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Growing evidence indicates that the pathophysiological link between the brain and heart underlies cardiovascular diseases, specifically acute myocardial infarction (AMI). Astrocytes are the most abundant glial cells in the central nervous system and provide support/protection for neurons. Astrocytes and peripheral glial cells are emerging as key modulators of the brain-heart axis in AMI, by affecting sympathetic nervous system activity (centrally and peripherally). This review, therefore, aimed to gain an improved understanding of glial cell activity and AMI risk. This includes discussions on the potential role of contributing factors in AMI risk, i.e., autonomic nervous system dysfunction, glial-neurotrophic and ischemic risk markers [glial cell line-derived neurotrophic factor (GDNF), astrocytic S100 calcium-binding protein B (S100B), silent myocardial ischemia, and cardiac troponin T (cTnT)]. Consideration of glial cell activity and related contributing factors in certain brain-heart disorders, namely, blood-brain barrier dysfunction, myocardial ischemia, and chronic psychological stress, may improve our understanding regarding the pathological role that glial dysfunction can play in the development/onset of AMI. Here, findings demonstrated perturbations in glial cell activity and contributing factors (especially sympathetic activity). Moreover, emerging AMI risk included sympathovagal imbalance, low GDNF levels reflecting prothrombic risk, hypertension, and increased ischemia due to perfusion deficits (indicated by S100B and cTnT levels). Such perturbations impacted blood-barrier function and perfusion that were exacerbated during psychological stress. Thus, greater insights and consideration regarding such biomarkers may help drive future studies investigating brain-heart axis pathologies to gain a deeper understanding of astrocytic glial cell contributions and unlock potential novel therapies for AMI.

OBJECTIVES: Low or high sympatho–adrenal–medullary axis (SAM) and hypothalamic–pituitary–adrenal axis (HPA) dysregulation reflect chronic stress. Retinal vessel dynamics may relate to SAM, HPA activity and stroke risk. Our objectives were therefore to assess the relationships between retinal vessel, SAM and HPA responses, and to determine stroke risk. METHODS: A prospective bi-ethnic gender cohort (n = 275, 45 ± 9 years) was included. Urine/serum/saliva samples for SAM [norepinephrine:creatinine ratio (u-NE)] and HPA [adrenocorticotrophic hormone (ACTH), cortisol] were obtained at baseline, three-year follow up and upon flicker light-induced provocation. Diastolic ocular perfusion pressure was measured as a marker of hypo-perfusion. Retinal arterial narrowing and venous widening calibres were quantified from digital images in the mydriatic eye. A validated stress and stroke risk score was applied. RESULTS: An interaction term was fitted for venous dilation in u-NE tertiles (p ≤ 0.05) and not in u-NE median/quartiles/ quintiles. Independent of race or gender, tertile 1 (low u-NE) had a 112% increase in u-NE, decreases in cortisol, and no changes in ACTH over three years (positive feedback). Tertile 3 (high u-NE) contradictorily had decreases in u-NE and cortisol, and increases in ACTH (negative feedback). In tertile 1, reduced arterial dilation, and faster arterial vasoconstriction and narrowing were related to higher SAM activity and hypo-perfusion (p ≤ 0.05), whereas delayed venous dilation, recovery and widening were related to cortisol hypo-secretion (p ≤ 0.05). In tertile 1, delayed venous recovery responses predicted stress and stroke risk [odds ratio 4.8 (1.2–19.6); p = 0.03]. These associations were not found in u-NE tertiles 2 and 3. CONCLUSIONS: In response to low norepinephrine, a reflex increase in SAM activity occurred, enhancing arterial vasoconstriction and hypo-perfusion. Concomitant HPA dysregu- lation attenuated retinal vein vasoactivity and tone, reflecting delayed vein recovery responses and non-adaptation to stress. These constrained vein recovery responses are indicative of increased chronic stress and stroke risk.

Background We explored the association of N-terminal probrain natriuretic peptide (NT-proBNP) with metabolic traits in a bi-ethnic African-Caucasian cohort. Methods Baseline examinations of the Sympathetic activity and Ambulatory Blood Pressure in African (SABPA) prospective cohort study were performed between 2008 and 2009, and re-examination after a three-year follow up in South African teachers (black African, n = 194; Caucasian, n = 203). Results Each one standard deviation increment of NT-proBNP was significantly inversely associated with body mass index ( β -1.01), glycated haemoglobin ( β -0.14 %), waist circumference (β -1.82), HOMA-IR (β -0.47), insulin (β -1.66) and triglyceride levels (β -0.04). Each one standard deviation increment of NT-proBNP was also associated with reduced odds of incident diabetes, and subjects within the highest quartile of NT-proBNP were at lowest risk (OR: 0.24; 95% CI: 0.06-0.96; p = 0.041). Conclusions In the SABPA cohort, Africans and Caucasians had similar NT-proBNP levels; however, the associations for Africans were stronger. Those findings suggest that BNP may affect the propensity for metabolic disturbances differently in Africans and Caucasians.

Objective To determine the relationship between objectively measured physical activity (PA) and carotid intima-media thickness (CIMT) in teachers in South Africa. Methods A cross-sectional study was conducted among 215 teachers aged 25 to 65 years (mean age 49.67 ± 8.43 years) who participated in the Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA) prospective cohort study. CIMT was measured using the SonoSite Micromaxx ultrasound over seven consecutive days. Other measurements obtained included body mass index (BMI), waist circumference, 24-hour ambulatory blood pressure, and C-reactive protein (CRP) and fasting blood total cholesterol levels. Data were analysed using Statistical Package for Social Sciences (SPSS) version 25. Results The prevalence of obesity according to BMI and sedentary behaviour was above 30%; hypertension was 38.9% and CRP 41.1 mg/dl. Male teachers showed higher mean values for CIMT than female teachers (0.75 ± 0.16 vs 0.66 ± 0.12 mm; p ≤ 0.05). A borderline negative association existed between CIMT and mean seven-day awake metabolic equivalent of task (r = -0.19; p = 0.08) in female teachers in the light-PA group. CIMT was inversely associated with total energy expenditure (r = -0.31; p = 0.05) in sedentary male teachers. Conclusions Participation in light PA was associated with lower CIMT values in female teachers. Given the health implications of cardiovascular disease risk among teachers, PA intervention studies are recommended to determine effective interventions to provide information on how to decrease the progression of subclinical atherosclerosis in this population.

