BackgroundGlobally hypertension is stabilising, but in sub-Saharan Africa the incidence
of hypertension remains on an increase. Although this might be attributed to
poor healthcare and ineffective antihypertensive treatment, there is a
limited understanding of population and individual-specific cardiovascular
pathophysiology – necessary for effective prevention and treatment
strategies in Africa. As there is a lack of longitudinal studies tracking
the early pathophysiological development of hypertension in black
populations, the African-PREDICT study was initiated. The purpose of this
paper is to describe the detailed methodology and baseline cohort profile of
the study.Methods and resultsFrom 2013 to 2017, the study included 1202 black (N = 606)
and white (N = 596) men and women (aged 20–30 years) from
South Africa – screened to be healthy and clinic normotensive. At baseline,
and each 5-year follow-up examination, detailed measures of health
behaviours, cardiovascular profile and organ damage are taken. Also,
comprehensive biological sampling for the ‘omics’ and biomarkers is
performed. Overall, the baseline black and white cohort presented with
similar ages, clinic and 24-hour blood pressures, but black adults had lower
socioeconomic status and higher central systolic blood pressure than white
individuals.ConclusionsThe prospective African-PREDICT study in young black and white adults will
contribute to a clear understanding of early cardiovascular disease
development.
The WHtR threshold of >0.5 appears to be more consistently supported and may provide a better predictor of future cardiometabolic risk in sub-Saharan Africa.
Brain-derived neurotrophic factor (BDNF) has been linked to neurological pathologies, but its role in cardiometabolic disturbances is limited. We aimed to assess the association between serum BDNF levels and structural endothelial dysfunction (ED) as determined by cross-sectional wall area (CSWA) and albumin/creatinine ratio (ACR) in black Africans. Ambulatory blood pressure (BP) and ultrasound CSWA values were obtained from 82 males and 90 females. Fasting blood and 8 h overnight urine samples were collected to determine serum BDNF and cardiometabolic risk markers, that is, glycated haemoglobin (HbA1c), lipids, inflammation and ACR. BDNF median split × gender interaction effects for structural ED justified stratification of BDNF into low and high (⩽/>1.37 ng ml(-1)) gender groups. BDNF values (0.86-1.98 ng ml(-1)) were substantially lower than reference ranges (6.97-42.6 ng ml(-1)) in the African gender cohort, independent of age and body mass index. No relationship was revealed between BDNF and renal function and was opposed by an inverse relationship between BDNF and CSWA (r=-0.17; P=0.03) in the African cohort. Linear regression analyses revealed a positive relationship between systolic BP and structural remodelling in the total cohort and low-BDNF gender groups. In the high-BDNF females, HbA1C was associated with structural remodelling. Attenuated or possible downregulated BDNF levels were associated with hypertrophic remodelling, and may be a compensatory mechanism for the higher BP in Africans. In addition, metabolic risk and hypertrophic remodelling in women with high BDNF underpin different underlying mechanisms for impaired neurotrophin homeostasis in men and women.
This study presents a detailed profile of the renin-angiotensin-aldosterone system (RAAS), electrolytes, volume loading, blood pressure (BP), and total peripheral resistance in healthy young Black and White adults. We also explored longitudinal associations between BP and RAAS. We included normotensive Black (N=543) and White (N=573) adults (20–30 years) and followed N=324 over ≈4.5 years. We measured clinic (central, brachial) and 24-hour BP, total peripheral resistance and left ventricular dimensions. We determined serum NT-proBNP (N-terminal prohormone B-type natriuretic peptide), RAAS, and 24-hour urinary and serum Na
+
and K
+
. RAAS components, left ventricular internal diameter (diastole), end diastolic volume and NT-proBNP were lower (
P
<0.001) in Black than White adults, despite similar clinic SBP. However, central systolic BP and total peripheral resistance were higher in Black adults (
P
<0.001). Plasma renin activity and angiotensin II were comparable between Black and White groups (
P
>0.05) only in quartile 1 of Na
+
/K
+
values. In both groups, RAAS was lower in the higher quartiles of 24-hour Na
+
and NT-proBNP (all
P
-trend≤0.014). Over 4.5 years, all BPs increased in the Black (
P
<0.001) but not White group. The increase in central systolic BP over time was associated with elevated serum aldosterone only in Black adults (β=0.18,
P
=0.038). We found that RAAS concentrations in healthy Black adults were half of those of White participants, which may not be explained by volume expansion. Yet, baseline aldosterone predicted BP elevation over time in Black adults. RAAS was similar in Black and White adults only at low Na
+
/K
+
scenarios, suggesting an essential role of potassium.
REGISTRATION:
URL:
https://www.clinicaltrials.gov;
Unique identifier: NCT03292094.
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