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Träfflista för sökning "WFRF:(Raitakari Olli) srt2:(2005-2009)"

Sökning: WFRF:(Raitakari Olli) > (2005-2009)

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2.
  • Juonala, Markus, et al. (författare)
  • Geographic Origin as a Determinant of Carotid Artery Intima-Media Thickness and Brachial Artery Flow-Mediated Dilation. The Cardiovascular Risk in Young Finns Study.
  • 2005
  • Ingår i: Arteriosclerosis, Thrombosis and Vascular Biology. - : Lippincott Williams & Wilkins. - 1524-4636. ; 25:2, s. 392-398
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective - People living in eastern Finland have approximate to 40% higher coronary heart disease mortality rates than western Finns. Whether this is because of genetic or environmental factors is unknown. We examined the effect of geographic family origin on subclinical atherosclerosis among young Finns. Methods and Results - As part of a longitudinal follow-up study, we measured carotid intima-media thickness (IMT) in 2264 and brachial flow-mediated dilation (FMD) in 2109 white adults, aged 24 to 39 years. Subjects from eastern Finland had greater IMT and lower FMD compared with western subjects. These differences accentuated when the subjects' family origin ( grandparents' birthplace) was taken into account and remained significant after adjusting for several environmental factors. Among subjects with all grandparents born in eastern or western Finland, IMTs were ( mean +/- SEM) 0.592 +/- 0.003 versus 0.565 +/- 0.005 mm ( P < 0.0001), respectively. The corresponding FMD values were 7.61 +/- 0.15% versus 8.75 +/- 0.26%; P < 0.01. The number of grandparents born in eastern Finland was directly related to IMT ( P < 0.0001) and inversely to FMD ( P < 0.05). Conclusions - Young adults originating from eastern Finland have greater carotid IMT and lower brachial FMD than western Finns. Consistent with a hereditable component predisposing to or protecting from atherosclerosis, these differences accentuated when subjects' family origin was taken into account.
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3.
  • Laaksonen, Marko, 1975-, et al. (författare)
  • Left-ventricular hypertrophy associates to impaired maximal myocardial perfusion in endurance-trained men
  • 2009
  • Konferensbidrag (refereegranskat)abstract
    • Long-term endurance training induces morphological adaptations in heart, such as left-ventricular (LV) hypertrophy caused by wall thickening and cavity enlargement. Interestingly, these anatomical changes in the heart are strikingly similar to certain pathophysiological changes (Pellicia 2000). Previous studies have shown that the perfusion response in myocardium during dipyridamole- or adenosine infusion is decreased in several pathophysiological states with LV hypertrophy (e.g. Stolen et al. 2004). However, studies in endurance athletes with LV hypertrophy have shown contradictory results on myocardial perfusion response ranging from reduced to increased myocardial perfusion during dipyridamole- or adenosine-induced vasodilation compared to untrained men (Kjaer et al. 2005; Kalliokoski et al. 2002). The degree of hypertrophy could explain the discrepant findings in studies in athletes, but it has not been thoroughly investigated. Thus, we examined totally 31 endurance athletes (ET) and 25 untrained (UT) men in order to study the association between myocardial functional and anatomical parameters measured with echocardiography, and myocardial perfusion (at rest and during maximal vasodilation induced by iv adenosine) measured with Positron Emission Tomography. Both VO2max (60+-5 vs 42+-8 ml/kg/min, p<0.001) and LVmass index (169+-27 vs 102+-15 g/m2, p<0.001) were markedly higher in ET. Resting myocardial perfusion was similar between the groups (ET 0.7+-0.2 vs UT 0.8+-0.2 ml/g/min, p=0.22) whereas adenosine-stimulated perfusion was lower in ET (2.9+-1.0 vs 3.7+-1.0 ml/g/min, p<0.01). VO2max correlated inversely with adenosine-stimulated perfusion in ET (r=-0.39, p=0.03) and with resting perfusion in UT (-0.49, p=0.01). Forward LV work correlated linearly with resting perfusion in both groups (ET r=0.54, p<0.01; UT r=0.50, p=0.01). ET group was further divided into three subgroups according to LVmass index (ET1: LVmass index <150g/m2, n=9; ET2 LVmass index 150-180 g/m2, n=12; ET3 LVmass index >180 gm2, n=10). Adenosine-induced myocardial perfusion decreased gradually when LVmass increased (UT 3.7+-1.+0 vs ET1 3.3+-0.9 vs ET2 2.7+-1.4 vs ET3 2.6+-0.5 mL g-1 min-1, p=0.008). LVmass index was also inversely related to adenosine-induced perfusion in entire study population (r=-0.46, p<0.01). Therefore, these results suggest that endurance training-induced severe cardiac hypertrophy impairs myocardial perfusion capacity. Kalliokoski K et al. (2002) Med Sci Sports Exerc 34:948-53 Kjaer A et al. (2005) Am J Cardiol 96:1692-98 Pellicia A (2000) Curr Cardiol Rep 2(2):166-71 Stolen KQ et al (2004) 10(2):132-40
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4.
  • Owen, Christopher G, et al. (författare)
  • Does initial breastfeeding lead to lower blood cholesterol in adult life? A quantitative review of the evidence.
  • 2008
  • Ingår i: American Journal of Clinical Nutrition. - 0002-9165 .- 1938-3207. ; 88:2, s. 305-14
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Earlier studies have suggested that infant feeding may program long-term changes in cholesterol metabolism. OBJECTIVE: We aimed to examine whether breastfeeding is associated with lower blood cholesterol concentrations in adulthood. DESIGN: The study consisted of a systematic review of published observational studies relating initial infant feeding status to blood cholesterol concentrations in adulthood (ie, aged >16 y). Data were available from 17 studies (17 498 subjects; 12 890 breastfed, 4608 formula-fed). Mean differences in total cholesterol concentrations (breastfed minus formula-fed) were pooled by using fixed-effect models. Effects of adjustment (for age at outcome, socioeconomic position, body mass index, and smoking status) and exclusion (of nonexclusive breast feeders) were examined. RESULTS: Mean total blood cholesterol was lower (P = 0.037) among those ever breastfed than among those fed formula milk (mean difference: -0.04 mmol/L; 95% CI: -0.08, 0.00 mmol/L). The difference in cholesterol between infant feeding groups was larger (P = 0.005) and more consistent in 7 studies that analyzed "exclusive" feeding patterns (-0.15 mmol/L; -0.23, -0.06 mmol/L) than in 10 studies that analyzed nonexclusive feeding patterns (-0.01 mmol/L; -0.06, 0.03 mmol/L). Adjustment for potential confounders including socioeconomic position, body mass index, and smoking status in adult life had minimal effect on these estimates. CONCLUSIONS: Initial breastfeeding (particularly when exclusive) may be associated with lower blood cholesterol concentrations in later life. Moves to reduce the cholesterol content of formula feeds below those of breast milk should be treated with caution.
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