Globally, the prevalence of physical inactivity and obesity are on the rise, which may increase carotid intima-media thickness (CIMT) as a marker of subclinical atherosclerosis. This study assessed the association between physical activity (PA), obesity, and CIMT. A cross-sectional study design was used, including a sub-sample (n = 216) of teachers who participated in the Sympathetic Activity and Ambulatory Blood Pressure in Africans (SAPBA) study. Measurements included the following: physical activity status (measured with ActiHeart devices over 7 consecutive days), body mass index (BMI), waist circumference (WC), waist-to-height ratio (WtHR), CIMT (measured by SonoSite Micromax ultrasound), blood pressure (BP), fasting C-reactive protein (CRP), and cholesterol and glucose levels. Data were analysed using the Statistical Package for Social Science. One-third of the teachers were physically inactive (33%) and had low-grade inflammation CRP ≥ 3 mg/L (41%). Males were more sedentary and had higher BP and CIMT (p < 0.05). Independent of age and sex, WC or central obesity was 2.63 times more likely (p = 0.02) to contribute to atherosclerosis, especially in females (OR: 4.23, p = 0.04). PA levels were insignificantly and negatively (β −0.034; 0.888; 0.240) related to subclinical atherosclerosis. The cardiovascular disease risk profiles and limited PA status may have curbed the beneficial impact of PA on the obesity and atherosclerosis.

We examined whether there were differences in the circadian variation in blood pressure and the morning surge in blood pressure between black and white Africans. Clinic and ambulatory blood pressure data obtained from the Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA) study was examined (n = 406; 49% black African). Ambulatory blood pressure readings were fitted to a six-parameter double logistic equation to determine the power and rate of the morning surge in blood pressure. Multiple linear regression analysis was used to examine differences in blood pressure between black and white participants. Clinic and ambulatory blood pressure were higher in black participants throughout the day and night. In those taking medications, blood pressure was less well controlled in black subjects. Despite the higher systolic blood pressure, the day-night difference estimated by the logistic function was similar in black and white participants. However, the rate of rise and power in the morning surge in blood pressure was lower in black participants. We conclude that black participants of the SABPA study present with higher blood pressure throughout the day and night but have a lower power of the morning surge in blood pressure due to a slower morning rate of increase. Moreover, they had an increased prevalence of undiagnosed hypertension and, in those taking medication, were less likely to have their blood pressure controlled than their white counterparts.

Background Defensive coping (DefS) was associated with cardiovascular disease (CVD) susceptibility in Blacks. Whether coping strategies will associate with sub-clinical left ventricular hypertrophy (electrocardiographic-left ventricular hypertrophy [ECG-LVH] or Cornell product), cardiomyocyte injury and blood pressure (BP), is unclear. Therefore, we assessed relationships between ECG-LVH, cardiac troponin T (cTnT) and 24-hour BP in bi-ethnic groups when habitually utilising a certain coping style, and these groups when having a stress-related cTnT cut-point of 4.2 ng/L. Methods A target population study included a Black (n = 190) and White (n = 204) teachers’ gender cohort (20–65 years) from South Africa. The Coping Strategy Indicator determined DefS, social support and avoidance coping scores. Fasting blood samples, 10-lead ECG, 24-hour BP and ECG data were obtained. Results Interaction effects showed no gender, social support and avoidance coping differences. Stratification of groups was done for ethnicity and DefS. Blacks sought more social support, used less avoidance coping and presented with higher CVD susceptibility. Hypertension prevalence and ECG-LVH levels in DefS Blacks (63%) were higher compared to DefS Whites (40%). Multivariate regression analyses showed positive associations between Cornell product, cTnT and BP [p ≤ 0.05] in DefS Blacks only. Their 24-hour systolic blood pressure (SBP) was associated with time-domain depressed heart-rate-variability and prolonged ST-segment-depression especially when applying an established stress-related cTnT ≥ 4.2 ng/L cut-point. Conclusions Defensive coping facilitated autonomic hyperactivity, myocardial injury and subsequent compensatory BP elevations as possible homeostatic reflexes to alleviate myocardial perfusion deficits. The resulting pressure overload increased sub-clinical wall remodelling and ischaemic heart disease risk in Blacks utilising habitual defensiveness. We therefore recommend regular ECG and high sensitivity cTnT screening in asymptomatic patients with emotional stress susceptibility. Longitudinal evidence is needed to confirm causality and progression of cardiomyopathy risk.

The aim of this study was to validate the Teacher Stress Inventory (TSI) for use in a South African context. The process of scale validation also sheds significant light on this culturally diverse group of participants’ levels of psychological well-being and physical health, and its association with the level of stress that teachers reported. Using a cross-sectional survey design, Caucasian ( n = 209) and African ( n = 200) educators’ subsiding in the North-West Province of South Africa, completed the TSI, together with a number of self-report and physiological measures of stress and well-being. In contrast to the five factors of the TSI identified in US samples, statistical analysis yielded a two-factor model (i.e. General circumstance-related stress and Learner-related stress ) with satisfactory reliability indices. Significant correlation with measures of psychological and physiological health also reflected positively on the criterion-related validity of the scale. The TSI proved to be a useful, brief self-report questionnaire for the assessment of teacher stress in this cohort of South African teachers. Keywords: psychological well-being; reliability; South African context; stress; Teacher Stress Inventory (TSI); validity

Objective In past studies, a lack of social support has been associated with cardiovascular disease (CVD) risk, particularly in black Africans. However, whether or not coping strategies have beneficial effects on blood pressure (BP) and emotional well-being is not clear. We therefore assessed the relationship between BP levels, depression and coping strategies. Methods A prospective bi-ethnic cohort followed 359 black and white South African school teachers (aged 20-65 years) over a three-year period. Data on ambulatory 24-hour blood pressure, depression, coping strategies (defensiveness, social support, avoidance) and culture-specific coping scores (cognitive/emotional debriefing, spiritual-, collectivistic and ritualcentred) were obtained. Results Over three years, chronic depression (38 vs 19%) and hypertension (68 vs 35%) were apparent in blacks ( d-values > 0.3) as opposed to whites. In both groups, depression was accompanied by more avoidance (loss-of-control) coping. Consistent spiritual and increasing collectivistic coping were apparent in whites. Over time, increasing defensiveness (OR 1.08, p ≤ 0.05) and ritual coping (OR 1.27, p ≤ 0.01; d-values > 0.5), predicted chronic depression in blacks. The change in their symptoms of depression predicted 24-hour hypertension (OR 1.11, p = 0.04). No similar associations existed in whites. Conclusions Blacks showed increasing defensiveness and ritual- and spiritual-centred coping in an attempt to combat chronic depression, which may be costly, as reflected by their chronic hypertensive status. Whites showed consistent spiritual- centred coping while utilising avoidance or loss-of-control coping, with a trend of seeking less social support or isolation as a coping mechanism. During counselling of depressed patients with hypertension, the beneficial effects of social support and spiritual coping may be of great importance.

