Hypertension In Blacks Research Articles

A11974 SNX1 Loss Manifests with Increased Oxidative Stress and Hypertension

Objectives: Acute depletion of renal sorting nexin 1 (SNX1) results in blunted natriuretic response and hypertension in mice due to impaired dopamine D5 receptor (D5R) activity. We elucidated the molecular mechanisms for these phenotypes in Snx1−/− mice, which have a congenital absence of SNX1. Methods: Basal reactive oxygen species (ROS) levels, NOX activity, and blood pressure of Snx1−/− mice and the activity of cAMP and sodium transport of renal proximal tubule cells from hypertensive (HT) were measured. Results: These mice had increased renal expression of AT1R, NADPH oxidase (NOX) components, D5R, sodium-chloride cotransporter, and the antioxidant paraoxonase 2. Basal reactive oxygen species (ROS) levels, NOX activity, and blood pressure were also markedly higher in Snx1−/− mice, which were normalized by apocynin, a drug that prevents NOX assembly. HT renal proximal tubule cells from Caucasian males have deficient SNX1, impaired D5R endocytosis, and increased ROS compared with cells from normotensive (NT) male subjects. siRNA - mediated depletion of SNX1 in NT cells led to a blunting of agonist-induced increase in cAMP production and decrease in sodium transport, while gene rescue via over-expression of SNX1 in HT cells normalized the D5R agonist-mediated stimulation of cAMP production and inhibition of sodium transport. Three of the 12 single nucleotide polymorphisms interrogated for the SNX1 gene associated with poor blood pressure response to thiazide among hypertensive blacks. Conclusion: Our data demonstrate a new paradigm for the development of hypertension.

Cluster Randomized Clinical Trial of FAITH (Faith-Based Approaches in the Treatment of Hypertension) in Blacks.

Therapeutic lifestyle change (TLC) is a recommended treatment for patients with hypertension, but its effectiveness in community-based settings remains untested, particularly in black churches-an influential institution for health promotion in black communities. The FAITH study (Faith-Based Approaches in the Treatment of Hypertension) evaluated the comparative effectiveness of a TLC intervention plus motivational interviewing (MINT) sessions versus health education (HE) alone, on blood pressure (BP) reduction among blacks with uncontrolled hypertension. Data were collected on 373 participants meeting eligibility criteria (self-identification as black, age ≥18 years, self-reported diagnosis of hypertension, and uncontrolled BP [BP ≥140/90 or ≥130/80 mm Hg with diabetes mellitus or chronic kidney disease]) from 32 New York City churches. The MINT-TLC intervention plus motivational interviewing treatment comprised 11 weekly group sessions on TLC plus 3 MINT sessions delivered monthly by lay health advisors. The HE control group received 1 TLC session plus 10 sessions on health topics delivered by local experts. The outcomes were BP reduction at 6 months (primary) and BP control and BP reduction at 9 months (secondary). The sample mean age was 63 years; 76% women, with mean BP of 153/87 mm Hg. Using linear mixed-effects regression models, the MINT-TLC intervention plus motivational interviewing group had a significantly greater systolic BP reduction of 5.79 mm Hg compared with the HE group at 6 months ( P=0.029). The treatment effect on systolic BP persisted at 9 months but had reduced significance (5.21 mm Hg; P=0.068). The between-group differences in diastolic BP reduction (0.41 mm Hg) and mean arterial pressure (2.24 mm Hg) at 6 months were not significant. Although the MINT-TLC intervention plus motivational interviewing group had greater BP control than the HE group at 9 months, the difference was not statistically significant (57.0% versus 48.8%; odds ratio, 1.43; 95% CI, 0.90-2.28). A community-based lifestyle intervention delivered in churches led to significantly greater reduction in systolic BP in hypertensive blacks compared with HE alone. URL: https://www.clinicaltrials.gov . Unique identifier: NCT01065831.

