Ethnicity-Specific Changes in Cardiac Troponin T in Response to Acute Mental Stress and Ethnicity-Specific Cutpoints for the R Wave of the aVL Lead.

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.

Coping and Cardiac Troponin T - A Risk for Hypertension and Sub-Clinical ECG Left Ventricular Hypertrophy: The SABPA Study.

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 4.2ng/L. METHODS: A target population study included a Black (n=190) and White (n=204) teachers' gender cohort (20-65years) 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 ≥ 4.2ng/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.

A Scoping Review of Trials Designed to Achieve Remission of Type 2 Diabetes with Lifestyle Intervention Alone: Implications for Sub-Saharan Africa.

According to the International Diabetes Federation, sub-Saharan Africa is experiencing the highest anticipate increase in the prevalence of type 2 diabetes (T2D) in the world and has the highest percent of people living with T2D who are undiagnosed. Therefore, diagnosis and treatment need prioritization. However, pharmacological hypoglycemics are often unavailable and bariatric surgery is not an option. Therefore, the ability to induce T2D remission through lifestyle intervention alone (LSI-alone) needs assessment. This scoping review evaluated trials designed to induce T2D remission by LSI-alone. PubMed, Embase, Cochrane, and CINAHL databases were searched for trials designed to induce T2D remission through LSI-alone. Of the 928 identified, 63 duplicates were removed. With abstract review, 727 irrelevant articles were excluded. After full-text review, 112 inappropriate articles were removed. The remaining 26 articles described 16 trials. These trials were published between 1984 and 2021 and were conducted in 10 countries, none of which were in Africa. Remission rates varied across trials. Predictors of remission were 10% weight loss and higher BMI, lower A1C and shorter T2D duration at enrollment. However, LSI-alone regimens for newly diagnosed and established T2D were very different. In newly diagnosed T2D, LSI-alone were relatively low-cost and focused on exercise and dietary counseling with or without calorie restriction (~1500 kcal/d). Presumably due to differences in cost, LSI-alone trials in newly diagnosed T2D had higher enrollments and longer duration. For established T2D trials, the focus was on arduous phased dietary interventions; phase 1: low-calorie meal replacement (<1000 kcal/day); phase 2: food re-introduction; phase 3: weight maintenance. In short, LSI-alone can induce remission in both newly diagnosed and established T2D. To demonstrate efficacy in Africa, initial trials could focus on newly diagnosed T2D. Insight gained could provide proof of concept and a foundation in Africa on which successful studies of LSI-alone in established T2D could be built.

Sleep and Economic Status Are Linked to Daily Life Stress in African-Born Blacks Living in America.

To identify determinants of daily life stress in Africans in America, 156 African-born Blacks (Age: 40 ± 10 years (mean ± SD), range 22-65 years) who came to the United States as adults (age ≥ 18 years) were asked about stress, sleep, behavior and socioeconomic status. Daily life stress and sleep quality were assessed with the Perceived Stress Scale (PSS) and Pittsburgh Sleep Quality Index (PSQI), respectively. High-stress was defined by the threshold of the upper quartile of population distribution of PSS (≥16) and low-stress as PSS < 16. Poor sleep quality required PSQI > 5. Low income was defined as <40 k yearly. In the high and low-stress groups, PSS were: 21 ± 4 versus 9 ± 4, p < 0.001 and PSQI were: 6 ± 3 versus 4 ± 3, p < 0.001, respectively. PSS and PSQI were correlated (r = 0.38, p < 0.001). The odds of high-stress were higher among those with poor sleep quality (OR 5.11, 95% CI: 2.07, 12.62), low income (OR 5.03, 95% CI: 1.75, 14.47), and no health insurance (OR 3.01, 95% CI: 1.19, 8.56). Overall, in African-born Blacks living in America, daily life stress appears to be linked to poor quality sleep and exacerbated by low income and lack of health insurance.

