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  • 1
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    Online Resource
    Alcohol Consumption and Hemostatic Factors : Analysis of the Framingham Offspring Cohort
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Circulation Vol. 104, No. 12 ( 2001-09-18), p. 1367-1373
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 104, No. 12 ( 2001-09-18), p. 1367-1373
    Abstract: Background — Moderate alcohol consumers have lower rates of cardiovascular disease than abstainers. One proposed mechanism is a beneficial effect on hemostatic parameters, but previous studies have provided conflicting results. Methods and Results — We measured levels of fibrinogen, plasma viscosity, von Willebrand factor, factor VII, plasminogen activator inhibitor antigen-1, and tissue plasminogen activator antigen in a cross-sectional analysis of 3223 adults free of cardiovascular disease enrolled in the Framingham Offspring Study. We assessed their alcohol consumption with a standardized questionnaire. Light-to-moderate alcohol consumption was associated with lower levels of fibrinogen, plasma viscosity, von Willebrand factor, and factor VII. This association was most pronounced for consumers of 3 to 7 drinks weekly for viscosity and 7 to 21 drinks weekly for the other hemostatic measures. Alcohol intake of 7 to 21 drinks weekly or more was associated with impaired fibrinolytic potential, reflected by higher levels of plasminogen activator inhibitor antigen-1 and tissue plasminogen activator antigen. Wine drinkers had lower plasminogen activator inhibitor antigen-1 levels than other drinkers, particularly at 3 to 21 drinks weekly, but beverage type did not otherwise consistently affect the results. Conclusions — Light-to-moderate alcohol consumption is associated with lower levels of coagulatory factors, but higher intake is associated with impaired fibrinolytic potential. These findings are consistent with the hypothesis that a balance between hemostatic and fibrinolytic activity may contribute to the complex relation of alcohol use with coronary heart disease.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/hc3701.096067
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
    detail.hit.zdb_id: 1466401-X
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  • 2
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    Hypobetalipoproteinemia Is Associated With Low Levels of Hemostatic Risk Factors in the Framingham Offspring Population
    Ovid Technologies (Wolters Kluwer Health) ; 1997
    In:  Circulation Vol. 95, No. 4 ( 1997-02-18), p. 825-830
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 95, No. 4 ( 1997-02-18), p. 825-830
    Abstract: Background Given the importance of thrombosis in causation of acute coronary syndromes, it is possible that the beneficial effect of low lipid levels on the risk of coronary events is achieved by lowering thrombotic potential of the blood. Hypobetalipoproteinemia is characterized by plasma concentrations of apolipoprotein B and LDL cholesterol that are one third of those observed in the general population. The aim of this study was to utilize subjects with hypobetalipoproteinemia to examine the relation between thrombotic potential and low levels of LDL cholesterol. Methods and Results Hemostatic risk factors were measured in 1878 individuals (1003 women and 875 men) participating in cycle 5 of the Framingham Offspring Study. The subjects were divided into five groups on the basis of LDL cholesterol level. Subjects with hypobetalipoproteinemia (LDL cholesterol 〈 70 mg/dL) had the lowest levels of fibrinogen, plasminogen activator inhibitor–1 antigen, and tissue plasminogen activator antigen. As LDL cholesterol increased, there was a significant increase in the levels of the hemostatic risk factors, with the exception of von Willebrand factor antigen. Adjustment with multivariate regression analyses for the covariates age, sex, body mass index, diabetes mellitus, smoking, alcohol intake, triglyceride level, and use of antihypertensive medication did not materially alter the results. Conclusions Decreasing levels of LDL cholesterol are associated with decreasing levels of hemostatic risk factors. Subjects with hypobetalipoproteinemia have the lowest levels of hemostatic risk factors and may be protected against thrombotic complications of atherosclerotic cardiovascular disease because of reduced thrombotic potential. One mechanism by which lipid-lowering therapy may decrease clinical cardiac events is through a reduction in thrombotic tendency.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.95.4.825
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1997
    detail.hit.zdb_id: 1466401-X
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  • 3
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    Factor VII Gene Polymorphism, Factor VII Levels, and Prevalent Cardiovascular Disease : The Framingham Heart Study
