| 5. |
- Wamala, S. P, et al.
(författare)
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Socioeconomic status and determinants of hemostatic function in healthy women
- 1999
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Ingår i: Arteriosclerosis, Thrombosis and Vascular Biology. - Karolinska Inst, Dept Publ Hlth Sci, Div Prevent Med, S-14157 Huddinge, Sweden. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Karolinska Hosp, Dept Cariol, S-10401 Stockholm, Sweden. Karolinska Hosp, King Gustaf V Res Inst, Atherosclerosis Res Unit, S-10401 Stockholm, Sweden. : LIPPINCOTT WILLIAMS & WILKINS. - 1079-5642 .- 1524-4636. ; 19:3, s. 485-492
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Tidskriftsartikel (refereegranskat)abstract
- Hemostatic factors are reported to be associated with coronary heart disease (CHD). Socioeconomic status (SES) is 1 of the determinants of the hemostatic profile, but the factors underlying this association are not well known. Our aim was to examine determinants of the socioeconomic differences in hemostatic profile. Between 1991 and 1994, we studied 300 healthy women, aged 30 to 65 years, who were representative of women living in the greater Stockholm area. Fibrinogen, factor VII mass concentration (FVII:Ag), activated factor VII (FVIIa), von Willebrand factor (vWF), and plasminogen activator inhibitor-1 (PAI-1) were measured. Educational attainment was used as a measure of SES. Low educational level and an unfavorable hemostatic profile were both associated with older age, unhealthful life style, psychosocial stress, atherogenic biochemical factors, and hypertension. Levels of hemostatic factors increased with lower educational attainment. Independently of age, the differences between the lowest (mandatory) and highest (college/university) education in FVII:Ag levels were 41 mu g/L (95% confidence interval [CI] 15 to 66 mu g/L, P=0.001), 0.26 g/L (95% CI, 0.10 to 0.42 g/L, P=0.001) in fibrinogen levels, and 0.11 U/mL (95% CI, 0.09 to 0.12 U/mL, P=0.03) in levels of vWF. The corresponding differences in FVIIa and PAI-1 were not statistically significant. With further adjustment for menopausal status, family history of CHD, marital status, psychosocial stress, lifestyle patterns, biochemical factors, and hypertension, statistically significant differences between mandatory and college/university education were observed in FVII:Ag (difference=34 mu g/L; 95% CI, 2 to 65 mu g/L, P=0.05) but not in fibrinogen (difference 0.03 g/L; 95% CI, -0.13 to 0.19 g/L, P=0.92) or in VWF (difference=0.06 U/mL; 95% CI, -0.10 to 0.22 U/mL, P=0.45). An educational gradient was most consistent and statistically significant for FVII:Ag, fibrinogen, and VWF. Age, psychosocial stress, unhealthful life style, atherogenic biochemical factors, and hypertension mediated the association of low educational level with elevated levels of fibrinogen and vWF. Psychosocial stress and unhealthful life style were the most important contributing factors. There was an independent association between education and FVII:Ag, which could not be explained by any of these factors.
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| 10. |
- Garpenstrand, H, et al.
(författare)
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Plasma semicarbazide-sensitive amine oxidase in stroke
- 1999
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Ingår i: European neurology. - : S. Karger AG. - 0014-3022 .- 1421-9913. ; 41:1, s. 20-23
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Tidskriftsartikel (refereegranskat)abstract
- Semicarbazide-sensitive amine oxidase (SSAO) has been suggested to be involved in the development of vascular endothelial damage. The source of the soluble form of SSAO found in the blood serum is unknown. However, it has been speculated that it is secreted from cells within the vascular wall where high activity of the enzyme is found. Altered SSAO activity has been reported in atherosclerotic plaques of the human aorta. Stroke is a manifestation of long-term atherosclerotic disease, and in this study, plasma SSAO activities were estimated in 42 patients with cerebral thrombosis and 26 patients with cerebral embolism, and compared to two control groups of 45 individuals in total. No statistically significant differences were found between the patient groups and controls regarding plasma SSAO activity, suggesting that changes in the soluble form of SSAO found in the circulation do not play a major role in this type of acute cerebrovascular event. Furthermore, it does not seem likely that the involvement of vascular tissue occurring in stroke results in release of the enzyme into the circulation. Nevertheless, further studies on tissue-bound SSAO in cerebral vessels would be of great interest.
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