Sympathetic activation may trigger acute coronary syndromes. We examined the relation between circulating neurotrophic factors and hemostatic risk factors of atherothrombotic cardiovascular disease at baseline and in response to acute mental stress to establish a brain–heart link. In 409 black and white South Africans, brain-derived neurotrophic factor (BDNF) and fibrinolytic measures were assessed at baseline. Glial cell-derived neurotrophic factor (GDNF), S100 calcium-binding protein (S100B), von Willebrand factor (VWF), fibrinogen and D-dimer were assessed at baseline and 10 min after the Stroop test. Neurotrophins were regressed on hemostatic measures adjusting for demographics, comorbidities, cardiometabolic factors and health behaviors. Higher baseline BDNF was associated with greater stress-induced increase in fibrinogen (p = 0.003) and lower D-dimer increase (p = 0.016). Higher baseline S100B was significantly associated with higher baseline VWF (p = 0.031) and lower fibrinogen increase (p = 0.048). Lower baseline GDNF was associated with higher baseline VWF (p = 0.035) but lower VWF increase (p = 0.001). Greater GDNF (p = 0.006) and S100B (p = 0.042) increases were associated with lower VWF increase. All associations showed small-to-moderate effect sizes. Neurotrophins and fibrinolytic factors showed no significant associations. The findings support the existence of a peripheral neurothrophin-hemostasis interaction of small-to-moderate clinical relevance. The implications for atherothrombotic cardiovascular disease need further exploration.

Background Psychobiological processes linking stress and vascular diseases remain poorly understood. The retina and the brain share a common embryonic-diencephalon origin and blood-barrier physiology e.g. ongoing ischemia facilitates S100B release with astrocytic activity and glial-fibrillary-acidic-protein expression (GFAP). However, GFAP decreases revealed astrocyte pathology in the prefrontal cortex of depression/suicide cases; and might be a key mechanism in stress – disease pathways. Methods A chronic emotional stress phenotype independent of age, ethnicity or sex was used to stratify the current prospective cohort (N ​= ​359; aged 46 ​± ​9 years) into Stress (N ​= ​236) and no-Stress groups (N ​= ​123). Prospective data for glia ischemia risk markers were obtained, including 24 ​h BP, fasting S100B, GFAP, HbA1C and tumor-necrosis-factor-α (TNF-α). At 3-yr follow-up: diastolic-ocular-perfusion-pressure (indicating hypo-perfusion risk) was measured and retinal vessel calibers were quantified from digital images in the mydriatic eye. Results Higher hypertension (75% vs. 16%), diabetes (13% vs. 0%) and retinopathy (57% vs. 45%) prevalence was observed in Stress compared to no-Stress individuals. Stressed individuals had consistently raised S100B, TNF-α, HbA1C and higher diastolic-ocular-perfusion-pressure, but decreases in GFAP and GFAP:S100B. Furthermore stroke risk markers, arterial narrowing and venous widening were associated with consistently raised S100B, GFAP:S100B (p ​= ​0.060), TNF-α and higher diastolic-ocular-perfusion-pressure [Adj. R2 0.39–0.41, p ​≤ ​0.05]. No retinal-glia associations were evident in the no-Stress group. Conclusions Retinal-glia ischemia and inflammation was induced by chronic stress. Persistent higher inflammation and S100B with GFAP decreases further reflected stress-induced astrocyte pathology in the human retina. It is recommended to increase awareness on chronic stress and susceptibility for brain ischemia., Highlights • Hypertension, retinopathy and perfusion deficits are enhanced in chronic stressed individuals. • Stress-induced ischemia facilitated consistent S100B and TNF-α release but GFAP decreases. • Retinal arterial narrowing and venous widening reflected ischemia and endothelial dysfunction. • Stress-induced astrocyte ischemia pathology was evident in the human retina. • It is recommended to increase awareness on chronic stress and susceptibility for brain ischemia.

Background Low-renin levels in Blacks have been associated with volume-loading hypertension (HT). Depression symptoms, frequently co-occurring with vascular dysregulation, might reflect a disturbed renin-angiotensin-aldosterone-system (RAAS). We aimed to assess prospective changes (∆) in depression symptoms, RAAS (renin, aldosterone), diastolic blood pressure (DBP), and estimated glomerular filtration rate (eGFR) in a bi-ethnic sex cohort. Methods We included 195 Black and White teachers (43.7 ± 9 years) from a South African 3-year prospective study. Hypertension medication users, diabetics and human immunodeficiency virus infected individuals were excluded. Depression symptoms (Patient-Health-Questionnaire-9/PHQ-9), 24 h blood pressure measurements and fasting blood samples were obtained. Results Blacks had lower renin but higher DBP and eGFR levels at baseline (p ≤ .01) when compared to Whites. Blacks and Whites with depression (PHQ-9 ≥ 10) at baseline developed co-morbidity for having both depression plus DBP-HT at follow-up (Blacks, 49.1%; Whites, 13.1%). At 3-year follow-up, chronic depression symptoms were related to chronic lower renin in Blacks [Adjusted R2 0.20; β −0.37 (−0.66, −0.08), p = .02]. Chronic depression symptoms also predicted DBP hypertension in Blacks [ROC AUC = 0.61 (0.48–0.75); sensitivity/specificity 78.1/46.3%]. No prospective associations existed between depression symptoms, aldosterone and eGFR. Conclusion Chronic depression symptoms in Blacks activated the RAAS system activity with apparent desensitization of renin activity. Chronic depression could be causal to hypertension and in turn, lowers renin activity as a protective mechanism against volume-loading. These findings emphasize the potential impact of depression on the low renin-hypertension phenotype in Blacks in terms of diagnosis and treatment.

