between COMP (quartile (Q) 4 vs. Q1: hazard ratio 0.81 (95% confidence interval: 0.67-0.98)) and YKL-40 (Q4 vs. Q1: hazard ratio 0.77 (0.62-0.95)) with incidence of MI after full multivariable adjustment. Serum CD147 was not associated with MI risk in adjusted analysis. Conclusion High levels of COMP and YKL-40 were associated with lower risk of incident MI, suggesting a potential beneficial role in promoting plaque stability in individuals without incident cardiovascular disease.
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Vik, K. L., Romundstad, P., Carslake, D., Davey Smith, G., & Nilsen, T. I. (2014). Transgenerational effects of parental cardiovascular disease and risk factors on offspring mortality: family-linkage data from the HUNT Study, Norway. Eur J Prev Cardiol, .
Abstract: BACKGROUND: Cardiovascular risk factors are known to be associated between parents and offspring. However, whether these associations are reflected in increased offspring mortality has not been extensively studied. DESIGN: This was a family study of 32,536 father-offspring and 39,614 mother-offspring pairs who participated in the HUNT Study, Norway. METHODS: Adjusted hazard ratios (HRs) for offspring total and cardiovascular mortality associated with parental levels of cardiovascular disease risk factors were estimated using Cox regression. RESULTS AND CONCLUSIONS: Fathers' and mothers' reporting of cardiovascular disease (HRs: 1.18; 95% CI 1.04-1.32 and 1.20; 1.07-1.35, respectively), diabetes (HRs: 1.22; 95% CI 1.00-1.49 and 1.21; 1.05-1.40, respectively), and current smoking (HRs: 1.21; 95% CI 1.08-1.36 and 1.30; 1.15-1.47, respectively) was associated with total mortality in offspring. An inverse association was found with maternal height (HR: 0.95; 95% CI 0.91-0.99), and a suggestive inverse association with paternal height (HR: 0.98; 95% CI 0.93-1.03). Relations with offspring cardiovascular mortality were less clear and consistent. Offspring whose parents both had a risk factor did not seem to have higher mortality than would be expected from the independent effects of each parent.
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