53 research outputs found

    Risk factor profile of coronary artery disease in black South Africans

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    Objectives: The aim of this study was to investigate the risk factor profile of coronary artery disease (CAD) in black South Africans. The study was motivated by the increased prevalence of CAD in South Africa, probably as a result of urbanisation. Despite this increase, however, very little is known regarding the cause, risk factor profile and clinical presentations of CAD in the black South African population. Design: A case control study was performed investigating 40 (33 men, 7 women) angiographically defined CAD patients and 20 (13 men and 7 women) age and body composition matched controls. Results: There was no difference in physical activity, sociodemographic factors or dietary intakes between the CAD and control group, except for the CAD patients consuming less vit C (40.9 vs 61.3 mg). The CAD group had significantly higher LDL-C, fasting glucose and CRP. There was also a significantly higher prevalence of smokers (35 vs 10%), hypertension (95 vs 75%) small dense LDL (73 vs 15%) and insulin resistance (M-value of 4.15 vs 12.5 mg/kg/min) in the CAD compared to the control group. In a logistic regression model, small dense LDL and insulin resistance were the main predictors of CAD. Conclusions: Black South African CAD patients had increased levels of the same risk factors that are typically seen in Caucasians with insulin resistance and small dense LDL being particularly significant in their contribution

    Plasma Clot Lysis Time and Its Association with Cardiovascular Risk Factors in Black Africans

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    Studies in populations of European descent show longer plasma clot lysis times (CLT) in patients with cardiovascular disease (CVD) than in controls. No data are available on the association between CVD risk factors and fibrinolytic potential in black Africans, a group undergoing rapid urbanisation with increased CVD prevalence. We investigated associations between known CVD risk factors and CLT in black Africans and whether CLTs differ between rural and urban participants in light of differences in CVD risk. Data from 1000 rural and 1000 urban apparently healthy black South Africans (35-60 years) were cross-sectionally analysed. Increased PAI-1act, BMI, HbA1c, triglycerides, the metabolic syndrome, fibrinogen concentration, CRP, female sex and positive HIV status were associated with increased CLTs, while habitual alcohol consumption associated with decreased CLT. No differences in CLT were found between age and smoking categories, contraceptive use or hyper- and normotensive participants. Urban women had longer CLT than rural women while no differences were observed for men. CLT was associated with many known CVD risk factors in black Africans. Differences were however observed, compared to data from populations of European descent available in the literature, suggesting possible ethnic differences. The effect of urbanisation on CLT is influenced by traditional CVD risk factors and their prevalence in urban and rural communities

    In black south africans from rural and urban communities, the 4G/5G PAI-1 polymorphism influences PAI-1 activity, but not plasma clot lysis time

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    Data on genetic and environmental factors influencing PAI-1 levels and their consequent effect on clot lysis in black African populations are limited. We identified polymorphisms in the promoter area of the PAI-1 gene and determined their influence on PAI-1act levels and plasma clot lysis time (CLT). We also describe gene-environment interactions and the effect of urbanisation. Data from 2010 apparently healthy urban and rural black participants from the South African arm of the PURE study were cross-sectionally analysed. The 5G allele frequency of the 4G/5G polymorphism was 0.85. PAI-1act increased across genotypes in the urban subgroup (p = 0.009) but not significantly in the rural subgroup, while CLT did not differ across genotypes. Significant interaction terms were found between the 4G/5G polymorphism and BMI, waist circumference and triglycerides in determining PAI-1act, and between the 4G/5G polymorphism and fibrinogen and fibrinogen gamma prime in determining CLT. The C428T and G429A polymorphisms did not show direct relationships with PAI-1act or CLT but they did influence the association of other environmental factors with PAI-1 act and CLT. Several of these interactions differed significantly between rural and urban subgroups, particularly in individuals harbouring the mutant alleles. In conclusion, although the 4G/5G polymorphism significantly affected PAI-1act, it contributed less than 1% to the PAI-1 act variance. (Central) obesity was the biggest contributor to PAI-1act variance (12.5%). Urbanisation significantly influenced the effect of the 4G/5G polymorphism on PAI-1act as well as gene-environment interactions for the C428T and G429A genotypes in determining PAI-1act and CLT

    Educating and training a workforce for nutrition in a post-2015 world.

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    Nearly all countries in the world today are burdened with malnutrition, manifesting as undernutrition, micronutrient deficiencies, and/or overweight and obesity. Despite some progress, efforts to alleviate malnutrition are hampered by a shortage in number, skills, and geographic coverage, of a workforce for nutrition. Here, we report the findings of the Castel Gandolfo workshop, a convening of experts from diverse fields in March 2014 to consider how to develop the capacity of a global cadre of nutrition professionals for the post-2015 development era. Workshop participants identified several requirements for developing a workforce for nutrition, including an ability to work as part of a multisectoral team; communication, advocacy, and leadership skills to engage decision makers; and a set of technical skills to address future challenges for nutrition. Other opportunities were highlighted that could immediately contribute to capacity development, including the creation of a consortium to link global North and South universities, online training modules for middle managers, and practical, hands-on experiences for frontline nutrition workers. Institutional and organizational support is needed to enable workshop recommendations on education and training to be effectively implemented and sustained. The findings from the Castel Gandolfo workshop can contribute to the delivery of successful nutrition-relevant actions in the face of mounting external pressures and informing and attaining the forthcoming Sustainable Development Goals

    Die effek van simvastatien, 'n HMG-KoA-reduktase-inhibeerder op die hemostatiese balans in hipercholesterolemiese pasiënte

