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Consistent reports indicate that hypertension is a particularly common finding in black populations. Hypertension occurs at younger ages and is often more severe in terms of blood pressure levels and organ damage than in whites, resulting in a higher incidence of cardiovascular disease and mortality. This review provides an outline of recent advances in the pathophysiological understanding of blood pressure elevation and the consequences thereof in black populations in Africa. This is set against the backdrop of populations undergoing demanding and rapid demographic transition, where infection with the human immunodeficiency virus predominates, and where under and over-nutrition coexist. Collectively, recent findings from Africa illustrate an increased lifetime risk to hypertension from foetal life onwards. From young ages black populations display early endothelial dysfunction, increased vascular tone and reactivity, microvascular structural adaptions as well as increased aortic stiffness resulting in elevated central and brachial blood pressures during the day and night, when compared to whites. Together with knowledge on the contributions of sympathetic activation and abnormal renal sodium handling, these pathophysiological adaptations result in subclinical and clinical organ damage at younger ages. This overall enhanced understanding on the determinants of blood pressure elevation in blacks encourages (a) novel approaches to assess and manage hypertension in Africa better, (b) further scientific discovery to develop more effective prevention and treatment strategies and (c) policymakers and health advocates to collectively contribute in creating health-promoting environments in Africa.

Objectives Insulin-like growth factor-1 (IGF-1) has potent endothelial-protective, anti-platelet and anti-thrombotic activities, and also exerts mitogenic and proliferatory actions on vascular smooth muscle cells. Conflicting reports exist regarding the role of IGF-1 in vascular protection and atherogenesis. We therefore investigated the relationships of ambulatory blood pressure (BP) and carotid intima-media thickness (cIMT) with a range of components of the IGF-1 axis in a bi-ethnic population. Methods We included black (N = 86) and white (N = 101) men and measured growth hormone, total IGF-1, insulin-like growth factor binding protein-3 (IGFBP-3), and pregnancy-associated plasma protein-A (PAPP-A) levels. Results Ambulatory BP was almost 10 mmHg higher in black men (137/88 mmHg versus 128/80 mmHg; both p < 0.001), accompanied by an adverse profile of the IGF-axis for all measured components (all p < 0.01), including reduced bioavailable IGF-1 (IGF-1/IGFBP-3; p = 0.006) and tissue IGF-1 accessibility index as represented by IGF-1.PAPP-A/IGFBP-3 (p < 0.001). Single, partial and multiple regression analyses confirmed an independent inverse association between ambulatory systolic BP and bioavailable IGF-1 in black men (R2 = 0.24; β = −0.22; p = 0.035). cIMT was similar in the ethnic groups (p = 0.34), and was negatively associated with bioavailable IGF-1 in white men (R2 = 0.42; β = −0.17; p = 0.039) prior to adjustment for γ-glutamyl transferase (R2 = 0.45; β = −0.10; p = 0.25). Conclusion Ambulatory systolic BP is inversely related to bioavailable IGF-1 in black men who displayed low IGF-1 concentrations. An inverse relation was found between cIMT and IGF-1 in white men, which disappeared after correction for γ-glutamyl transferase – opposing reports of a detrimental role of IGF-1 in the early stages of atherogenesis.

Globally the prevalence of non-communicable diseases, such as hypertension and type 2 diabetes, are escalating. Metabolomic studies indicated that circulating branched chain amino acids (BCAAs) are associated with insulin resistance, coronary artery disease and increased risk for cardiovascular events. We aimed to extend the current understanding of the cardiovascular risk associated with BCAAs. We explored whether BCAAs are related to markers of cardiovascular disease in a bi-ethnic population and whether this relationship was influenced by chronic hyperglycaemia. We included 200 African and 209 Caucasian participants, and determined their ambulatory blood pressure and carotid intima-media thickness (cIMT). We analysed blood samples for glycated haemoglobin (HbA1c) and BCAAs. Participants were stratified into two groups according to their HbA1c value using the median cut-off value of 5.6 %. Ambulatory BP, cIMT and BCAAs were significantly higher (all p < 0.001) in the high HbA1c group. Single regression analyses indicated significant positive associations of ambulatory blood pressure and cIMT with BCAAs (all p < 0.05) in both the groups. These associations between ambulatory systolic blood pressure (SBP) (r = 0.16, p = 0.035) and cIMT (r = 0.22, p = 0.004) with BCAAs remained in the high HbA1c group after adjusting for age, gender, ethnicity and body mass index (BMI) and were confirmed in multiple regression analyses (ambulatory SBP: R2 = 0.17, β = 0.21, p = 0.005 and cIMT: R2 = 0.30, β = 0.19, p = 0.003). Our results demonstrate that BCAAs are independently related to ambulatory BP and cIMT in individuals with high HbA1c levels and suggest that potential cardiovascular deterioration accompany the rise in BCAAs in conditions of hyperglycaemia.