Sodium Reduction, miRNA Profiling and CVD Risk in Untreated Hypertensives: a Randomized, Double-Blind, Placebo-Controlled Trial

Sodium reduction decreases blood pressure (BP) and cardiovascular mortality. However, the underlying molecular mechanisms are not well understood. We tested the hypothesis that reduction of sodium intake would change miRNA expression in hypertensive patients, and those changes would be associated with improved cardiovascular phenotypes. A whole genome RNA sequencing was performed in paired serum samples collected at the end of usual sodium intake and reduced sodium intake periods from 10 (age 56.8 ± 8.9) untreated black male hypertensives, selected from a randomized crossover trial of sodium reduction as the discovery cohort. Validation was carried out by the PCR Serum/Plasma Focus panel profiling in paired samples in all 64 (50% males, age 50.2 ± 9.5) untreated black hypertensives from the same trial. Fifteen respondent miRNAs were identified in the discovery stage. miR-143-3p was replicated. Sodium reduction up-regulated miR-143-3p. The increase in miR-143-3p was associated with the reduction of BP and arterial stiffness and the increase in skin capillary density. In conclusion, dietary sodium reduction alters circulating miRNA expressions, and those miRNA changes are associated with reduced BP and improved arterial compliance in untreated black hypertensives, suggesting that miRNA regulation may be one of the underlying mechanisms that dietary sodium regulates cardiovascular health.

Hydralazine/Isosorbide Dinitrate, Blood Pressure and Mortality in Patients with Heart Failure with Reduced Ejection Fraction

Introduction The use of hydralazine and isosorbide dinitrate (H-ISDN) has been shown to reduce mortality in African American patients with heart failure with reduced ejection fraction (HFrEF). We aimed to evaluate the association of H-ISDN use with all-cause mortality among HFrEF patients with and without hypertension in large health system serving an inner city population. Hypothesis H-ISDN is associated with lower mortality in patients with hypertension, and this association differs by race/ethnicity. Methods We queried electronic health records to identify all patients ≥18 years old diagnosed with HFrEF (EF Results Of 11,962 patients included, mean age was 65.2±15.6, mean EF 22.7±7.3%, 60% were male, 31% were non-Hispanic black, 69% were hypertensive, and 13% were prescribed H-ISDN. Overall, H-ISDN was not significantly associated with mortality among hypertensive (HR 0.88; 0.77-1.01, p=0.084), nor among normotensive patients (HR 1.12; 0.92-1.37, p=0.254). H-ISDN was associated with significant mortality reduction in hypertensive blacks (HR 0.78; 0.63-0.97, p=0.025), but not in hypertensive whites (HR 0.95; 0.69-1.32, p=0.76) or hypertensive Hispanics (HR 1.12; 0.85-1.49, p=0.422). There was no evidence of effect modification by gender in any race/ethnic group (p-interaction >0.05). H-ISDN was not significantly associated with mortality among normotensives in any race/ethnic group. Conclusion In real-world practice in a large urban center, there was a suggestion of an inverse association between H-ISDN use and mortality among hypertensive patients, but this was not statistically significant. Use of H-ISDN did show a significant association with lower mortality among hypertensive blacks, which lends support to the benefits of this drug combination in this race/ethnic group.

Cumulative Incidence of Hypertension by 55Years of Age in Blacks and Whites: The CARDIA Study.

BackgroundBlacks have higher blood pressure levels compared with whites beginning in childhood. Few data are available on racial differences in the incidence of hypertension from young adulthood through middle age.Methods and ResultsWe calculated the cumulative incidence of hypertension from age 18 to 55 years among participants in the CARDIA (Coronary Artery Risk Development in Young Adults) study. Incident hypertension was defined by the first visit with mean systolic blood pressure ≥130 mm Hg, mean diastolic blood pressure ≥80 mm Hg, or self‐reported use of antihypertensive medication. Among 3890 participants without hypertension at baseline (aged 18–30 years), cumulative incidence of hypertension by age 55 years was 75.5%, 75.7%, 54.5%, and 40.0% in black men, black women, white men, and white women, respectively. Among participants with systolic blood pressure/diastolic blood pressure <110 and 70, 110 to 119/70 to 74, and 120 to 129/75 to 79 mm Hg at baseline, blacks were more likely than whites to develop hypertension: multivariable‐adjusted hazard ratios 1.97 (95% confidence interval, 1.65, 2.35), 1.80 (95% confidence interval, 1.52, 2.14), and 1.59 (95% confidence interval, 1.31, 1.93), respectively. Parental history of hypertension and higher body mass index, serum uric acid, and systolic blood pressure/diastolic blood pressure categories were associated with a higher risk for hypertension among blacks and whites. A higher Dietary Approaches to Stop Hypertension diet adherence score was associated with a lower risk for hypertension in blacks and whites.ConclusionsRegardless of blood pressure level in young adulthood, blacks have a substantially higher risk for hypertension compared with whites through 55 years of age.

