Individual and area-level socioeconomic correlates of hypertension prevalence, awareness, treatment, and control in uMgungundlovu, KwaZulu-Natal, South Africa.

BACKGROUND: Hypertension is the second leading risk factor for death in South Africa, and rates have steadily increased since the end of Apartheid. Research on the determinants of hypertension in South Africa has received considerable attention due to South Africa's rapid urbanization and epidemiological transition. However, scant work has been conducted to investigate how various segments of the Black South African population experience this transition. Identifying the correlates of hypertension in this population is critical to the development of policies and targeted interventions to strengthen equitable public health efforts. METHODS: This analysis explores the relationship between individual and area-level socioeconomic status and hypertension prevalence, awareness, treatment, and control within a sample of 7,303 Black South Africans in three municipalities of the uMgungundlovu district in KwaZulu-Natal province: the Msunduzi, uMshwathi, and Mkhambathini. Cross-sectional data were collected on participants from February 2017 to February 2018. Individual-level socioeconomic status was measured by employment status and educational attainment. Ward-level area deprivation was operationalized by the most recent (2011 and 2001) South African Multidimensional Poverty Index scores. Covariates included age, sex, BMI, and diabetes diagnosis. RESULTS: The prevalence of hypertension in the sample was 44.4% (n = 3,240). Of those, 2,324 were aware of their diagnosis, 1,928 were receiving treatment, and 1,051 had their hypertension controlled. Educational attainment was negatively associated with hypertension prevalence and positively associated with its control. Employment status was negatively associated with hypertension control. Black South Africans living in more deprived wards had higher odds of being hypertensive and lower odds of having their hypertension controlled. Those residing in wards that became more deprived from 2001 to 2011 had higher odds of being aware of their hypertension, yet lower odds of receiving treatment for it. CONCLUSIONS: Results from this study can assist policymakers and practitioners in identifying groups within the Black South African population that should be prioritized for public health interventions. Black South Africans who have and continue to face barriers to care, including those with low educational attainment or living in deprived wards had worse hypertension outcomes. Potential interventions include community-based programs that deliver medication to households, workplaces, or community centers.

Underweight, overweight and obesity among South African adolescents: results of the 2002 National Youth Risk Behaviour Survey.

OBJECTIVE: The present paper reports the prevalence of underweight, overweight and obesity by gender, ethnicity and grade, among participants in a 2002 national survey among South African school-going youth that included height and weight measurements. DESIGN: A stratified two-stage sample was used. Nationally representative rates of underweight, overweight and obesity were calculated using weighted survey data and compared using chi2 analysis. SETTING: In all, 9224 grade 8 to grade 11 students, present at school in selected classes within selected South African government-funded schools in all nine provinces, participated in this study. Most of the students were between 13 and 19 years of age. RESULTS: Higher rates of underweight were observed for males than females as well as for black and 'coloured' than white students. Within each gender group, black and 'coloured' students had significantly higher rates of underweight than their white counterparts. Higher percentages of females than males were overweight and obese, overall and among black students. Furthermore, white male students had significantly higher rates of overweight than their black and 'coloured' counterparts. Among females, black and white students had significantly higher rates than 'coloured' students. Students in higher grades showed significantly lower rates of underweight and higher rates of overweight. DISCUSSION: These data confirm that South Africa, a developing nation in socio-economic transition, is experiencing both undernutrition and overnutrition. However, these problems are disproportionately distributed by gender, socio-economics and ethnicity. Continued surveillance of nutritional status may be one important component of a national strategy to prevent and control malnutrition.

Coronary artery disease and risk factors in Black South Africans--a comparative study.