Background Hypertensive heart disease is a rising concern, especially among black South African women. As high sensitivity cardiac troponin T (cTnT) is a marker of cardiomyocyte damage, we determined the potential link of (i) systemic endothelial dysfunction (reflected by urinary albumin-to-creatinine ratio), (ii) large artery stiffness, (iii) cardiac volume load (estimated by the N-terminal prohormone B-type natriuretic peptide (Nt-proBNP)), and (iv) ECG left ventricular hypertrophy in post-menopausal black women. Methods In 121 (50 normotensive and 71 hypertensive) black women (mean age: 60.6 years), basic cardiovascular assessments including blood pressure and ECG were performed, along with plasma and urinary biomarkers including cTnT. Results The cTnT levels (p=0.049) along with Nt-proBNP (p=0.003), pulse pressure (p

The overall growth of the global AIDS epidemic appears to have stabilised and the number of new infections is declining.1 This and the significant reduction in mortality could be attributed to the effectiveness of antiretroviral therapy (ART). Human immunodeficiency virus (HIV) infection, although still fatal, has become a chronic and manageable disease. The therapy has increased the life expectancy of HIV-infected individuals and therefore more people are living with HIV. The region affected the most by HIV remains sub-Saharan Africa, and South Africa continues to be the country housing the largest population of people (an estimated 5.6 million people in 2009) living with HIV worldwide.1 Besides some very uncomfortable side effects due to both HIV infection and the therapy, another more serious side effect has emerged, namely an increased risk for cardiovascular disease (CVD).2,3 HIV infection paradoxically affects cardiovascular risk factors and circulatory disease within populations and individuals. Researchers have associated HIV infection and especially the use of ART with an increase in insulin resistance, dyslipidaemia,4 lipodystrophy5,6 endothelial dysfunction,7 accelerated atherosclerosis8 and coagulation disorders.9 In the past 15 years South Africa has experienced a rise in noncommunicable diseases, such as cardiovascular disease, which is predicted to increase in the next decades.10 This rise in incidence of non-communicable diseases is masked by the overwhelming presence of communicable diseases such as HIV and tuberculosis.11 Therefore, cardiovascular complications in the HIV-infected population could become a serious health problem in South Africa by increasing the burden of non-communicable diseases once patients are receiving ART for longer periods.11 Recent research has shown that atherosclerotic disease, historically not common in black Africans, is increasing in South Africa.12 The South African HIV-infected population has had access to free antiretroviral treatment since 2004 and the influence of ART on the cardiovascular system in this population is not yet established. The South African National AIDS Council updated the HIV treatment guidelines and adopted some of the recent recommendations made by the World Health Organisation (WHO), which will lead to more people receiving treatment.13 This expansion of antiretroviral therapy and the effect thereof on the burden of non-communicable diseases (such as cardiovascular disease) in South Africa is yet to be determined. The predominant virus responsible for the infections in South Africa is HIV-1, group M (major), subtype C,14,15 which accounts for 55 to 60% of all HIV-1 infections worldwide,16 and differs as much as 30% in its genome from HIV-1 subtype B, responsible for most infections in North America, Europe and Australia.14,16,17 The clinical consequences of these subtype variations remain unclear.18 Although the risk for the development of cardiovascular disease has been described in many different HIV-1-infected populations, data on the risk facing the South African HIV-infected population is scarce, as most of the research is done on Caucasians infected with HIV-1 subtype B. Therefore, the risk of cardiovascular disease in HIV-infected South Africans and how it is affected by the roll-out programme of ART remains largely unknown. The various effects of the virus itself – including its cardiovascular effects – are also important, since many HIV-infected South Africans are still without therapy and/or unaware of their infection status. Various factors seem to contribute to the latter, such as the lack of knowledge, poverty, stigma, scepticism and lack of interest.19 The Hypertension in Africa Research Team (HART) therefore individually matched 300 newly identified HIV-infected Africans from the South African Prospective Urban and Rural Epidemiology (PURE) study with 300 uninfected controls. They were matched according to age, gender, body mass index and locality (urban/rural). The larger PURE study is an epidemiological study that will address questions regarding the cause and development of cardiovascular risk factors and disease within populations, including South Africa.20 A minimum follow up of 10 years is planned. The South African leg of the study was performed in the North