Chronic depression symptoms desensitize renin activity to protect against volume-loading hypertension in Blacks: The SABPA study.

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. 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. 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. 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.

Hypertension in Blacks: Individualized Therapy Based on Renin/Aldosterone Phenotyping.

The prevalence of hypertension in blacks is higher than in other groups. The following is quoted from the 2015 statistical report of the American Heart Association1: “In 2009 to 2012, the age-adjusted prevalence of hypertension was 44.9% and 46.1% among non-Hispanic black men and women, respectively; 32.9% and 30.1% among non-Hispanic white men and women, respectively; and 29.6% and 29.9% among Hispanic men and women, respectively.” In the national REGARDS cohort (Reasons for Geographic and Racial Differences in Stroke)2, among 27 744 participants followed up for 4.4 years (2003–2010), the overall age- and sex-adjusted black/white incidence rate ratio for ischemic stroke was 1.51, but for ages 45 to 54 years, it was 4.02, whereas for those ≥85 years of age, it was 0.86. This suggests that those who survived to 85 years of age did not have resistant hypertension. Among blacks, compared with whites, the relative risk of intracranial atherosclerotic stroke was 5.85; of extracranial atherosclerotic stroke, 3.18; of lacunar stroke, 3.09; and of cardioembolic stroke, 1.58.3 Similarly, Markus et al4 reported that in South London, United Kingdom, the relative risk of stroke because of small vessel disease in black patients was 2.94 (95% confidence interval, 1.97–4.39; P 20 years of age, the age-adjusted relative risk of intracerebral hemorrhage among blacks compared with white patients was 2.4 for men and 3.2 for women.5 In the Northern Kentucky study, “The greatest excess risk of ICH in blacks compared with whites was found among young to middle-aged (35 to 54 years) persons with brain stem (RR, 9.8; 95% CI, 4.2 to 23.0) and deep cerebral (RR, 4.5; 95% CI, 3.0 to 6.8) hemorrhage.”6 Strokes due to small vessel disease …

Abstract P181: Contribution of C-Reactive Protein to Racial Disparities in Incident Hypertension: The REasons for Geographic And Racial Differences in Stroke Study (REGARDS)

Introduction: In the US, blacks are at higher risk of hypertension than whites. The single largest contributor to this disparity is the Southern Diet pattern. Inflammation biomarkers are associated with risk of hypertension, and C-reactive protein (CRP) is higher in blacks than whites. We studied whether elevated CRP in blacks relative to whites contributes to the racial disparity in hypertension in blacks. Methods: We included 6,548 black and white men and women age ≥45 years from the REGARDS cohort without hypertension at baseline ('03-'07) and who completed visit 2 in '13-'16. Incident hypertension was defined as BP ≥140/90 mm Hg or hypertension medication use at visit 2. Using logistic regression, the black:white odds ratio (OR) for incident hypertension was calculated adjusting for age, sex, race, and baseline SBP. We assessed the percent change in the black:white OR for incident hypertension after adding CRP. The 95% CI was calculated using 1,000 bootstrapped samples. We determined the impact of known hypertension risk factors and anti-inflammatory medications on the percent mediation by CRP. Results: Hypertension developed in 46% of blacks and 33% of whites. Adjusting for demographics, the black:white OR (95% CI) was 1.51, which was reduced to 1.46, a 9.3% reduction (95% CI 5.4%, 13.2%) by CRP (Table). In models including exercise, waist circumference, BMI, and depressive symptoms, the percent mediation by CRP was 3.7% (1.0%, 6.4%). Similar patterns were seen for models incorporating socioeconomic factors and medication use. After adding Southern diet pattern and dietary Na/K ratio, CRP no longer attenuated the association (1.3% mediation; -1.5, 4.1). Conclusions: CRP significantly attenuated the black-white difference in incident hypertension; however, once dietary factors were accounted for, CRP had no impact on the black:white difference in incident hypertension. Thus, inflammation as measured by CRP, may be part of the reason that dietary factors influence the black:white disparity in incident hypertension.