Non-invasive type 2 diabetes risk scores do not identify diabetes when the cause is ß-cell failure: The Africans in America study.

Background: Emerging data suggests that in sub-Saharan Africa ß-cell-failure in the absence of obesity is a frequent cause of type 2 diabetes (diabetes). Traditional diabetes risk scores assume that obesity-linked insulin resistance is the primary cause of diabetes. Hence, it is unknown whether diabetes risk scores detect undiagnosed diabetes when the cause is ß-cell-failure. Aims: In 528 African-born Blacks living in the United States [age 38 ± 10 (Mean ± SE); 64% male; BMI 28 ± 5 kg/m2] we determined the: (1) prevalence of previously undiagnosed diabetes, (2) prevalence of diabetes due to ß-cell-failure vs. insulin resistance; and (3) the ability of six diabetes risk scores [Cambridge, Finnish Diabetes Risk Score (FINDRISC), Kuwaiti, Omani, Rotterdam, and SUNSET] to detect previously undiagnosed diabetes due to either ß-cell-failure or insulin resistance. Methods: Diabetes was diagnosed by glucose criteria of the OGTT and/or HbA1c ≥ 6.5%. Insulin resistance was defined by the lowest quartile of the Matsuda index (≤ 2.04). Diabetes due to ß-cell-failure required diagnosis of diabetes in the absence of insulin resistance. Demographics, body mass index (BMI), waist circumference, visceral adipose tissue (VAT), family medical history, smoking status, blood pressure, antihypertensive medication, and blood lipid profiles were obtained. Area under the Receiver Operator Characteristics Curve (AROC) estimated sensitivity and specificity of each continuous score. AROC criteria were: Outstanding: >0.90; Excellent: 0.80-0.89; Acceptable: 0.70-0.79; Poor: 0.50-0.69; and No Discrimination: 0.50. Results: Prevalence of diabetes was 9% (46/528). Of the diabetes cases, ß-cell-failure occurred in 43% (20/46) and insulin resistance in 57% (26/46). The ß-cell-failure group had lower BMI (27 ± 4 vs. 31 ± 5 kg/m2 P < 0.001), lower waist circumference (91 ± 10 vs. 101 ± 10cm P < 0.001) and lower VAT (119 ± 65 vs. 183 ± 63 cm3, P < 0.001). Scores had indiscriminate or poor detection of diabetes due to ß-cell-failure (FINDRISC AROC = 0.49 to Cambridge AROC = 0.62). Scores showed poor to excellent detection of diabetes due to insulin resistance, (Cambridge AROC = 0.69, to Kuwaiti AROC = 0.81). Conclusions: At a prevalence of 43%, ß-cell-failure accounted for nearly half of the cases of diabetes. All six diabetes risk scores failed to detect previously undiagnosed diabetes due to ß-cell-failure while effectively identifying diabetes when the etiology was insulin resistance. Diabetes risk scores which correctly classify diabetes due to ß-cell-failure are urgently needed.

The Africans in America study demonstrates that subclinical cardiovascular risk differs by etiology of abnormal glucose tolerance.