OBJECTIVE: The purpose of this study was to identify and compare coronary risk factors in different South African ethnic groups with angiographically documented significant coronary artery disease (CAD). DESIGN: An observational retrospective analysis. METHODS: Hospital records of 500 consecutive patients with no previous coronary interventions who underwent coronary angiography at Chris Hani Baragwanath Hospital, Soweto over a 2-year period were reviewed. Patients with significant CAD were selected for this study. Data analyzed included demographics, presenting diagnoses, coronary risk factors, number of coronary arteries significantly affected and extent of CAD, left ventricular ejection fraction (LVEF), and the main treatment modality for CAD. RESULTS: Of the 206 patients with significant CAD, 85 were Africans and 121 were non-Africans. There were significantly more females in the African group (31% vs 12%, P=.0023) and hypertension was more prevalent in the same group (78% vs 55%, P=.0006). Serum total (TC) and low-density lipoprotein (LDL) cholesterol were significantly lower in African than in non-African patients [189.5 (96.67-313.2) vs 228.2 (127.6-464) mg/dL; P=.0006 and 100.5 (34.8-282.3) vs 146.9 (42.54-313.2) mg/dL; P=.0001, respectively]. CONCLUSION: Cholesterol levels in this group of African patients with angiographically significant CAD are within the target range recommended by the adult treatment panel III (ATP III) guidelines of the National Cholesterol Education Program (NCEP). These data have implications for risk assessment using cholesterol and the role of cholesterol lowering treatment in populations of developing countries.

A prospective study of serum lipoproteins after coronary artery bypass surgery.

We examined the acute and long-term effects of coronary artery bypass (CABG) surgery on serum lipid, lipoprotein and apolipoprotein levels. One series of 34 patients having CABG surgery was studied pre-operatively and for six weeks afterwards, and another 22 patients were investigated before and two years after CABG surgery. None of the patients studied received any lipid-lowering drug therapy or specific dietary advice. In both groups, pre-operative serum lipoprotein (a) (Lp(a)) and serum triglyceride concentrations were raised and serum high-density lipoprotein (HDL) cholesterol and apolipoprotein AI (apo AI) were low compared to healthy people. Acutely, there were profound decreases of 40-60% in the serum levels of cholesterol (p < 0.001), low-density lipoprotein cholesterol (p < 0.05), triglycerides (p < 0.01), Lp(a) (p < 0.05) and apolipoprotein B (apo B) (p < 0.05). There was a small decrease in serum apo A1 (p < 0.05), and serum HDL cholesterol showed no change. All these variables regained their pre-operative values within six weeks. Two years postoperatively, serum Lpa was 40% less than its pre-operative concentration (p < 0.001) and HDL cholesterol had increased (p < 0.001). Triglyceride levels decreased (p < 0.02) when beta-blockade was withdrawn. The long-term decrease in Lp(a) following surgery is unlikely to be due either to stopping beta-blockers or to life-style changes. Myocardial ischaemia relieved by the operation may have been partially responsible for its previously raised concentration.

Serum Lp(a) lipoprotein concentration and outcome of thrombolytic treatment for myocardial infarction.

BACKGROUND: Lp(a) lipoprotein has structural homology with plasminogen and has been shown to inhibit plasminogen activation in vitro. OBJECTIVE: To determine whether the serum concentration of Lp(a) lipoprotein present when streptokinase was given in acute myocardial infarction influenced the outcome as judged by electrocardiographic methods. PATIENTS AND DESIGN: Serum Lp(a) lipoprotein concentration was measured in 135 consecutive patients admitted with a diagnosis of acute myocardial infarction who received streptokinase treatment. Recovery from myocardial injury was assessed by the reduction in the sum of ST segment elevation measured from the J point (STJ) in the electrocardiogram immediately before streptokinase was given compared with that three hours later. RESULTS: The serum Lp(a) lipoprotein concentrations were measured within 12 hours of the onset of symptoms of myocardial infarction and were higher than in healthy reference populations. Recovery from myocardial infarction could be assessed from the STJ in 116 patients (86% of the series). Those in whom it could not had bundle branch block, left ventricular hypertrophy, did not survive three hours, or had started intravenous nitrate treatment or some other clinical procedure before or at the time the second electrocardiogram was to be recorded. Patients with reductions in STJ after streptokinase that were > 4 mm (the median decrease) had mean (range) serum Lp(a) lipoprotein concentrations of 41.0 (0.8-220) mg/dl and those with a smaller reduction in STJ had concentrations of 29.1 (1.7-151) mg/dl. The difference was not statistically significant. CONCLUSION: In this study Lp(a) lipoprotein concentration did not significantly influence the outcome of thrombolytic treatment with streptokinase.

The immediate effect of streptokinase on serum lipoprotein(a) concentration and the effect of myocardial infarction on serum lipoprotein(a), apolipoproteins A1 and B, lipids and C-reactive protein.