Disparities in hypertension and cardiovascular disease in blacks: The critical role of medication adherence.

Blacks are two to three times as likely as whites to die of preventable heart disease and stroke. Declines in mortality from heart disease have not eliminated racial disparities. Control and effective treatment of hypertension, a leading cause of cardiovascular disease, among blacks is less than in whites and remains a challenge. One of the driving forces behind this racial/ethnic disparity is medication nonadherence whose cause is embedded in social determinants. Eight practical approaches to addressing medication adherence with the potential to attenuate disparities were identified and include: (1) patient engagement strategies, (2) consumer-directed health care, (3) patient portals, (4) smart apps and text messages, (5) digital pillboxes, (6) pharmacist-led engagement, (7) cardiac rehabilitation, and (8) cognitive-based behavior. However, while data suggest that these strategies may improve medication adherence, the effect on ameliorating racial/ethnic disparities is not certain. This review describes the relationship between disparities and medication adherence, which likely plays a role in persistent disparities in cardiovascular morbidity and mortality.

Cardiovascular Health and Incident Hypertension in Blacks: JHS (The Jackson Heart Study).

Several modifiable health behaviors and health factors that comprise the Life's Simple 7-a cardiovascular health metric-have been associated with hypertension risk. We determined the association between cardiovascular health and incident hypertension in JHS (the Jackson Heart Study)-a cohort of blacks. We analyzed participants without hypertension or cardiovascular disease at baseline (2000-2004) who attended ≥1 follow-up visit in 2005 to 2008 or 2009 to 2012 (n=1878). Body mass index, physical activity, diet, cigarette smoking, blood pressure (BP), total cholesterol, and fasting glucose were assessed at baseline and categorized as ideal, intermediate, or poor using the American Heart Association's Life's Simple 7 definitions. Incident hypertension was defined at the first visit wherein a participant had systolic BP ≥140 mm Hg, diastolic BP ≥90 mm Hg, or self-reported taking antihypertensive medication. The percentage of participants with ≤1, 2, 3, 4, 5, and 6 ideal Life's Simple 7 components was 6.5%, 22.4%, 34.4%, 25.2%, 10.0%, and 1.4%, respectively. No participants had 7 ideal components. During follow-up (median, 8.0 years), 944 (50.3%) participants developed hypertension, including 81.3% with ≤1 and 11.1% with 6 ideal components. The multivariable-adjusted hazard ratios (95% confidence interval) for incident hypertension comparing participants with 2, 3, 4, 5, and 6 versus ≤1 ideal component were 0.80 (0.61-1.03), 0.58 (0.45-0.74), 0.30 (0.23-0.40), 0.26 (0.18-0.37), and 0.10 (0.03-0.31), respectively (Ptrend <0.001). This association was present among participants with baseline systolic BP <120 mm Hg and diastolic BP <80 mm Hg and separately systolic BP 120 to 139 mm Hg or diastolic BP 80 to 89 mm Hg. Blacks with better cardiovascular health have lower hypertension risk.

Chronic defensiveness and neuroendocrine dysfunction reflect a novel cardiac troponin T cut point: The SABPA study

BackgroundSympatho-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. MethodsA prospective bi-ethnic cohort, excluding atrial fibrillation, myocardial infarction and stroke cases, was followed for 3 years (N=342; 45.6±9.0years). We obtained serum high-sensitive cTnT and exposure measures [Coping-Strategy-Indicator, depression/Patient-Health-Questionnarie-9, 24h BP, 24h heart-rate-variability (HRV) and 24h urinary catecholamines]. ResultsBlacks showed moderate depression (45% vs. 16%) and 24h hypertension (67% vs. 42%) prevalence compared to Whites. A receiver-operating-characteristics cTnT cut-point 4.2ng/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]; 24h 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 3year 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 5.6ng/L cTnT predicting hypertension was not associated with exposure measures. ConclusionCentral 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 4.2ng/L cTnT cut-point in Blacks.