Abnormal-glucose tolerance (Abnl-GT) is due to an imbalance between ß-cell function and insulin resistance (IR) and is a major risk factor in cardiovascular disease (CVD). In sub-Saharan Africa, ß-cell failure is emerging as an important cause of Abnl-GT (Abnl-GT-ß-cell-failure). Visceral adipose tissue (VAT) volume and hyperlipidemia are major contributors to CVD risk when Abnl-GT is due to IR (Abnl-GT-IR). Yet, the CVD profile associated with Abnl-GT-ß-cell failure is unknown. Therefore, our goals in 450 African-born Blacks (Male: 65%; Age: 39 ± 10 years; BMI 28 ± 5 kg/m2), living in America were to: (1) determine Abnl-GT prevalence and etiology; (2) assess by Abnl-GT etiology, associations between four understudied subclinical CVD risk factors in Africans: (a) subclinical myocardial damage (high-sensitivity troponin T (hs-cTnT)); (b) neurohormonal regulation (N-terminal pro-Brain-natriuretic peptide (NT-proBNP)); (c) coagulability (fibrinogen); (d) inflammation (high-sensitivity C-reactive protein (hsCRP)), as well as HbA1c, Cholesterol/HDL ratio and VAT. Glucose tolerance status was determined by the OGTT. IR was defined by the threshold at the lowest quartile for the Matsuda Index (≤ 2.97). Abnl-GT-IR required both Abnl-GT and IR. Abnl-GT-ß-cell-failure was defined as Abnl-GT without IR. VAT was assessed by CT-scan. For both the Abnl-GT-ß-cell-failure and Abnl-GT-IR groups, four multiple regression models were performed for hs-cTnT; NT-proBNP; fibrinogen and hsCRP, as dependent variables, with the remaining three biomarkers and HbA1c, Cholesterol/HDL and VAT as independent variables. Abnl-GT occurred in 38% (170/450). In the Abnl-GT group, ß-cell failure occurred in 58% (98/170) and IR in 42% (72/170). VAT and Cholesterol/HDL were significantly lower in Abnl-GT-ß-cell-failure group vs the Abnl-GT-IR group (both P < 0.001). In the Abnl-GT-ß-cell-failure group: significant associations existed between hscTnT, fibrinogen, hs-CRP, and HbA1c (all P < 0.05), and none with Cholesterol/HDL or VAT. In Abnl-GT-IR: hs-cTnT, fibrinogen and hsCRP significantly associated with Cholesterol/HDL (all P < 0.05) and NT-proBNP inversely related to fibrinogen, hsCRP, HbA1c, Cholesterol/HDL, and VAT (all P < 0.05). The subclinical CVD risk profile differed between Abnl-GT-ß-cell failure and Abnl-GT-IR. In Abnl-GT-ß-cell failure subclinical CVD risk involved subclinical-myocardial damage, hypercoagulability and increased inflammation, but not hyperlipidemia or visceral adiposity. For Abnl-GT-IR, subclinical CVD risk related to subclinical myocardial damage, neurohormonal dysregulation, inflammation associated with hyperlipidemia and visceral adiposity. ClinicalTrials.gov Identifier: NCT00001853.

Circulating neurotrophins and hemostatic risk factors of atherothrombotic cardiovascular disease at baseline and during sympathetic challenge: the SABPA study.

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.

Exploring biomarkers associated with deteriorating vascular health using a targeted proteomics chip: The SABPA study.

ABSTRACT: In this observational study, by the use of a multiplex proteomic platform, we aimed to explore associations between 92 targeted proteins involved in cardiovascular disease and/or inflammation, and phenotypes of deteriorating vascular health, with regards to ethnicity.Proteomic profiling (92 proteins) was carried out in 362 participants from the Sympathetic activity and Ambulatory Blood Pressure in Africans (SABPA) study of black and white African school teachers (mean age 44.7 ±â€Š9.9 years, 51.9% women, 44.5% Black Africans, 9.9% with known cardiovascular disease). Three proteins with <15% of samples below detectable limits were excluded from analyses. Associations between multiple proteins and prevalence of hypertension as well as vascular health [Carotid intima-media thickness (cIMT) and pulse wave velocity (PWV)] measures were explored using Bonferroni-corrected regression models.Bonferroni-corrected significant associations between 89 proteins and vascular health markers were further adjusted for clinically relevant co-variates. Hypertension was associated with growth differentiation factor 15 (GDF-15) and C-X-C motif chemokine 16 (CXCL16). cIMT was associated with carboxypeptidase A1 (CPA1), C-C motif chemokine 15 (CCL15), chitinase-3-like protein 1 (CHI3L1), scavenger receptor cysteine-rich type 1 protein M130 (CD163) and osteoprotegerin, whereas PWV was associated with GDF15, E-selectin, CPA1, fatty acid-binding protein 4 (FABP4), CXCL16, carboxypeptidase B (CPB1), and tissue-type plasminogen activator. Upon entering ethnicity into the models, the associations between PWV and CPA1, CPB1, GDF-15, FABP4, CXCL16, and between cIMT and CCL-15, remained significant.Using a multiplex proteomic approach, we linked phenotypes of vascular health with several proteins. Novel associations were found between hypertension, PWV or cIMT and proteins linked to inflammatory response, chemotaxis, coagulation or proteolysis. Further, we could reveal whether the associations were ethnicity-dependent or not.