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 20, No. 2 ( 2000-02), p. 593-600
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 20, No. 2 ( 2000-02), p. 593-600
    Abstract: Abstract —Elevated factor VII levels have been associated with increased cardiovascular risk in some studies. The arginine/glutamine (Arg/Gln) polymorphism of the factor VII gene has been previously shown to modify factor VII levels. However, the presence of a gene/environment interaction on factor VII levels or a link with cardiovascular disease (CVD) remains uncertain. We studied subjects from the Framingham Heart Study to determine (1) the extent to which this genetic polymorphism affects factor VII levels; (2) whether interactions exist between this polymorphism and environmental factors on factor VII levels; and (3) the association between the polymorphism and CVD. Genotype data and factor VII antigen levels were available in 1816 subjects. Factor VII levels differed significantly among genotypes in an additive fashion: Gln homozygous, 82.7±2.5%; heterozygous, 92.2±0.7%; and Arg homozygous, 100.5±0.4% ( P 〈 0.0001). The polymorphism was the strongest, single predictor of factor VII levels, explaining 7.7% of the total variance of factor VII levels, whereas other traditional risk factors combined explained an additional 11.5% of the variance. There was an interaction ( P =0.02) between the genotype and total cholesterol on factor VII levels, such that the correlation coefficient and slope (factor VII level/total cholesterol) were greatest in Gln/Gln subjects. Among 3204 subjects characterized for genotype and CVD, there was no significant relationship between the genotype and CVD ( P =0.12). In the Framingham Heart Study, the Arg/Gln polymorphism was significantly associated with factor VII antigen levels. The strength of the association suggests that genetic variation plays an important role in determining factor VII levels. However, despite being associated with factor VII levels, the Arg/Gln polymorphism was not associated with prevalent CVD.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/01.ATV.20.2.593
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
    detail.hit.zdb_id: 1494427-3
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  • 4
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    Association of Blood Pressure With Fibrinolytic Potential in the Framingham Offspring Population
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Circulation Vol. 101, No. 3 ( 2000-01-25), p. 264-269
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 101, No. 3 ( 2000-01-25), p. 264-269
    Abstract: Background —Hypertension is an established risk factor for acute coronary events. Because fibrinolytic and hemostatic factors are also associated with cardiovascular disease, we examined the relations of systolic and diastolic blood pressures (SBP and DBP) to levels of plasminogen activator inhibitor antigen, tissue plasminogen activator antigen, fibrinogen, factor VII, von Willebrand factor, fibrinogen, and plasma viscosity in subjects of the Framingham Offspring Study. Methods and Results —We studied 1193 men and 1459 women after the exclusion of subjects with known cardiovascular disease and those receiving anticoagulant or antihypertensive therapy. Linear regression models were used to evaluate SBP and DBP as predictors of fibrinolytic and hemostatic factor levels in separate sex models, with adjustment for age, body mass index, smoking, diabetes, total cholesterol, HDL, triglycerides, alcohol intake, and estrogen use (in women). In both sexes, levels of plasminogen activator inhibitor and tissue plasminogen activator antigen were positively related to SBP and DBP ( P 〈 0.001). Plasma viscosity was positively related to SBP ( P =0.008) and DBP ( P =0.001) in women only. There was no association between SBP or DBP and fibrinogen, factor VII, or von Willebrand factor in either sex. Conclusions —These data suggest that impaired fibrinolysis may play an important role in the pathogenesis of cardiovascular disease in hypertensive patients.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.101.3.264
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
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  • 5
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    Online Resource
    Platelet Glycoprotein IIIa Pl A Polymorphism, Fibrinogen, and Platelet Aggregability : The Framingham Heart Study
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Circulation Vol. 104, No. 2 ( 2001-07-10), p. 140-144
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 104, No. 2 ( 2001-07-10), p. 140-144