The protective role of oestradiol against silent myocardial ischemia and hypertension risk in South African men: The SABPA study

BackgroundOestradiol has a protective effect on coronary artery health in women but the effect it has on men, is controversial. A translational approach was followed to assess whether sex hormone levels are associated with silent myocardial ischemia (SMI) and hypertension risk over a 3year period. MethodsParticipants included 89 Black and 91 White men (aged 21–63years) participating in both phases of the Sympathetic activity and Ambulatory Blood Pressure in Africans prospective study. Fasting blood samples, ambulatory blood pressure and 2-lead ECG recordings were obtained. ResultsNo difference in the levels of the various baseline serum T fractions between the two ethnic groups occurred. Oestradiol of the Black men increased by 54.2% compared to a decrease of 24.1% in the White men. Changes in total oestradiol (adjusted R2=0.33, β=−0.31, p=0.023) and free oestradiol (adjusted R2=0.34, β=−0.33, p=0.019) were inversely associated with changes in SMI in the Black men but not in White men. Baseline serum nitric oxide metabolites were inversely associated with ΔSMI in the Blacks only (adjusted R2=0.33, β=−0.28, p=0.047). Chronic SMI was associated with 24h hypertension in Blacks [cut point 1.5 events: Area under the curve 0.71 (95% CI: 0.60, 0.82); p=0.006; with sensitivity/specificity 44%/94%]. ConclusionsChronic SMI events facilitated future ischemic heart disease in Black men. Up-regulated free oestradiol seems to be involved in the protection of the heart against SMI and hypertension risk in Black but not in White men. A similar protective role for testosterone could however not be shown.

Hypokalemic Metabolic Alkalosis and Hypertension in Blacks

Hypokalemic Metabolic Alkalosis and Hypertension in Blacks

Hypertension in Blacks: Unanswered Questions and Future Directions for the JHS (Jackson Heart Study).

This report resulted from a working group assembled by the JHS (Jackson Heart Study) coordinating center as part of a symposium to identify, discuss, and refine key questions, related to hypertension in blacks, that can be addressed in the National Heart, Lung and Blood Institute (NHLBI)–sponsored study. The symposium and working group were assembled to assist in the preparation for the next phase of the JHS. The JHS is a longitudinal observational study designed to identify cardiovascular disease (CVD) risk factors among blacks and to develop the infrastructure for training the next generation of health disparities researchers.1 Between 2000 and 2004, 5306 community-dwelling blacks, aged ≥21 years, were enrolled from the tricounty area of Jackson, MS. In addition to a baseline study visit, follow-up visits were conducted in 2005 to 2008 and 2009 to 2013. JHS participants are contacted annually by telephone to identify potential CVD events that are adjudicated by trained clinicians.2 Hypertension is more common in blacks than any other race/ethnic group in the United States.3 In addition, blacks have a higher incidence of hypertension-related CVD and end-stage renal disease than other race/ethnic groups in the United States.4,5 The hypertension working group thought broadly about essential research questions related to hypertension in blacks. We considered research questions that could be addressed through continued observational follow-up of the JHS cohort or by conducting interventions among JHS participants. The working group benefited from reviewing the NHLBI Strategic Vision and a recently published report from an NHLBI working group addressing research needs to improve hypertension treatment and control in blacks.6,7 Also, this report builds on the published work in the area of hypertension from the JHS (Table 1). Some of the suggestions from the working group require new study visits and are …

Abstract MP019: Contributors to the Black-White Disparities in Incident Hypertension