Taxing psychosocial stress and defensive coping have been associated with hypoactivity in cortisol, a vasoconstrictive agent. Estradiol has vasodilatory properties with cardio- and neuroprotective effects. It can however also induce αAfrican (n = 168) and Caucasian (n = 207) men and women (46 ± 9 years) were included. Preferential use of defensive coping was determined from Coping Strategy Indicator questionnaire scores. 24h Ambulatory blood pressure was obtained. Fasting serum estradiol and cortisol samples were collected before 09h00 and Cort:E2 was calculated.Estradiol was higher in ethnic-coping groups. Smaller Cort:E2, higher estradiol levels, self-reported emotional stress (19.05% vs. 9.66%) and 24h blood pressure reaching hypertensive status (65% vs. 24%) were evident in African compared to Caucasian men (p ≤ .05). A smaller Cort:E2 was associated with augmented 24h SBP and 24h DBP in African men [Adj RA smaller Cort:E2 was associated with raised blood pressure in defensive coping African men. Defensive coping, possibly via highly activated α

Background Sympatho-adrenal responses are activated as an innate defense coping (DefS) mechanism during emotional stress. Whether these sympatho-adrenal responses drive cardiac troponin T (cTnT) increases are unknown. Therefore, associations between cTnT and sympatho-adrenal responses were assessed. Methods A prospective bi-ethnic cohort, excluding atrial fibrillation, myocardial infarction and stroke cases, was followed for 3 years (N = 342; 45.6 ± 9.0 years). We obtained serum high-sensitive cTnT and exposure measures [Coping-Strategy-Indicator, depression/Patient-Health-Questionnarie-9, 24 h BP, 24 h heart-rate-variability (HRV) and 24 h urinary catecholamines]. Results Blacks showed moderate depression (45% vs. 16%) and 24 h hypertension (67% vs. 42%) prevalence compared to Whites. A receiver-operating-characteristics cTnT cut-point 4.2 ng/L predicting hypertension in Blacks was used as binary outcome measure in relation to exposure measures [AUC 0.68 (95% CI 0.60-0.76); sensitivity/specificity 63/70%; P ≤ 0.001]. Bi-ethnic cTnT-incidence was similar (Blacks=27%, Whites=25%) with cTnT-recovery better in Blacks (9%) compared to Whites (5%), P = 0.001. In cross-sectional analyses, elevated cTnT was related to DefS [OR 1.08 (95% CI 0.99–1.16); P = 0.06]; 24 h BP [OR 1.03–1.04 (95% CI 1.01–1.08); P ≤ 0.02] and depressed HRV [OR 2.19 (95% CI 1.09–4.41); P = 0.03] in Blacks, but not in Whites. At 3 year follow-up, elevated cTnT was related to attenuated urine norepinephrine:creatinine ratio in Blacks [OR 1.46 (95% CI 1.01–2.10); P = 0.04]. In Whites, a cut point of 5.6 ng/L cTnT predicting hypertension was not associated with exposure measures. Conclusion Central neural control systems exemplified a brain-heart stress pathway. Desensitization of sympatho-adrenal responses occurred with initial neural- (HRV) followed by neuroendocrine dysfunction (norepinephrine:creatinine) in relation to elevated cTnT. Chronic defensiveness may thus drive the desensitization or physiological depression, reflecting ischemic heart disease risk at a novel 4.2 ng/L cTnT cut-point in Blacks

Background: Hypercoagulation is associated with coronary artery disease (CAD). Whether depression symptoms dysregulate inflammatory and hemostatic markers in an African cohort is not known; therefore, we assessed the relationship between depressive symptoms and inflammatory and hemostatic markers as potential CAD risk markers in an African sex cohort. Material and Methods: We included 181 black African urban-dwelling teachers (88 men, 93 women; aged 25-60 years) from the Sympathetic Activity and Ambulatory Blood Pressure in Africans Study. The Patient Health Questionnaire was used to assess depressive symptoms. Fasting plasma concentrations of C-reactive protein, fibrinogen, D-dimer, plasminogen activator inhibitor-1 (PAI-1) and 24-hour blood pressure measures were obtained. Results: Moderately severe depression symptom status was similar in the black sex groups. Both sex groups showed a mean hypertensive state and low-grade inflammation (C-reactive protein > 3 mg/L). Levels of PAI-1 were higher in depressed men, whereas D-dimer levels were lower in depressed women when considering concomitant confounders. In black men only, depressive symptoms were associated with levels of PAI-1 (adj. R2 = 0.12; [beta] = .22 [95% confidence interval, .0-.44]; P = .04) and D-dimer (adj. R2 = 0.12; [beta] = .28 [95% confidence interval, .08-.48]; P = .01), independent of confounders. Conclusion: In black men, depression symptoms accompanied by a mean hypertensive status may up-regulate inflammatory and thrombotic processes. Depression symptoms in black men facilitated hypercoagulation or fibrinolytic dysregulation and potentially increased their CAD risk. Early screening of fibrinolytic markers and for the presence of depressive symptoms is recommended

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.

Mitochondrial DNA (mtDNA) variation has been implicated in many common complex diseases, but inconsistent and contradicting results are common. Here we introduce a novel mutational load hypothesis, which also considers the collective effect of mainly rare variants, utilising the MutPred Program. We apply this new methodology to investigate the possible role of mtDNA in two cardiovascular disease (CVD) phenotypes (hypertension and hyperglycaemia), within a two-population cohort (n = 363; mean age 45 ± 9 yrs). Very few studies have looked at African mtDNA variation in the context of complex disease, and none using complete sequence data in a well-phenotyped cohort. As such, our study will also extend our knowledge of African mtDNA variation, with complete sequences of Southern Africans being especially under-represented. The cohort showed prevalence rates for hypertension (58.6%) and prediabetes (44.8%). We could not identify a statistically significant role for mtDNA variation in association with hypertension or hyperglycaemia in our cohort. However, we are of the opinion that the method described will find wide application in the field, being especially useful for cohorts from multiple locations or with a variety of mtDNA lineages, where the traditional haplogroup association method has been particularly likely to generate spurious results in the context of association with common complex disease.