Beta-cell failure rather than insulin resistance is the major cause of abnormal glucose tolerance in Africans: insight from the Africans in America study.

INTRODUCTION: Uncertainties exist on whether the main determinant of abnormal glucose tolerance (Abnl-GT) in Africans is ß-cell failure or insulin resistance (IR). Therefore, we determined the prevalence, phenotype and characteristics of Abnl-GT due to ß-cell failure versus IR in 486 African-born blacks (male: 64%, age: 38±10 years (mean±SD)) living in America. RESEARCH DESIGN AND METHODS: Oral glucose tolerance test were performed. Abnl-GT is a term which includes both diabetes and prediabetes and was defined as fasting plasma glucose (FPG) ≥5.6 mmol/L and/or 2-hour glucose ≥7.8 mmol/L. IR was defined by the lowest quartile of the Matsuda Index (≤2.98) and retested using the upper quartile of homeostatic model assessment of insulin resistance (HOMA-IR) (≥2.07). Abnl-GT-IR required both Abnl-GT and IR. Abnl-GT-ß-cell failure was defined as Abnl-GT without IR. Beta-cell compensation was assessed by the Disposition Index (DI). Fasting lipids were measured. Visceral adipose tissue (VAT) volume was obtained with abdominal CT scan. RESULTS: The prevalence of Abnl-GT was 37% (182/486). For participants with Abnl-GT, IR occurred in 38% (69/182) and ß-cell failure in 62% (113/182). Compared with Africans with Abnl-GT-IR, Africans with Abnl-GT-ß-cell failure had lower body mass index (BMI) (30.8±4.3 vs 27.4±4.0 kg/m2), a lower prevalence of obesity (52% vs 19%), less VAT (163±72 vs 107±63 cm2), lower triglyceride (1.21±0.60 vs 0.85±0.42 mmol/L) and lower FPG (5.9±1.4 vs 5.3±0.6 mmol/L) and 2-hour glucose concentrations (10.0±3.1 vs 9.0±1.9 mmol/L) (all p<0.001) and higher DI, high-density lipoprotein (HDL), low-density lipoprotein particle size and HDL particle size (all p<0.01). Analyses with Matsuda Index and HOMA-IR yielded similar results. Potential confounders such as income, education, alcohol and fiber intake did not differ by group. CONCLUSIONS: Beta-cell failure occurred in two-thirds of participants with Abnl-GT and may be a more frequent determinant of Abnl-GT in Africans than IR. As BMI category, degree of glycemia and lipid profile appeared more favorable when Abnl-GT was due to ß-cell failure rather than IR, the clinical course and optimal interventions may differ. TRIAL REGISTRATION NUMBER: NCT00001853.

Delayed retinal vein recovery responses indicate both non-adaptation to stress as well as increased risk for stroke: the SABPA study.

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 dysregulation 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.

Heart rate variability, the dynamic nature of the retinal microvasculature and cardiac stress: providing insight into the brain-retina-heart link: the SABPA study.

