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Sökning: L773:1741 8267 > Lind Lars

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1.
  • Arefalk, Gabriel, et al. (författare)
  • Smokeless tobacco (snus) and risk of heart failure : results from two Swedish cohorts
  • 2012
  • Ingår i: European Journal of Cardiovascular Prevention & Rehabilitation. - : Sage Publications. - 1741-8267 .- 1741-8275 .- 2047-4873 .- 2047-4881. ; 19:5, s. 1120-1127
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Oral moist snuff (snus) is discussed as a safer alternative to smoking, and its use is increasing. Based on its documented effect on blood pressure, we hypothesized that use of snus increases the risk of heart failure.Design: Two independent Swedish prospective cohorts; the Uppsala Longitudinal Study of Adult Men (ULSAM), a community-based sample of 1076 elderly men, and the Construction Workers Cohort (CWC), a sample of 118,425 never-smoking male construction workers. Methods: Cox proportional hazards models were used to investigate possible associations of snus use with risk of a first hospitalization for heart failure.Results: In ULSAM, 95 men were hospitalized for heart failure, during a median follow up of 8.9 years. In a model adjusted for established risk factors including past and present smoking exposure, current snus use was associated with a higher risk of heart failure [hazard ratio (HR) 2.08, 95% confidence interval (CI) 1.03-4.22] relative to non-use. Snus use was particularly associated with risk of non-ischaemic heart failure (HR 2.55, 95% CI 1.12-5.82). In CWC, 545 men were hospitalized for heart failure, during a median follow up of 18 years. In multivariable-adjusted models, current snus use was moderately associated with a higher risk of heart failure (HR 1.28, 95% CI 1.00-1.64) and non-ischaemic heart failure (HR 1.28, 95% CI 0.97-1.68) relative to never tobacco use.Conclusion: Data from two independent cohorts suggest that use of snus may be associated with a higher risk of heart failure.
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2.
  • Hansson, Jonas, et al. (författare)
  • Relations of serum MMP-9 and TIMP-1 levels to left ventricular measures and cardiovascular risk factors : a population-based study
  • 2009
  • Ingår i: European Journal of Cardiovascular Prevention & Rehabilitation. - 1741-8267 .- 1741-8275. ; 16:3, s. 297-303
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Extracellular matrix remodeling is a hallmark of pathological left ventricular (LV) hypertrophy and heart failure. This process is tightly controlled by the degrading matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs). We hypothesized that circulating MMP-9 and TIMP-1 levels are altered already in persons with the signs of LV remodeling that forego clinical heart failure. DESIGN: Cross-sectional study in the Prospective Investigation of the Vasculature in Uppsala Seniors , a community-based cohort of 891 70-year-old men and women free from valvular disease, heart failure, and myocardial infarction. METHODS: We examined relations of serum MMP-9 and TIMP-1 to echocardiographic LV geometry and function. All models were adjusted for sex, height, intra-arterial systolic and diastolic blood pressures, antihypertensive medication use, and serum freezer time. RESULTS: Serum TIMP-1 was positively related to LV mass and wall thickness (r=0.15, P<0.0001 and r=0.16, P<0.0001, respectively), with a 32 g higher LV mass and 2.2 mm thicker walls in the fourth compared with the first quartile of serum TIMP-1. Serum TIMP-1 was also inversely related to LV ejection fraction (r=-0.10, P=0.009), but not to LV dimension or diastolic function indices. Serum MMP-9 was only weakly related to LV wall thickness and isovolumic relaxation time (r=0.08, P=0.04 and r=-0.08, P=0.04). CONCLUSION: In this large population-based sample, serum TIMP-1 levels were related to LV mass, wall thickness, and inversely to systolic function. This may imply that extracellular matrix remodeling is involved already in the earliest stages of the process leading to heart failure.
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3.
  • Lind, Lars, et al. (författare)
  • Endothelium-dependent vasodilation is impaired in apparently healthy subjects with a family history of myocardial infarction
  • 2002
  • Ingår i: Journal of Cardiovascular Risk. - : Oxford University Press (OUP). - 1350-6277 .- 1473-5652. ; 9:1, s. 53-57
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: To investigate whether endothelial-dependent vasodilation is altered in healthy subjects with a family history of myocardial infarction. SETTING: Tertiary University Hospital SUBJECTS AND DESIGN: Fifty apparently healthy subjects selected from the general population were subjected to an evaluation of endothelial-dependent vasodilation (EDV) and endothelial-independent vasodilation (EIDV) by means of local infusion of methacholine (MCh, 2 and 4 microg/min) and sodium nitroprusside (SNP, 5 and 10 microg/min) with measurements of forearm blood flow with venous occlusion plethysmography. The occurrence of plaque and the intima-media thickness of the carotid arteries were determined by ultrasonography. RESULTS: Subjects reporting at least one parent suffering from myocardial infarction (n = 11) showed a significantly lower EDV than subjects without such a family history (21 +/- 3.7 vs. 26 +/- 6.7 ml/min/100 ml tissue at MCh 4 microg/min, P<0.05). EIDV was not significantly different between the groups (21 +/- 6.8 vs. 18 +/- 5.4 ml/min/100 ml tissue at SNP 10 microg/min). Age, sex distribution, body mass index, waist to hip ratio, blood pressure, lipids, fasting blood glucose, smoking habits and status of the carotid arteries were not significantly different between the groups. CONCLUSION: A family history of myocardial infarction was found to be associated with an impaired endothelial-dependent vasodilation in the forearm of apparently healthy subjects. The risk factor profile was not different from the control group, suggesting that genetic factors are responsible for the impaired endothelial-dependent vasodilation.
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