Defensive coping (DefS), oxidative stress, inflammation, and related amino acids (phenylalanine [Phe] and tyrosine [Tyr]) have been implicated in cardiovascular disease. This study assessed whether inflammation, oxidative stress, changes in essential amino acids, and altered coping strategies are correlated with subclinical vascular changes in African (n = 82) and Caucasian (n = 100) men from the Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA) study. The Coping Strategy Indicator questionnaire identified DefS participants. Ambulatory blood pressure (BP) was monitored for 24 h, whereas carotid intima media thickness (CIMT) and cross-sectional wall area (CSWA) were determined ultrasonically. Essential amino acids were analyzed with a liquid chromatography tandem mass spectrometry method. Oxidative-inflammatory markers were measured by spectrophotometry. African men had poorer health than Caucasian men, including higher alcohol abuse, elevated BP, abdominal obesity, physical inactivity, and elevated inflammation. Phe (p

Emotional distress has been associated with a poorer prognosis in myocardial infarction patients. Elevated adrenocorticotrophic hormone (ACTH), lower cortisol, dehydroepiandrosterone sulfate (DHEAS) and cortisol:DHEAS, as measures of emotional distress, might correlate with silent myocardial ischemia (SMI) and workload. Thus, we assessed the relationship between emotional distress, SMI and double product (systolic blood pressure (SBP) × heart rate). Cross-sectional South African biethnic single-set cohorts (N=378), aged 44.7±9.52 years, were investigated. Depressive symptoms (Patient Health Questionnaire-9), anthropometric, fasting blood, 24-h double product and 24-h 2-lead electrocardiogram (ST-segment depression) values were obtained. Blacks, mostly men, had increased depressive symptoms, hyperglycemia, SMI, double product, SBP hypertension and ACTH but lower cortisol, DHEAS and cortisol:DHEAS than their White counterparts. Black men had the highest combined SBP hypertension and below-median cortisol prevalence, 38%, compared with 5.9-13.8% in the other groups. Their SMI was associated with ACTH and cortisol:DHEAS (adj. R 0.29; β 0.27-0.31 (0.12-0.64); P≤ 1/20.05), double product (adj. R 0.29; β 0.38 (0.18-0.57); P=0.050) and SBP hypertension (area under the curve: 0.68 (95% CI: 0.56, 0.80); P=0.042; sensitivity/specificity 49/85%). Double product was positively associated with central obesity in all sex groups and with cortisol in the Black men (P

Introduction The evolving use of multiplex proteomic platforms provides an excellent tool for investigating associations between multiple proteins and subclinical atherosclerotic disease. In this study, we evaluated the impact of a multiplex protein panel, on carotid intima-media thickness (cIMT) as a marker of subclinical atherosclerosis. Purpose We used a multiplex proteomic platform to identify possible associations between proteins and subclinical carotid atherosclerosis as measured by carotid ultrasound in an African population. Methods In the Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA) study, 92 proteins from the Proseek Multiplex CVD III 96×96 (Olink Bioscience, Sweden) were analyzed in 378 participants (mean age 44.7±9.6 years, 50.6% women, 10.8% with known cardiovascular disease). Carotid ultrasound was performed for measurements of the carotid intima-media thickness (cIMT, mean 0.663±0.127 mm) and calculation of cross-sectional wall area (CSWA, mean 13.5±4.4mm2), a measure of target organ damage. Possible associations between the proteins, and cIMT and CSWA, respectively, were explored using linear regression models. A two-sided Bonferroni corrected P-value of 0.05/92=5.4x10–4 was considered statistically significant in the crude analysis. Results Of 18 proteins (1 standard deviation of change of ln-transformed values) that were Bonferroni-corrected (p≤5.4x10–4) significantly associated with cIMT and/or CWAS in crude analyses, the following remained significant after further adjustment for age, sex, waist circumference, systolic blood pressure, smoking and total cholesterol: growth-differentiation factor-15 (GDF15; β 0.017, p=0.050), E-selectin (SELE; β 0.019, p=0.017), carboxypeptidase A1 (CPA1; β 0.019, p=0.019), C-C motif chemokine 15 (CCL15; β 0.031, p Conclusion In an African population, we could confirm five proteins (GDF15, SELE, CHI3L1, CD163 and OPG) associated with cIMT, but in addition identified two proteins (CPA1 and CCL15) with novel associations with cIMT and/or CSWA. Acknowledgement/Funding North-West University; National Research Foundation (NRF); Medical Research Council (MRC-SA); Department of Education North-West Province; ROCHE

Purpose: The renin-angiotensin-aldosterone system (RAAS) plays an important role in maintaining hemodynamic homeostasis. Ethnic disparities exist regarding RAAS activity due to sympathetic activity and sodium-water retention, however the implications thereof on cardiac damage is unknown. This study investigated the associations of cardiac troponin T (cTnT), N-terminal pro-brain natriuretic peptide (NTproBNP) and subclinical LVH with components of the RAAS (renin, aldosterone and aldosterone-to-renin ratio (ARR)) and copeptin in a black and white South African cohort. Materials and methods: The study population consisted of 305 participants (black = 139, white = 166) aged 20–62 years. Serum cTnT, NTproBNP, Cornell product, components of the RAAS (active renin, aldosterone and ARR) and copeptin were determined. Results: The black group had lower renin (p

Background: Brain‐derived neurotrophic factor (BDNF) modulates brain health and cognition, which can interfere with executive cognitive function. BDNF was impli-cated with microcirculatory ischaemia and may reflect cardiomyocyte injury. We aimed to determine whether prospective changes (%Δ) in BDNF and cardiac tro-ponin T (cTnT) will be associated with executive cognitive function in a bi‐ethnic cohort.Design: A prospective investigation was conducted over a three‐year period in a bi‐ethnic sex cohort (N = 338; aged 20‐65 years) from South Africa. Fasting serum samples for BDNF and cTnT were obtained. The STROOP‐color‐word conflict test (CWT) was applied to assess executive cognitive function at baseline.Results: In Blacks, BDNF (P< 0.001) increased over the three‐year period while cTnT did not change. In contrast, in Whites, BDNF and cTnT decreased over three years. In Black men, no change in cTnT was associated with increased ΔBDNF (β= 0.25; 95% CI 0.05‐0.45; P= 0.02). In the Black men, constant cTnT levels were inversely associated with executive cognitive function (β= −0.33; 95% CI −0.53 to −0.12; P = 0.003). Three‐year increases in BDNF increased the likelihood for chronic lower cTnT levels at a pre‐established cut‐point of

Mitochondrial DNA (mtDNA) variation has been implicated in several common complex and degenerative diseases, including cardiovascular disease. Inflammation is seen as part of many of these conditions. Mitochondria feature in inflammatory pathways and it has been suggested that mtDNA variation or released mtDNA might be important in this phenomenon. To determine if mtDNA is involved in the mechanisms leading up to cardiovascular disease, we investigated the role of these variants in seven indicators of oxidative stress and inflammation. This study was done in participants of the Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA) cohort, a South African bi-ethnic cohort (N = 363). We applied a variant load hypothesis, which is an alternative approach to, and moves away from the classic haplogroup association approaches, to evaluate the cumulative effect of non-synonymous mtDNA variants on measurements of serum peroxides, nitric oxide metabolites, 8-hydroxy-deoxyguanosine, thiobarbituric acid reactive substances, whole blood reduced glutathione, C-reactive protein, and tumor necrosis factor alpha. We found no significant relationships between non-synonymous mtDNA variants and the seven biochemical parameters investigated here. Non-synonymous mtDNA variants are unlikely to impact on disease in this cohort, to an appreciable or measurable extent.