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    PhD (Voeding), North-West University, Potchefstroom CampusThe effect of simvastatin, a HMG-CoA reductase inhibitor, on the haemostatic balance in hypercholesterolaemic patients. Coronary heart disease (CHO) is an important cause of mortality and morbidity for a large proportion of the economically active persons in South Africa. Two hundred and twenty six out of each 100000 deaths amongst Asians, 11 O out of each 100000 deaths amongst coloureds, 139 out of each 100000 deaths amongst whites and 11 out of each 100000 deaths amongst Africans can be ascribed to CHO. The prevalence of familial hypercholesterolaemia (FH) amongst the Afrikaner is unusually high and is estimated to be 1 in 70. FH is characterised by elevated levels of low density lipoprotein cholesterol (LOL-C). The use of 3-hydroxy-3- methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors is the most effective way to lower high LOL-C levels in these patients. Previously reported primary and secondary prevention trials have shown that the use of HMG-CoA reductase inhibitors may reduce cardiovascular as well as all-cause mortality. Increased levels of plasma fibrinogen has been shown to be a CHO risk factor to the same or even greater extent than cholesterol. Hypercholesterolaemia is also associated with increased fibrinogen levels. Studies on the effect of HMG-CoA reductase inhibitors on plasma fibrinogen levels and other haemostatic variables have yielded conflicting results. The objective of this study was to study the treatment effects of the HMG-CoA reductase inhibitor, simvastatin, on the haemostatic balance in 29 unrelated FH patients. Twenty nine FH patients, 12 men and 17 women, were treated with 10 mg simvastatin daily for 4 weeks and then with 20 mg simvastatin for 1 O weeks. Serum lipids and various safety parameters were monitored throughout the study. The following haemostatic variables were measured: fibrinogen, antithrombin Ill, thrombin-antithrombin complex (TAT), d-dimer, az-antiplasmin, plasmin-az- antiplasmin complex (PAP}, tissue plasminogen activator and plasminogen activator inhibitor-1 . Women had significantly higher concentrations of fibrinogen (3.31 [0.99] g/L vs 2. 75 [0.75] g/L}, PAP (0.39 [0.39] mg/L vs 0.21 [0.13] mg/L) and d-dimer (12.0 [10.6] µg/L vs 3.90 [4.40] µg/L) than men. As was exp!3cted, simvastatin treatment significantly reduced LDL-C in both men (7.54 [3.12] mmol/L to 4.81 [0.92] mmol/L) and women (7.34 [1 .81] mmol/L to 5.11 [1.03] mmol/L). Simvastatin treatment significantly increased plasma fibrinogen levels in men (2.82 [0.67] g/L to 3.19 [0. 7 4] g/L) but not in women. This finding suggests that the hyperfibrinogenaemia associated with hypercholesterolaemia in FH patients is probably not caused by an abnormal lipid profile. The increases in fibrinogen in men were accompanied by compensatory profibrinolytic changes in the TAT:PAP ratio, a marker of the haemostatic balance. This study provides evidence that possible adverse changes in plasma fibrinogen in men, as a result of lipid lowering treatment with simvastatin occurs. This is accompanied by compensatory profibrinolytic changes in men. The clinical implications of this finding requires further investigation. The haemostatic system in men and women appears to respond differently to simvastatin therapy and may be influenced by different factors. The haemostatic balance in women appears to be at a "higher" level of activity that in men.Doctora

    Meganismes waardeur sommige plasminogeenaktiveerders en -inhibeerders plasmafibrinogeen en die risiko vir hartvatsiektes beïnvloed

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    MSc (Fisiologie), North-West University, Potchefstroom CampusIncreased levels of plasma fibrinogen is regarded as an independent risk factor for coronary heart disease (CHD). Factors which influence fibrinogen levels are poorly understood. There is a possibility that tPA and PAI-1 may influence fibrinogen levels through effects on the catabolism of fibrinogen. Plasminogen activator inhibitor 1 (PAl-1) is the principal inhibitor of the fibrinolytic enzyme system (Loskutoff et al., 1989). High levels of PAI-1, and consequent low fibrinolytic activity, is a risk factor for deep vein thrombosis (Paramo et al., 1985a) and recurrent myocardial infarction (Hamsten et al., 1987a). In comparison with whites, higher fibrinolytic activity has been reported for South African (Franz et al., 1980) and American (Dischinger et al., 1980) blacks. The objective of this study was to examine the possibility that ethnic differences in PAI-1 activity could contribute to ethnic differences in fibrinogen and fibrinolytic activity. A further objective was to establish whether there are any ethnic differences in tPA and PAil activity in response to venous occlusion. Two matched groups of healthy non-smoking ....Master

    Meganismes waardeur sommige plasminogeenaktiveerders en -inhibeerders plasmafibrinogeen en die risiko vir hartvatsiektes beïnvloed

    No full text
    MSc (Fisiologie), North-West University, Potchefstroom CampusIncreased levels of plasma fibrinogen is regarded as an independent risk factor for coronary heart disease (CHD). Factors which influence fibrinogen levels are poorly understood. There is a possibility that tPA and PAI-1 may influence fibrinogen levels through effects on the catabolism of fibrinogen. Plasminogen activator inhibitor 1 (PAl-1) is the principal inhibitor of the fibrinolytic enzyme system (Loskutoff et al., 1989). High levels of PAI-1, and consequent low fibrinolytic activity, is a risk factor for deep vein thrombosis (Paramo et al., 1985a) and recurrent myocardial infarction (Hamsten et al., 1987a). In comparison with whites, higher fibrinolytic activity has been reported for South African (Franz et al., 1980) and American (Dischinger et al., 1980) blacks. The objective of this study was to examine the possibility that ethnic differences in PAI-1 activity could contribute to ethnic differences in fibrinogen and fibrinolytic activity. A further objective was to establish whether there are any ethnic differences in tPA and PAil activity in response to venous occlusion. Two matched groups of healthy non-smoking ....Master
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