Introduction: While predictors of incident hypertension are well-studied, the factors explaining the black-white (B/W) disparity in the incidence of hypertension are unknown. Absent interactions, for a factor to contribute to this racial disparity, it must both : 1) have a large B/W difference in prevalence, and 2) be strongly associated with the risk of incident hypertension. Methods: We selected 20 established risk factors for hypertension to assess the degree to which they contribute to the black excess risk of incident hypertension. The B/W difference in hypertension risk factors was assessed by the standardized difference score (SDS: # standard errors difference in the B/W means) adjusting for age group. The impact of risk factors on incident hypertension was assessed by logistic regression adjusting for age group and baseline SBP. The mediation by each risk factor was calculated as the percent change in the regression coefficient for black race with additional adjustment for each risk factor. Results: Over a 10-year follow-up, 45% of 619 black and 36% of 2204 white men, and 52% of 994 black and 34% of 2409 white women, developed hypertension. The B/W difference in the mean southern diet score (assessed by a food frequency survey) was large for men (SDS =19.3) and women (SDS = 21.8). The diet score was also strongly associated with incident hypertension for men (OR = 1.17; 95% CI: 1.07-1.30) and women (OR = 1.18; 95% CI: 1.06-1.30). As such, the diet score was the most powerful mediator of the B/W difference in incident hypertension, accounting for 52% (95% CI: 19%-84%) of the black excess risk in men and 26% (95%CI: 10%-42%) in women. For women, BMI was the 2 nd most powerful mediator, accounting for 17% (95% CI: 6% - 15%) of the excess black risk of hypertension (SDS = 9.5; OR = 1.04; 95% CI: 1.03-1.06); however, because BMI was similar in black and white men (SDS = 1.4) it did not significantly mediate the risk in men (p = 0.63). Low education was the 2 nd most powerful mediator for men (14%: 95% CI: 3%-25%), but played a smaller role in women (4% mediation; 95% CI: 2% - 7%) because of a smaller B/W difference of the prevalence of low education in women (SDS = 1.4). The dietary sodium/potassium ratio (11%) was also a mediator in men; while in women (in decreasing order of mediation) low mobility (15%), low DASH diet score (11%), low income (10%), low neighborhood quality (8%), dietary sodium/potassium ratio (5%), low physical activity (5%) and low education (4%) also contributed to the excess black risk of incident hypertension. Other factors including exercise and discrimination did not significantly mediate the excess risk of hypertension in blacks. Conclusions: This report provides insights to the contributors of the higher incidence of hypertension in blacks, with a high consumption of southern foods being the most powerful contributor to black disparity in incidence of hypertension for both men and women.

Hypertension in blacks: insights from Africa.

Although the consequences of hypertension are universal, blacks (African-Americans or indigenous Africans) have been the subject of a differential approach to causation, outcome, and treatment. Blacks have a greater propensity to salt sensitivity and suppressed plasma renin suggesting a predisposition to sodium retention. Target organ damage is more frequent and blood pressure is more difficult to control. We explore potential underlying causes, both genetic and environmental, particularly in the South African population, and propose a more physiological approach to the treatment of resistant hypertension in blacks.

High Frequency of Variants of Candidate Genes in Black Africans with Low Renin-Resistant Hypertension.

Black subjects tend to retain salt and water, be more sensitive to aldosterone, and have suppression of plasma renin activity. Variants of the renal sodium channel (ENaC, SCNN1B) account for approximately 6% of resistant hypertension (RHT) in Blacks; other candidate genes may be important. Six candidate genes associated with low renin-resistant hypertension were sequenced in Black Africans from clinics in Kenya and South Africa. CYP11B2 was sequenced if the aldosterone level was high (primary aldosteronism phenotype); SCNN1B, NEDD4L, GRK4, UMOD, and NPPA genes were sequenced if the aldosterone level was low (Liddle phenotype). There were 14 nonsynonymous variants (NSVs) of CYP11B2: 3 previously described and associated with alterations in aldosterone synthase production (R87G, V386A, and G435S). Out of 14, 9 variants were found in all 9 patients sequenced. There were 4 NSV of GRK4 (R65L, A116T, A142V, V486A): at least one was found in all 9 patients; 3 were previously described and associated with hypertension. There were 3 NSV of SCNN1B (R206Q, G442V, and R563Q); 2 previously described and 1 associated with hypertension. NPPA was found to have 1 NSV (V32M), not previously described and NEDD4L did not have any variants. UMOD had 3 NSV: D25G, L180V, and T585I. A phenotypic approach to investigating the genetic architecture of RHT uncovered a surprisingly high yield of variants in candidate genes. These preliminary findings suggest that this novel approach may assist in understanding the genetic architecture of RHT in Blacks and explain their two fold risk of stroke.