Structural and functional similarities exist between the retinal, cerebral and, as previously suggested, the coronary microvasculature. Retinal microvascular structure and functionality (in response to flicker-light-induced-provocation (FLIP)) may relate to coronary artery disease risk and possible stroke risk. We investigated associations between retinal vessel structure, functionality and cardiac stress markers (cardiac troponin T [cTnT], amino-terminal B-type natriuretic peptide [NT-proBNP]) to translate these retina-heart relationships to stroke risk. We included 317 African and Caucasian teachers' (aged 23-68 years), who participated in the Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA) study. Fasting plasma and serum samples for cTnT and NT-proBNP were collected. Retinal vascular calibres were quantified from fundus images and dynamic retinal vessel calibre responses during FLIP. The University of California stroke risk score was applied to assess sub-clinical 10-year stroke risk. cTnT levels were similar in Africans and Caucasians, whereas NT-proBNP levels were lower in Africans. In Africans, a reduced arteriolar calibre and attenuated arteriolar dilation during FLIP was associated with higher cTnT (p 0.01). Their larger retinal-venular calibre (p 0.02) and attenuated arteriolar dilation during FLIP (p 0.05) were associated with lower NT-proBNP. Again, exclusively in Africans, increased cardiac stress, wider venular calibres and retinal arteriovenous nicking predicted an increased 10-year stroke risk with odds ratios of 1.57 (95% CI, 1.34; 1.68, p = 0.031), 1.51 (95% CI, 1.26; 1.59, p = 0.002), 1.10 (95% CI, 0.94; 2.85, p = 0.002) and 1.06 (95% CI 0.83; 1.56, p = 0.052), respectively. None of these associations were evident in the Caucasian group. Investigating the retinal vasculature may serve as a tool to approximate sub-clinical coronary and cerebral microvasculature damage or dysfunction. These cardiac stress-retinal associations additionally predicted a greater stroke risk in the SABPA African cohort. Observable changes in the retinal vasculature may serve as markers for the identification and prediction of cardio-systemic and cerebral vascular morbidities and risks, thereby establishing a brain-heart link. Graphical Abstract Proposed series of events during which sustained high pressure and increased cardiac stress may alter retinal reactivity and link to increased stroke risk.

Correction to: Eye https://doi.org/10.1038/s41433-019-0515-y Since the online publication of this article, the authors have noticed that the conclusion to the abstract contains an error. The correct abstract conclusion should read as follows: FLIP elicited increased SNS activity and modulation in this bi-ethnic cohort. In Africans, decreased HRV during FLIP accompanied arteriolar and venular dilatory responses and elevated systemic levels of cTnT, implying that the SNS exerted a significant effect on the smooth muscle tone of the retinal vasculature. Disrupted retinal autoregulation may imply general autonomic nervous system dysfunction; exemplifying central control by the brain on all systemic regulatory functions, across different vascular beds. The authors apologise for any inconvenience caused

Background Defensive coping (DefS) was associated with a vulnerable cardiovascular profile in blacks. The copeptin/vasopressin system is a manifestation of hypothalamic-pituitary-adrenal-axis activity and may act as an acute compensatory mechanism when there is a disruption in volume-loading homeostasis, i.e. when cardiac stress is evident. Whether DefS will influence associations between copeptin and cardiac stress markers, remains unclear. Here we aimed to determine associations between acute mental stress responses of copeptin, vascular responsiveness and biomarkers of cardiomyocyte injury [cardiac troponin T (cTnT)] and cardiac wall-stress [N-terminal pro-brain natriuretic peptide (NT-proBNP)] in DefS race groups. Methods South African black and white teachers (n = 378) of both sexes, participated in this target population study. Cases with a history of myocardial infarction, stroke and atrial fibrillation were excluded. We obtained coping scores (Coping Strategy Indicator), beat-to-beat blood pressure and fasting blood samples at rest and after 1-min exposure to the Stroop-Colour-Word-Conflict-test. Results Interaction effects (p

Objective: Glucose dysregulation is an independent risk factor for cardiovascular and neurodegenerative disease development through synaptic dysfunction resulting in cognitive decline. The aim of this study was to study the interplay between impaired glycaemic metabolism (hyperglycaemia and insulin resistance), cardiac stress (cardiac troponin T and N-terminal brain natriuretic peptide) and executive cognitive function prospectively, in a bi-ethnic sex cohort. Methods: Black and White teachers (N = 338, aged 20–63 years) from the Sympathetic activity and Ambulatory Blood Pressure in Africans study were monitored over a 3-year period. Fasting blood samples were obtained for cardiac troponin T, N-terminal brain natriuretic peptide, glycated haemoglobin and the homeostatic model assessment-insulin resistance for insulin resistance. The Stroop colour-word conflict test was applied to assess executive cognitive function at baseline. Results: Over the 3-year period, Black men revealed constant high levels of cardiac troponin T (⩾4.2 ng/L), pre-diabetes (glycated haemoglobin > 5.7%) and insulin resistance (homeostatic model assessment-insulin resistance >3). %Δ Glycated haemoglobin was associated with %Δ insulin resistance (p Conclusion: Progressive myocyte stretch and chronic myocyte injury, coupled with glucose dysregulation, may interfere with processes related to interference control in Black men.