West Province where a total of 2 010 participants (1 004 urban and 1 006 rural) were randomly recruited from a rural and urban setting and screened during the baseline phase in 2005. A follow up on the PURE South Africa study was done in 2010. The newly identified HIV-infected participants and their controls of the baseline (2005) study were also followed up in 2008. In a cross-sectional analysis on the baseline data we aimed to evaluate if HIV-1 infection itself is associated with dyslipidaemia, inflammation and the occurrence of the metabolic syndrome in newly identified HIV-1-infected black South Africans who had never received antiretroviral therapy. We concluded that HIV-1 is associated with dyslipidaemia and an inflammatory state in newly identified HIV-infected, never-treated African individuals and that it may increase their risk for cardiovascular disease. The study showed that HIV-1, most likely subtype C, seems to influence the components of the metabolic syndrome in South Africans in the same way as HIV-1 subtype B does in Caucasians. It also showed that the virus does not increase the prevalence of the metabolic syndrome in these never-treated, HIV-infected South Africans.21 In this edition of the Cardiovascular Journal of Africa, a study is published in which we assessed cross-sectionally whether these newly identified, never-treated, HIV-1-infected Africans showed signs of inflammatory injury of the endothelium. This could lead to endothelial dysfunction, accelerated atherosclerosis and increased coagulation, which could result in thrombosis. Our findings suggest inflammatory injury of the endothelium, which was probably worsened by the attenuation of the protective effect of high-density lipoprotein cholesterol (HDL-C). The high levels of protective HDL-C in black South Africans is thought to be the reason for the fairly low prevalence of ischaemic heart disease in the general population.22 Although there was no indication of a prothrombotic state which could result in atherosclerotic disease, there was an indication of accelerated vascular aging and probable early atherosclerosis in the older HIV-infected South Africans. The latter indicates a decrease in vascular function of the never-treated, HIV-1-infected older population.23 After being identified as HIV infected, the participants were referred to their nearest hospital or clinic for follow up on the diagnosis of HIV infection and commencement of treatment if needed. Some of the participants were eligible, by CD4 cell count, for enrollment in the ART roll-out programme but chose not to initiate treatment. During the 2008 follow up, our results showed lower systolic blood pressure and dyslipidaemia in the never-treated, HIV-1-infected South Africans compared to the control participants. In the treated HIV-infected participants, we observed an increase in systolic blood pressure, but no hypertension, and an improvement in lipid profile. Although the antiretroviral treatment stabilised the lipid profile, an increase in lipodystrophy was seen in the treated group, which may influence the development of future cardiovascular disease. Indeed, changes in body composition were one of the most prominent results of this study. These changes in the treated group confirm the possible development of lipodystrophy, expected after the introduction of antiretroviral treatment.5,6 Stavudine, the nucleoside reverse transcriptase inhibitor (NRTI) of the first-line therapy of the roll-out programme is incriminated in the development of lipodystrophy.24 New guidelines on the WHO’s first-line therapy, which came into effect on 1 April 2010 in South Africa, phase out the use of stavudine in favour of tenofovir.13 Whether this could have an effect on the development of lipodystrophy in the South African population remains to be seen. The novel biomarker, soluble urokinase plasminogen activator receptor (suPAR) is a stable plasma protein25 and is associated with inflammation and progression of disease in HIV-1 infection.26 It was suggested that suPAR may be a marker linking inflammatory and metabolic characteristics (lipid and glucose metabolism, as well as fat redistribution) of HIV-infected patients on ART.25 We therefore hypothesised that the HIV-1-infected black South Africans would have significantly higher suPAR levels than their uninfected controls. While the latter was confirmed by our results, the treated HIV-1-infected Africans unexpectedly showed a significantly greater increase in blood suPAR levels than never-treated infected or uninfected Africans after a three-year period. Furthermore, this study indicates an association of suPAR with the development of lipodystrophy in HIV-1-infected black South Africans on the WHO’s recommended first-line antiretroviral therapy.27 In summary, our results clearly indicate a detrimental health profile in the HIV-infected black population of South Africa (whether receiving treatment or not). Therefore it remains of the utmost importance to gain knowledge about the influence of HIV infection and the treatment thereof on the cardiovascular system of the South African population.