BACKGROUND AND AIMS: Decreased heart-rate-variability (HRV) indicates increased sympathetic nervous system (SNS) activity and modulation with a shift in the sympatho-vagal balance towards SNS predominance. Increased SNS activity may precede volume-loading hypertension, contribute to increases in cardiac troponin T (cTnT), endothelial dysfunction and small vessel disease. Therefore, we investigated the retinal vasculature, HRV during flicker-light-induced-provocation (FLIP) and systemic cTnT, a marker of cardiac stress, to provide further evidence in support of the brain-retina-heart link. METHODS: Cross-sectional observations were obtained from a bi-ethnic cohort (N = 264), aged 23-68 years. Fasting serum samples for cTnT were obtained. Retinal vascular calibres were quantified from mydriatic eye fundus images and dynamic retinal vessel calibre responses were determined during FLIP. Time-and frequency domain parameters of HRV were calculated during FLIP for each participant. RESULTS: Africans had wider venules and attenuated time domain parameters during FLIP. In Africans, inverse associations emerged between arteriolar dilation and both cTnT and root-mean squared of the standard deviations of successive RR-intervals (rMSSD) (p = 0.030), and between arteriolar constriction and both low-frequency expressed in normalised units (LFnu) (p = 0.003) and high-frequency expressed in normalised units (p = 0.021). Wider venules inversely associated with standard deviation of the NN intervals (SDNN) as well as LFnu (p = 0.009) in Africans. An opposite profile was observed in Caucasians with both time-and frequency domain parameters of HRV in relation to retinal vessel structure and function. CONCLUSION: FLIP elicited increased SNS activity and modulation in this bi-ethnic cohort. In Africans, decreased HRV during FLIP accompanied arteriolar and venular 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.

Correction to: Heart rate variability, the dynamic nature of the retinal microvasculature and cardiac stress: providing insight into the brain-retina-heart link: the SABPA study.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Africans Who Arrive in the United States before 20 Years of Age Maintain Both Cardiometabolic Health and Cultural Identity: Insight from the Africans in America Study.

The overall consensus is that foreign-born adults who come to America age < 20 y achieve economic success but develop adverse behaviors (smoking and drinking) that lead to worse cardiometabolic health than immigrants who arrive age ≥ 20 y. Whether age of immigration affects the health of African-born Blacks living in America is unknown. Our goals were to examine cultural identity, behavior, and socioeconomic factors and determine if differences exist in the cardiometabolic health of Africans who immigrated to America before and after age 20 y. Of the 482 enrollees (age: 38 ± 1 (mean ± SE), range: 20-65 y) in the Africans in America cohort, 23% (111/482) arrived age < 20 y, and 77% (371/482) arrived age ≥ 20 y. Independent of francophone status or African region of origin, Africans who immigrated age < 20 y had similar or better cardiometabolic health than Africans who immigrated age ≥ 20 y. The majority of Africans who immigrated age < 20 y identified as African, had African-born spouses, exercised, did not adopt adverse health behaviors, and actualized early life migration advantages, such as an American university education. Due to maintenance of cultural identity and actualization of opportunities in America, cardiometabolic health may be protected in Africans who immigrate before age 20. In short, immigrant health research must be cognizant of the diversity within the foreign-born community and age of immigration.

Retinal-glia ischemia and inflammation induced by chronic stress: The SABPA study.

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 â€‹= â€‹359; aged 46 â€‹± â€‹9 years) into Stress (N â€‹= â€‹236) and no-Stress groups (N â€‹= â€‹123). Prospective data for glia ischemia risk markers were obtained, including 24 â€‹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 â€‹= â€‹0.060), TNF-α and higher diastolic-ocular-perfusion-pressure [Adj. R2 0.39-0.41, p â€‹≤ â€‹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.

Retinal Vasculature Reactivity During Flicker Light Provocation, Cardiac Stress and Stroke Risk in Africans: The SABPA Study.

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.

QTc prolongation, increased NT-proBNP and pre-clinical myocardial wall remodeling in excessive alcohol consumers: The SABPA study.

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.