Type 3 diabetes (T3D) accurately reflects that dementia, e.g., Alzheimer’s disease, represents insulin resistance and neurodegeneration in the brain. Similar retinal microvascular changes were observed in Alzheimer’s and chronic stressed individuals. Hence, we aimed to show that chronic stress relates to T3D dementia signs and retinopathy, ultimately comprising a Stress syndrome prototype reflecting risk for T3D and stroke. A chronic stress and stroke risk phenotype (Stressed) score, independent of age, race or gender, was applied to stratify participants (N = 264, aged 44 ± 9 years) into high stress risk (Stressed, N = 159) and low stress risk (non-Stressed, N = 105) groups. We determined insulin resistance using the homeostatic model assessment (HOMA-IR), which is interchangeable with T3D, and dementia risk markers (cognitive executive functioning (cognitiveexe-func), telomere length, waist circumference (WC), neuronal glia injury, neuron-specific enolase/NSE, S100B). Retinopathy was determined in the mydriatic eye. The Stressed group had greater incidence of HOMA-IR in the upper quartile (≥5), larger WC, poorer cognitiveexe-func control, shorter telomeres, consistently raised neuronal glia injury, fewer retinal arteries, narrower arteries, wider veins and a larger optic cup/disc ratio (C/D) compared to the non-Stressed group. Furthermore, of the stroke risk markers, arterial narrowing was related to glaucoma risk with a greater C/D, whilst retinal vein widening was related to HOMA-IR, poor cognitiveexe-func control and neuronal glia injury (Adjusted R2 0.30, p ≤ 0.05). These associations were not evident in the non-Stressed group. Logistic regression associations between the Stressed phenotype and four dementia risk markers (cognitiveexe-func, telomere length, NSE and WC) comprised a Stress syndrome prototype (area under the curve 0.80, sensitivity/specificity 85%/58%, p ≤ 0.001). The Stress syndrome prototype reflected risk for HOMA-IR (odds ratio (OR) 7.72) and retinal glia ischemia (OR 1.27) and vein widening (OR 1.03). The Stressed phenotype was associated with neuronal glia injury and retinal ischemia, potentiating glaucoma risk. The detrimental effect of chronic stress exemplified a Stress syndrome prototype reflecting risk for type 3 diabetes, neurodegeneration and ischemic stroke.

Atrial fibrillation (AF) is the most common sustained arrhythmia associated with significant morbidity and mortality. The mechanisms underlying the pathogenesis of AF are poorly understood, although electrophysiological remodeling has been described as an important initiating step. There is growing evidence that oxidative stress is involved in the pathogenesis of AF. Many known triggers of oxidative stress, such as age, diabetes, smoking, and inflammation, are linked with an increased risk of arrhythmia. Numerous preclinical studies and clinical trials reported the importance of antioxidant therapy in the prevention of AF, using vitamins C and E, polyunsaturated fatty acids, statins, or nitric oxide donors. The aim of our work is to give a current overview and analysis of opportunities, challenges, and benefits of antioxidant therapy in AF.

Adverse changes in retinal microvasculature caliber are associated with incident hypertension, coronary heart disease and stroke. The absence of a nocturnal dipping in arterial pressure may induce changes throughout the vascular tree, including the retinal microvasculature, but the later link is not sufficiently studied. We explored the relationship between retinal vessel caliber and dipping status in a group of black and white teachers. The study included black (n=68) and white (n=81) men (24-66 years) from the SABPA study. We measured 24 h ambulatory blood pressure and the percentage mean arterial pressure dipping(%MAPdip) was calculated as (diurnal MAP-nocturnal MAP)/diurnal MAP × 100. Retinal images were captured and the central retinal artery equivalent (CRAE) and central retinal vein equivalent (CRVE) calculated. Black men demonstrated higher diurnal and nocturnal MAP (P⩽0.001) and a lesser %MAPdip compared with white men (P=0.047). When stratified by dipping status, black non-dippers (n=33) revealed an increased CRVE (P0.001) compared with their dipper counterparts (n=35). In black men, CRVE was negatively (R

Acute mental stressor–induced cardiac stress responses might contribute to excessive myocardial strain and resultant cardiovascular episode risk. We assessed ethnicity-specific acute cardiac stress (by measuring cardiac troponin T (cTnT) and N-terminal prohormone of brain natriuretic peptide) related to hemodynamic activity. The prospective Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA) study was conducted during 2007–2008 in South Africa. In the cross-sectional phase of the SABPA study, 388 black and white participants underwent a 1-minute acute mental stressor, during which blood pressure was continuously measured. Fasting blood samples for cardiac stress markers were obtained before and 10 minutes after stress (% change). Resting 10-lead electrocardiogram measured the R wave of the aVL lead (RaVL). Black participants exhibited greater cardiac stress responses (P < 0.001), diastolic blood pressure, total peripheral resistance, and stroke volume compared with white participants, who displayed decreases in cardiac stress and increases in cardiac output. Prestress and stressor cTnT cutpoints of 4.2 pg/mL predicted 24-hour, daytime, and nighttime diastolic hypertension in black participants (P < 0.001). These cTnT cutpoints were associated with an ethnicity-specific RaVL cutpoint of 0.28 mV (odds ratio = 3.49, 95% confidence interval: 2.18, 5.83; P = 0.021). Acute mental stress elicited an α-adrenergic activation pattern and cardiac stress hyperreactivity only in black participants. Mental stress might increase the black population’s risk for ischemic episodes and heart disease.

Inflammation was cross-sectionally associated with subclinical wall remodeling and hypertension. Whether longitudinal changes (∆) in inflammation, myocyte injury (troponin T), and stretch (N-terminal-pro-B-type natriuretic peptide) are associated with hypertension and ECG left ventricular hypertrophy (ECG-LVH) is unclear. The first prospective analysis in Africa assessing these associations included a cohort of Black and White teachers (N = 338; aged 20-63 years). Fasting blood samples were obtained to measure tumor necrosis factor-alpha (TNF-α), cardiac troponin T (cTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP). Ambulatory blood pressure, 2-lead ECG and resting 10-lead ECG values were obtained. A higher mean hypertensive status (62%) was evident in Blacks compared to Whites (44%, p