    Abstract: Background — Recent data suggest that the Pl A2 allele of the platelet glycoprotein IIIa receptor may be a genetic risk factor for cardiovascular disease. We previously reported that the Pl A2 allele was associated with increased platelet aggregability, as indicated by lower epinephrine threshold concentrations. Paradoxically, however, it has been reported that Pl A2 -positive platelets have reduced fibrinogen binding. Because fibrinogen mediates platelet aggregability, we hypothesized that plasma fibrinogen levels may interact with Pl A genotype in modulating platelet aggregability. Methods and Results — Glycoprotein IIIa Pl A genotype, fibrinogen level, and platelet aggregability were ascertained in 1340 subjects enrolled into the Framingham Offspring Study. Platelet aggregability was evaluated by the Born method. Higher fibrinogen levels were associated with increased epinephrine-induced aggregation ( P =0.002) and a trend for ADP-induced aggregation ( P =0.07). The fibrinogen effect was genotype specific, however, in that the increase in platelet aggregability with higher fibrinogen was present for the Pl A1/A1 genotype ( P =0.0005 and P =0.03 for epinephrine- and ADP-induced aggregation, respectively) but not for the Pl A2 -positive genotype ( P 〉 0.90). Conclusion — Higher fibrinogen levels were associated with increased platelet aggregability. However, the association between fibrinogen and platelet aggregability was genotype specific. This interaction may be responsible for the conflicting findings regarding Pl A genotype and platelet aggregability. Further study of this gene-environment interaction may provide insight into cardiovascular disease risk.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.104.2.140
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
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  • 6
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    Association between obesity and a prothrombotic state: the Framingham Offspring Study
    Georg Thieme Verlag KG ; 2004
    In:  Thrombosis and Haemostasis Vol. 91, No. 04 ( 2004), p. 683-689
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 91, No. 04 ( 2004), p. 683-689
    Abstract: Although obesity is associated with increased cardiovascular risk, the mechanism has not been fully explained. Since thrombosis is a critical component of cardiovascular disease, we examined the relationship between obesity and hemostatic factors. We studied 3230 subjects (55% females, mean age 54 years) without a history of cardiovascular disease in cycle 5 of the Framingham Offspring Study. Obesity was assessed by body mass index and waist-to-hip ratio. Fasting blood samples were obtained for fibrinogen, plasminogen activator inhibitor (PAI-1) antigen, tissue plasminogen activator (tPA) antigen, factor VII antigen, von Willebrand factor (VWF), and plasma viscosity. Body mass index was directly associated with fibrinogen, factor VII, PAI-1 and tPA antigen in both men and women (p 〈 0.001) and with VWF and viscosity in women. Similar associations were present between waist-to-hip ratio and the hemostatic factors. With minor exceptions for VWF and viscosity, all associations persisted after controlling for age, smoking, total and HDL cholesterol, triglycerides, glucose level, blood pressure, and use of antihypertensive medication. The association between increased body mass index and waist-to-hip ratio and prothrombotic factors and impaired fibrinolysis suggests that obesity is a risk factor whose effect is mediated in part by a prothrombotic state.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1160/TH03-01-0014
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2004
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  • 7
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    Online Resource
    Hemostatic state and atrial fibrillation (The Framingham Offspring Study)
    Elsevier BV ; 2001
    In:  The American Journal of Cardiology Vol. 87, No. 2 ( 2001-01), p. 168-171
    Details
    In: The American Journal of Cardiology, Elsevier BV, Vol. 87, No. 2 ( 2001-01), p. 168-171
    Type of Medium: Online Resource
    ISSN: 0002-9149
    URL: Article
    DOI: 10.1016/S0002-9149(00)01310-2
    RVK:
    XA 18500
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2001
    detail.hit.zdb_id: 2019595-3
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  • 8
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    Online Resource
    Alcohol Consumption and Platelet Activation and Aggregation Among Women and Men: The Framingham Offspring Study
    Wiley ; 2005
    In:  Alcoholism: Clinical & Experimental Research Vol. 29, No. 10 ( 2005-10), p. 1906-1912
    Details
    In: Alcoholism: Clinical & Experimental Research, Wiley, Vol. 29, No. 10 ( 2005-10), p. 1906-1912
    Type of Medium: Online Resource
    ISSN: 0145-6008
    URL: Article
    DOI: 10.1097/01.alc.0000183011.86768.61
    Language: English
    Publisher: Wiley
    Publication Date: 2005
    detail.hit.zdb_id: 2046886-6
    detail.hit.zdb_id: 3167872-5
    SSG: 15,3
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  • 9
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    Online Resource
    Increased Platelet Aggregability Associated With Platelet GPIIIa Pl A2 Polymorphism : The Framingham Offspring Study