The renin–angiotensin–aldosterone system can be activated by sympathetic nervous input and is thought to have an important role in the prevalence of hypertension and cardiovascular risk in black Africans. We examined (1) the association between plasma renin responses to mental stress and a marker of sub-clinical atherosclerosis; and (2) associations between resting renin and 24-h ambulatory blood pressure. Participants were 143 urbanized black African men and women (43.1±7.7 years) drawn from a study of Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA). After an overnight fast, participants completed the Stroop mental stress task. Blood samples were drawn during baseline and 10 min after the task to assess the concentration of active renin in plasma. Blood pressure assessments included continuous Finometer measures during the stress testing and 24-h ambulatory monitoring. Carotid intima–media thickness (CIMT) was measured using high-resolution ultrasound. Approximately 50% of the sample responded to the task with an increase in renin concentration. Multiple linear regression analysis revealed an association between the renin stress response and CIMT (β=0.024, 95% confidence interval, 0.004–0.043), after adjustment for conventional risk factors, blood pressure stress responses and basal levels of renin activity (R2 for model=0.37). In addition, resting renin was inversely associated with ambulatory blood pressure. In summary, heightened release of renin during a laboratory mental stressor was associated with a marker of sub-clinical atherosclerosis; thus, it may be a potential mechanism in explaining the increased burden of cardiovascular disease in urbanized black Africans. http://dx.doi.org/10.1038/jhh.2010.82

Severe underweight may be a risk factor for hypertension in developing countries, although the manner whereby this occurs is unknown. Leptin is known to exert both beneficial and detrimental vascular effects, and is predictive of poor cardiovascular outcome at high levels, but also at low levels. We explored the relationship between blood pressure and leptin in black men from South Africa with a body mass index (BMI) in the underweight to normal range. We included 113 African men (BMI≤25 kg/m 2 ) and took anthropometric, biochemical and cardiovascular measures. The blood pressure-leptin relationship was then investigated along quintiles of leptin and within BMI stratified median split (20 kg/m 2 ) groups. Blood pressure increased across leptin quintiles 1–3 (p for trend≤0.040), whereas no relationship was observed along quintiles 3 to 5 (p for trend≥0.14) (adjusted for age and waist circumference). Blood pressure was similar in the two BMI median split groups (p≥0.083). In the low BMI group only, blood pressure associated positively with leptin following unadjusted, partial, and full adjustment (systolic blood pressure and diastolic blood pressure: R 2 =0.20–0.27, β=0.32–0.34, p≤0.009). Decreasing leptin levels are not likely to contribute to hypertension prevalence in the underweight. Rather, in African men with a BMI≤20 kg/m 2 , low leptin levels are positively and independently associated with elevated blood pressure, which is not seen at higher BMI (20–25 kg/m 2 ). Our findings suggest a differential concentration dependent vascular effect of leptin in underweight and normal weight African men.