Alcohol contributes greatly to vascular and structural modifications. Due to differences in the metabolism and tolerance of alcohol between ethnic groups, the manner of these modifications may differ. We investigated the association between alcohol consumption - measured via ethnic-specific gamma glutamyl transferase (γ-GT) cut-points - and markers of cardiac perfusion, electrical activity, and pre-clinical structural alterations. A South African target population study was performed in a bi-ethnic cohort (n = 405). Alcohol consumption was determined according to previously defined ethnic-specific γ-GT cut-points, where γ-GT ≥ 19.5 U/L and γ-GT ≥ 55 U/L indicated excessive alcohol consumption in Caucasians and Africans, respectively. Ambulatory 24-h blood pressure and electrocardiograms (ECG), 10-lead ECG left ventricular hypertrophy (LVH), ischemic events, N-terminal pro-brain natriuretic peptide (NT-proBNP), and QTc prolongation were assessed. Fasting blood samples were obtained. A poorer cardio-metabolic profile and mean 24-h hypertensive and ECG-LVH values were evident in high γ-GT groups of both ethnicities, when compared to their low counterparts. The African high γ-GT group reported a higher intake of alcohol and presented significant increases in NT-proBNP (p 0.001), QTc prolongation (p = 0.008), and ischemic events (p = 0.013). Regression analyses revealed associations between ECG-LVH and NT-proBNP, QTc prolongation, ischemic events, and SBP, in the African high γ-GT group exclusively. High alcohol consumers presented delayed electrical conduction in the heart accompanied by ECG-LVH, ischemic events, and increased vaso-responsiveness, predominantly in Africans. Ultimately, increased left ventricular distension on a pre-clinical level may elevate the risk for future cardiovascular events in this population.

Supplemental material, dvdres-sep-2018-00172-File007 for Prospective associations between cardiac stress, glucose dysregulation and executive cognitive function in Black men: The Sympathetic activity and Ambulatory Blood Pressure in Africans study by Esmé Jansen van Vuren, Leoné Malan, Roland von Känel, Martin Magnusson, Leandi Lammertyn and Nicolaas T Malan in Diabetes & Vascular Disease Research

Background and objectives: It is widely accepted that regular physical exercise reduces the BP, particularly in hypertensive individuals. It is recommended in the prevention of hypertension to assist in BP control. The BP lowering mechanisms of exercise remain largely elusive, we therefore evaluated the RAAS as a regulator of arterial BP. Methods: The sub-study was embedded in the African Prospective study on the Early Detection and Identification of Cardiovascular disease and Hypertension (African- PREDICT) and included 111 white and 99 black participants aged 20–30 years. Office- and central blood pressure as well as other cardiovascular variables were measured. Renin was analysed with an ELISA- and aldosterone with a RIA kit. Results: The BP decreased significantly in the white but not in the black participants when tertiles for physical activity levels were compared. The total renin (renin + prorenin) level decreased significantly from 789.2 to 700.0 pg/ml (p = 0.04) in the white but not in the black participants (821.6 to 806.6 pg/ml; p = 0.84) with high physical activity level. In multiple regression analysis, in the white participants, MAP and aldosterone contributed significantly and independently to the low renin in the third percentile for physical activity level. This was not evident in the black participants. Conclusion: Only in white participants high physical activity levels were associated with decreased blood pressure and the RAAS may be an important mechanism in this regard.

OBJECTIVES Defensive coping (DefS) in Blacks has been associated with greater cardiovascular risk than in their White counterparts. We examined associations between endothelial function mental stress responses and markers of vascular structure in a bi-ethnic cohort. METHODS We examined vascular function and structure in 368 Black (43.84±8.31years) and White Africans (44.78±10.90years). Fasting blood samples, 24h blood pressure, left carotid intima-media thickness of the far wall (L-CIMTf), and left carotid cross-sectional wall area (L-CSWA) values were obtained. von Willebrand factor (VWF), endothelin-1 (ET-1) and nitric oxide metabolite (NOx) responses to the Stroop mental stress test were calculated to assess endothelial function. DefS was assessed using the Coping Strategy Indicator questionnaire. Interaction between main effects was demonstrated for 283 participants with DefS scores above the mean of 26 for L-CIMTf. RESULTS Blunted stress responses for VWF (men 16.71% vs. 51.10%; women 0.85% vs. 42.09%, respectively) and NOx (men -64.52% vs. 74.89%; women -76.16% vs. 113.29%, respectively) were evident in the DefS Blacks compared to the DefS Whites (p

This study examined the association between nutritional awareness and diet quality, as indicated by energy density, dietary diversity and adequacy to achieve dietary recommendations, while considering the potentially important role of socioeconomic status (SES). Data were derived from 1351 subjects, aged 18–69 years and enrolled in the ORISCAV-LUX study. Energy density score (EDS), dietary diversity score (DDS) and Recommendation Compliance Index (RCI) were calculated based on data derived from a food frequency questionnaire. Nutritional awareness was defined as self-perception of the importance assigned to eating balanced meals, and classified as high, moderate, or of little importance. Initially, a General Linear Model was fit that adjusted for age, sex, country of birth, and body mass index (BMI). Furthermore, simultaneous contributions to diet quality of individual-level socioeconomic factors, education, and household income were examined across levels of nutritional awareness. Attributing high importance was associated inversely with energy density (p = 0.02), positively with both dietary diversity (p &lt, 0.0001), and adequacy to dietary recommendations (p &lt, 0.0001), independent of demographic factors, weight status and SES. Further adjustment for household income in the EDS-related multivariable model, reduced the β coefficient by 47% for the “moderate importance” category and 36% for the “high importance” category. Likewise, the β coefficient decreased by 13.6% and 10.7% in the DDS-related model, and by 12.5%, and 7.1% in the RCI-related model, respectively, across awareness categories. Nutritional awareness has a direct effect on diet quality, with a minor component of variance explained by improved income. The impact of nutritional awareness on diet quality seems to be a promising area for both health promotion and health policy research.

Evidence of the relationship between left ventricular hypertrophy and urinary albumin excretion is contradictory and limited in black adults in whom hypertensive heart disease is common. We aimed to investigate the relationship between subclinical left ventricular hypertrophy and albuminuria in non-diabetic hypertensive blacks. Urinary albumin-to-creatinine ratio (UACR) was determined from 8-hour overnight urine collection. We recorded ambulatory blood pressure and 12-lead electrocardiogram during a typical working day. Cornell product (P = .002), UACR (P = .042), 24-hour systolic pressure (P .0001), and 24-hour pulse pressure (P .0001) were higher in the hypertensive group. Cornell product was associated with UACR in single (r = 0.25; P = .012), partial (P trend = .002), and multiple regression (β = 0.326; P = .0005) analyses in the hypertensive group only, even below the threshold for microalbuminuria and independent of 24-hour systolic pressure. Urinary albumin excretion is associated with subclinical left ventricular hypertrophy in non-diabetic hypertensive blacks and may be a useful marker of early cardiovascular disease in blacks.