Lipoprotein(a) (Lp(a)) has close structural homology with plasminogen and, at least in vitro, may interfere with fibrinolysis. Any changes in the serum Lp(a) concentration during and following myocardial infarction (MI) and whether the serum Lp(a) level is affected by streptokinase (SK) are therefore of interest. Serum Lp(a) levels immediately before and 3 h after completion of an intravenous infusion of SK in 39 patients with acute MI were not significantly different (median 31.3 mg/dl before and 35.9 mg/dl after). Furthermore, SK added during the serum Lp(a) assay did not affect the result, except at very high concentrations of SK (1000 units/ml). Serum Lp(a) and fasting lipids were measured daily for 3 days following definite MI in 13 patients and then after 14 and 42 days. There was no significant change in serum Lp(a) following MI. In marked contrast, C-reactive protein levels in these patients increased steeply immediately following MI. Thus, there was no early 'acute-phase response' in serum Lp(a) levels after MI. However, greater variation in its concentration was observed at day 14 than at other times. Serum cholesterol, apolipoprotein B and apolipoprotein A1 concentrations decreased significantly following MI, whereas a significant transient increase in serum triglycerides occurred. Forty-two days after MI all lipid and lipoprotein values had regained their day 1 levels, except for apo A1, which remained depressed.

A cross-sectional evaluation of cardiovascular risk factors in coronary heart disease associated with type 1 (insulin-dependent) diabetes mellitus.

The contribution from lipoproteins, blood pressure, albuminuria and demographic variables to coronary heart disease in 90 adult subjects with and 172 without Type 1 diabetes mellitus was examined in order to investigate whether risk factors were of equivalent importance in diabetic and non-diabetic coronary heart disease. Coronary heart disease (CHD) was present in roughly 25% of subjects in each group. In Type 1 diabetes those with CHD had significantly higher levels of systolic blood pressure, albumin excretion, serum creatinine, triglycerides, VLDL cholesterol and C-peptide, and reductions in serum concentrations of HDL and HDL2 cholesterol, in comparison to those without. However, the prevalence of smokers, and concentrations of Lp(a), ApoB and fibrinogen were comparable. Blood pressure and HDL cholesterol were higher in the CHD group with Type 1 diabetes in comparison to the nondiabetic group with CHD, although LDL concentrations and the prevalence of Lp(a) concentrations > 200 mg/l were lower. Logistic regression analysis revealed the strongest independent predictors of CHD in Type 1 diabetes were serum triglycerides, systolic blood pressure, age, serum LDL cholesterol, and the daily insulin dosage, whereas in the non-diabetic control group HDL2 cholesterol, Lp(a), ApoA1 and ApoB, total serum cholesterol and body mass index were additional predictors. CHD in Type 1 diabetes appears to be most closely associated with increasing age and levels of blood pressure and total serum lipids. Apolipoproteins and albuminuria did not seem to be important independent predictors of CHD in Type 1 diabetes, whereas the former were more clearly associated with CHD in non-diabetic controls.

Serum lipoprotein(a) in patients heterozygous for familial hypercholesterolemia, their relatives, and unrelated control populations.

Serum lipoprotein(a) (Lp[a]) levels were significantly higher in 89 patients with heterozygous familial hypercholesterolemia (FH) (geometric mean, 22.7 mg/dl) than in 109 normocholesterolemic controls (10.0 mg/dl, p less than 0.05) and 40 controls (9.1 mg/dl, p less than 0.05) with similarly elevated low density lipoprotein cholesterol levels due to other primary hypercholesterolemias. To provide further evidence that the increased serum Lp(a) concentration was due to inheritance of the FH gene, 24 unaffected first-degree relatives were compared with their FH probands. Serum Lp(a) in affected individuals was significantly greater than in unaffected relatives (geometric means, 26.5 versus 13.7 mg/dl, respectively; p less than 0.05). Family membership exerted an effect on serum Lp(a) concentrations, indicating that other genetic influences were also operating, as is known to be the case in general populations. Serum Lp(a) in 30 of the FH patients, who had coronary heart disease, was not significantly different from 30 age- and sex-matched controls with FH but with coronary heart disease (geometric means, 23.6 versus 24.7 mg/dl, respectively). FH is associated with an increase in serum Lp(a). Elevated serum Lp(a) concentrations should probably now be regarded as a component of the clinical syndrome of FH. However, within our FH population Lp(a) did not distinguish those with clinically overt coronary heart disease from those without the disease.