Background. The prevalence of HIV is the highest in sub-Saharan Africa; South Africa (SA) is one of the most affected countries with the highest number of adults living with HIV infection in the world. Besides the traditional risk factors for cardiovascular disease (CVD) in the general population, in people living with HIV there are specific factors – chronic inflammation, metabolic changes associated with the infection, therapy, and lipodystrophy – that potentially increase the risk for developing CVD. Objective. This study proposes a screening discriminant model to identify the most important risk factors for the development of CVD in a cohort of 140 HIV-infected black Africans from the North West Province, SA. Methods. Anthropometric measures, systolic blood pressure, diastolic blood pressure and the carotid-dorsalis pedis pulse wave velocity were determined. Blood was analysed to determine the levels of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol, triglycerides (TGs) and glucose. Partial least squares discriminant analysis was performed as a supervised pattern recognition method. Independent Student’s t -tests were further employed to compare the means of risk factors on interval scales; for comparison of categorical risk factors between groups, χ 2 tests were used. Results . A TG:HDL-C ratio ≥1.49, TC:HDL-C ratio ≥5.4 and an HDL-C level ≤0.76 mmol/l indicated CVD risk in this cohort of patients living with HIV. Conclusion. The results have important health implications for black Africans living with HIV as these lipid levels may be a useful indicator of the risk for CVD.

Various studies indicate a relationship between increased oxidative stress and hypertension, resulting in increased DNA damage and consequent excretion of 8-oxo-7,8-dihydro-2’-deoxyguanosine (8-oxodG). The aim of this study was to compare urinary 8-oxodG levels in African and Caucasian men and to investigate the association between ambulatory blood pressure (BP) and pulse pressure (PP) with 8-oxodG in these groups. We included 98 African and 92 Caucasian men in the study and determined their ambulatory BP and PP. Biochemical analyses included, urinary 8-oxodG, reactive oxygen species (ROS) (measured as serum peroxides), ferric reducing antioxidant power (FRAP), total glutathione (GSH), glutathione peroxidase (GPx) and glutathione reductase (GR) activity. The African men had significantly higher systolic (SBP) and diastolic blood pressure (DBP) (both p < 0.001). Assessment of the oxidative stress markers indicated significantly lower 8-oxodG levels (p < 0.001) in the African group. The African men also had significantly higher ROS (p = 0.002) with concomitant lower FRAP (p < 0.001), while their GSH levels (p = 0.013) and GR activity (p < 0.001) were significantly higher. Single and partial regression analyses indicated a negative association between urinary 8-oxodG levels with SBP, DBP and PP only in African men. These associations were confirmed in multiple regression analyses (SBP: R$^2$ = 0.41; β = −0.25; p = 0.002, DBP: R$^2$ = 0.30; β = −0.21; p = 0.022, PP: R$^2$ = 0.30; β = −0.19; p = 0.03). Our results revealed significantly lower urinary 8-oxodG in African men, accompanied by a negative association with BP and PP. We propose that this may indicate a dose-response relationship in which increased oxidative stress may play a central role in the up-regulation of antioxidant defence and DNA repair mechanisms

Objectives: In developing countries, urbanization leads to changes in behavioural lifestyle and malnutrition which may lead to higher rates of cardiovascular disease .1,2 We aimed to assess the association between low body mass index and markers of cardiovascular function like pulse wave velocity in Africans. Methods: We included 496 Africans, aged between 35–65 years, with a low socio-economic status. They were stratified into a low BMI group with BMI ≤ 20 kg/m2 and a normal BMI group with BMI ≤ 20 kg/m2 and ≤ 25 kg/m2. Blood pressure (OMRON HEM-757) and PWV (Complier SP) were recorded. Results: African men with low BMI revealed significantly higher DBP (88.0 ± 13.4 mm/Hg) compared to the normal BMI group (84.2 ± 12.2 mm/Hg) and an increased arterial stiffness with significantly higher PWV (12.6 ± 2.47 m/s) compared to the normal BMI group (11.6 ± 2.00 m/s). The significant higher DBP and PWV remained after adjusting for confounders. The BMI scatter plot illustrated a negative tendency towards PWV in Africans (r= −0.28; p