    Ovid Technologies (Wolters Kluwer Health) ; 1999
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 19, No. 4 ( 1999-04), p. 1142-1147
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 19, No. 4 ( 1999-04), p. 1142-1147
    Abstract: Abstract —The platelet glycoprotein IIb/IIIa (GP IIb/IIIa) plays a pivotal role in platelet aggregation. Recent data suggest that the Pl A2 polymorphism of GPIIIa may be associated with an increased risk for cardiovascular disease. However, it is unknown if there is any association between this polymorphism and platelet reactivity. We determined GP IIIa genotype and platelet reactivity phenotype data in 1422 subjects from the Framingham Offspring Study. Genotyping was performed using PCR-based restriction fragment length polymorphism analysis. Platelet aggregability was evaluated by the Born method. The threshold concentrations of epinephrine and ADP were determined. Allele frequencies of Pl A1 and Pl A2 were 0.84 and 0.16, respectively. The presence of 1 or 2 Pl A2 alleles was associated with increased platelet aggregability as indicated by incrementally lower threshold concentrations for epinephrine and ADP. For epinephrine, the mean concentrations were 0.9 μmol/L (0.9 to 1.0) for homozygous Pl A1 , 0.7 mmol/L (0.7 to 0.9) for the heterozygous Pl A1 / Pl A2 , and 0.6 μmol/L (0.4 to 1.0) for homozygous Pl A2 individuals, P =0.009. The increase in aggregability induced by epinephrine remained highly significant ( P =0.007) after adjustment for covariates. For ADP-induced aggregation, the respective mean concentrations were 3.1 μmol/L (3.0 to 3.2), 3.0 μmol/L (2.9 to 3.2), and 2.8 μmol/L (2.4 to 3.3); P =0.19 after adjustment for covariates. Our findings indicate that molecular variants of the gene encoding GP IIIa play a role in platelet reactivity in vitro. Our observations are compatible with and provide an explanation for the reported association of the Pl A2 allotype with increased risk for cardiovascular disease.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/01.ATV.19.4.1142
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1999
    detail.hit.zdb_id: 1494427-3
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  • 10
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    Relations of Inflammatory Biomarkers and Common Genetic Variants With Arterial Stiffness and Wave Reflection
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Hypertension Vol. 51, No. 6 ( 2008-06), p. 1651-1657
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 51, No. 6 ( 2008-06), p. 1651-1657
    Abstract: Inflammation causes vascular dysfunction and perpetuates proatherosclerotic processes. We hypothesized that a broad panel of inflammatory biomarkers and single nucleotide polymorphisms in inflammatory genes is associated with vascular stiffness. We assessed 12 circulating inflammatory biomarkers (C-reactive protein, fibrinogen, interleukin-6, intercellular adhesion molecule-1, lipoprotein-associated phospholipase-A2 [mass and activity], monocyte chemoattractant protein-1, myeloperoxidase, CD40 ligand, osteoprotegerin, P-selectin, and tumor necrosis factor receptor-II) in relation to tonometry variables (central pulse pressure, mean arterial pressure, forward pressure wave, reflected pressure wave, carotid-femoral pulse wave velocity, and augmentation index) measured in 2409 Framingham Heart Study participants (mean age: 60 years; 55% women; 13% ethnic/racial minorities). Single nucleotide polymorphisms (n=2195) in 240 inflammatory candidate genes were related to tonometry measures in 1036 white individuals. In multivariable analyses, biomarkers explained 〈 1% of any tonometry measure variance. Applying backward elimination, markers related to tonometry ( P 〈 0.01) were as follows: tumor necrosis factor receptor-II (inversely) with mean arterial pressure; C-reactive protein (positively) and lipoprotein-associated phospholipase-A2 (inversely) with reflected pressure wave; and interleukin-6 and osteoprotegerin (positively) with carotid-femoral pulse wave velocity. In genetic association analyses, lowest P values (false discovery rate 〈 0.50) were observed for rs10509561 ( FAS ), P =6.6×10 −5 for central pulse pressure and rs11559271 ( ITGB2 ), P =1.1×10 −4 for mean arterial pressure. These data demonstrate that, in a community-based sample, circulating inflammatory markers tumor necrosis factor receptor-II (mean arterial pressure), C-reactive protein, lipoprotein-associated phospholipase-A2 activity (reflected pressure wave), interleukin-6, and osteoprotegerin (carotid-femoral pulse wave velocity) were significantly but modestly associated with measures of arterial stiffness and wave reflection. Additional studies are needed to determine whether variation in inflammatory marker genes is associated with tonometry measures.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.107.105668
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
    detail.hit.zdb_id: 2094210-2
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