Twenty-four hour urinary albumin excretion reflects general endothelial damage, relates to arterial stiffness, and predicts adverse health outcomes. Albumin determined from easily collected spot urine samples is also predictive. No prognostic evidence for albumin excretion from any means of urine collection exists for Africans. We followed health outcomes in 1061 randomly selected non-diabetic, HIV negative Africans (mean age: 51.5 years; 62.0% women). We determined the baseline urinary albumin-to-creatinine ratio from spot urine samples. Over a median follow-up of 4.52 years, 132 deaths occurred of which 47 were cardiovascular-related. The urinary albumin-to-creatinine ratio averaged 0.68 (5th to 95th percentile interval; 0.13, 4.54 mg/mmol). In multivariable-adjusted analyses, albumin excretion predicted all-cause mortality (hazard ratio, 1.26; 95% confidence interval, 1.07, 1.48; P=0.006), and a tendency existed for cardiovascular (1.26; 0.97, 1.63; P=0.087) mortality, which seemed driven by stroke (1.72; 1.17, 2.54; P=0.006) and not cardiac mortality (0.67; 0.41, 1.07; P=0.094). The predictive value remained in 528 hypertensives for both all-cause (1.38; 1.13, 1.69; P=0.001) and cardiovascular mortality (1.45; 1.07, 1.96; P=0.017), but again driven by stroke. Our findings remained significant after excluding participants with macroalbuminuria and those on anti-hypertensive treatment. In conclusion, in non-diabetic HIV-negative Africans, albumin excretion from spot urine samples predicts all-cause and stroke mortality.

Background: Hypertension and increased blood glucose are associated with subclinical kidney damage, atherosclerosis and with low testosterone values. Low testosterone in men is often accompanied by increased levels of estradiol. Objectives and methods: In this study, the association between estradiol, subclinical kidney damage and atherosclerosis in African and white men in a South African cohort was investigated. Cardiovascular variables were studied by means of B-mode ultrasound and ambulatory blood pressure (BP) monitoring. The sex hormones and other biochemical values were measured from fasting venous blood and overnight urine samples. The ethnic groups were stratified into low and high testosterone groups by means of median split. Results: The low testosterone African group demonstrated a higher cardiovascular risk compared with the low testosterone white men with 91% being hypertensive and having increased albumin-to-creatinine ratio (ACR), left carotid intima–media thickness (L-CIMTf) and estradiol-to-testosterone ratio. In the low-testosterone African men, estradiol explained 33% of the variance in ACR, whereas the estradiol-to-testosterone ratio explained 22% of the variance in L-CIMTf, respectively. Estradiol-to-testosterone ratio was positively associated with ACR in the low testosterone whites. Conclusion: We conclude that increased levels of estradiol may play a role in the development of subclinical kidney damage in both African and white men as well as atherosclerosis in low-testosterone African men. http://dx.doi.org/10.1097/HJH.0b013e3283599bb5

The aetiology for an increasing incidence of hypertensive cardiovascular disease amongst Africans in southern Africa is unclear. Hypertension may be induced by inadequate release of L-arginine-derived nitric oxide impairing vascular tone regulation. In addition, asymmetric dimethylarginine (ADMA) is associated with cardiovascular disease. We compared profiles of L-arginine in African and Caucasian men of similar age with cardiovascular risk factors. We studied 163 Caucasian and 132 African men, respectively, (20 to 70 years) measuring serum L-arginine, ADMA, creatinine, urea, symmetric dimethylarginine (SDMA) and blood pressure. L-arginine levels were significantly lower, whereas blood pressure and pulse wave velocity were significantly higher in African men. Simple linear regression showed ADMA more strongly associated with L-arginine in Caucasians (r=0.59 vs 0.19), whereas association of SDMA with L-arginine was significant only in Caucasians (r=0.43 vs 0.001). The stronger association of L-arginine with ADMA in Caucasian men was confirmed by multiple regression analysis (β=0.46 vs 0.25). Our findings show that the relationship of cardiovascular risk factors with serum L-arginine and some of its catabolites is different in African and Caucasian men and that this may be associated with a relatively higher prevalence of hypertension in African men. http://www.nature.com/jhh/journal/v26/n12/pdf/jhh2011103a.pdf http://dx.doi.org/10.1038/jhh.2011.103

Background Dissociation between behavioural defensive active coping (AC) control albeit physiological "loss of control" responses was associated with silent ischaemia and structural wall abnormalities in African men. Whether it applies to structural alterations and endothelial dysfunction is uncertain. We therefore aimed to determine AC ethnic-gender specific receiver operating characteristic (ROC) carotid intima media far wall (CIMTf) cut points best associated with 24-h BP, -silent ischaemia and glycated haemoglobin (HbA1c). Methods Participants included African and Caucasians (N=317) without pre-existing stroke or atrial fibrillation, aged 45±9years. The Coping Strategy Indicator was used to measure AC. Ultrasound CIMTf, ambulatory BP, silent ischaemia and fasting blood samples were obtained. Results Between 69 and 77% of AC African men showed above normal diastolic BP and HbA1c levels compared to 44–48% of AC Caucasian men. In AC African women, 41–60% showed above normal BP, silent ischaemia and HbA1c levels compared to 17–44% of their Caucasian counterparts. ROC curve analyses, detecting optimal CIMTf cut points, ranged between 0.57 and 0.65mm (BP) and 0.71 and 0.74mm (silent ischaemia) in AC ethnic-gender groups. Only HbA1C (>5.7%), with a sensitivity/specificity 47%/74%, after controlling for confounders, predicted structural alterations at an optimal cut point of 0.69mm in AC African men (OR 4.5; 95% CI 2.93–18.73). Conclusion Novel findings of behavioural resilience were apparent in the AC African female despite a high prevalence of risk markers. In AC males, chronic hyperglycaemia facilitated endothelial dysfunction, i.e. a physiological "loss of control" and susceptibility to stroke risk.

Objective:The current study aimed to determine the prevalence of masked hypertension (i.e. normotensive office blood pressure [BP] and hypertensive ambulatory BP) in a young, bi-ethnic South African population who were recruited on to the AFRICAN-PREDICT study based on normotensive office BP reading

Objective:Elevated inflammatory markers such as C-reactive protein (CRP) and interleukin-6 (IL-6) are well-known risk factors for cardiovascular mortality. The less familiar marker, soluble urokinase plasminogen activator receptor (suPAR), is known to predict cancer, infections and all-cause mortali

The objective was to study the changes in vascular function of HIV-1 (subtype C) infected black Africans over three years. In a longitudinal study (2005–2008) we compared the vascular function of 140 HIV+ (newly diagnosed) black Africans from the North-West province, South Africa. Seventy seven of the same HIV+ participants, received by choice no ARV treatment while 63 received treatment. Systolic (SBP), diastolic (DBP) blood pressure, heart rate (HR) (Omron HEM 757), and the pulse wave velocity (PWV) (Complior SP device) were determined. Sonar images were obtained with the MicroMaxx sonar device. Blood was analyzed with known methods to determine total cholesterol, high density lipoprotein (HDL-c), low density lipoprotein (LDL-c), triglycerides (TG), glucose and C-reactive protein (CRP). Blood pressure increased significantly (dependent T-test) if the HIV+ (2005) were compared to the 2008 participants (received ARV’s). The PWV showed no significant changes in both groups. Although the weight stayed constant over three years, the waist circumference increased significantly in the ARV treated group. The HDL-c decreased significantly from 1.37 to 0.83mmol/L in the treatment naive group and the HDL-c showed no changes in the treatment group compared to the 2005 participants. The CRP was high in both groups. To conclude: the ARV treatment group showed lipodystrophy, an increase in blood pressure and a lower plaque score (6.5% vs 10.5%). It seems that ARV treatment stabilizes the lipids and results in a higher blood pressure, whereas in the treatment naive group a significant decrease in HDL – cholesterol over three years were encountered.