Neighborhood Socioeconomic Disadvantage; Neighborhood Racial Composition; and Hypertension Stage, Awareness, and Treatment Among Hypertensive Black Men in New York City: Does Nativity Matter?

Neighborhood-level poverty and racial composition may contribute to racial disparities in hypertension outcomes. Little is known about how the effects of neighborhood social environments may differ by nativity status among diverse urban Black adults. We aimed to characterize the influence of neighborhood-level socio-demographic factors on hypertension outcomes among US- and foreign-born Black men with uncontrolled blood pressure. We conducted a cross-sectional analysis of baseline data from two large community-based trials of hypertensive Black men aged 50 and over linked with census tract data from the 2012 American Community Survey 5-year estimates. We defined census tracts with high racial segregation as those where 60% or more self-identified as Black and high-poverty census tracts as those where 20% or more lived below the poverty line. Multivariable general estimating equation models were used to measure associations between neighborhood characteristics and stage of hypertension, hypertension awareness, and treatment to yield adjusted prevalence ratios (aPR). Models were run separately for US- and foreign-born Black men. Over 64% of the 1139 participants lived in a census tract with a high percentage of Black residents and over 71% lived in high-poverty census tracts. Foreign-born Black men living in neighborhoods with a high concentration of Black residents were less likely to be treated for their high blood pressure (aPR 0.44, 95% CI 0.22-0.88), but this result did not hold for US-born Black men. There were no significant associations between neighborhood poverty and hypertension outcomes. Neighborhood context may impact treatment for hypertension, one of the most important factors in hypertension control and decreasing hypertension-related mortality, particularly among foreign-born Black men.

Cystatin C Based Evaluation of Renal Function in Hypertensive Patients in Ubth, Benin City

Background: Hypertension is a recognized cause of chronic kidney disease. Hypertension in blacks is most important because it is volume dependent and its ensuing renal complication. The widely accepted marker to assess renal function is creatinine and its estimated glomerular filtration rate. However, this is limited in assessing early renal impairment. This necessitate a need to evaluate other renal markers such as cystatin C. Objective: To measure and compare serum cystatin C and creatinine for early renal impairment among hypertensive patients on treatment. Methodology: A total of 48 hypertensive patients attending cardiology clinic for follow up were recruited in this study. Serum specimen were collected and assayed for creatinine and cystatin C. estimated glomerular filtration (eGFR) rate was calculated for the analytes. The two eGFR were compared in assessing renal function. Results: The BMI, Blood pressure and Abdominal circumference of the subjects were significantly higher than the controls (31.5±7.5kg/m 2 , 144/82mmHg and 102.3cm vs 26.1±4.3kg/m 2 , 116/80mmHg and 93cm) respectively Table 1. The hypertensives had a significantly higher serum levels of creatinine and cystatin C when compared with the controls (105µmol/L vs 88µmol/L and 2.9mg/L vs 1.1mg/L) respectively Table 2. Calculated estimated GFR for both serum creatinine and cystatin C were significantly lower among the subjects (89.1ml/min/1.73m 2 vs 110ml/min/1.73m 2 and 67.7ml/min/1.73m 2 vs 118ml/min/1.73m 2 ). Estimated GFR based on cystatin C was significantly lower than eGFR-Cr among the subjects (67.7ml/min/1.73m 2 vs 89.1ml/min/1.73m 2 ). There was a significant correlation between BMI and eGFR-Cr, abdominal circumference also had a significant correlation with fasting plasma glucose among the subjects and controls. Conclusion: serum levels of cystatin C appears to be a better predictor of GFR among hypertensive patients.

What Is the Significance of Masked Hypertension Versus Incident Hypertension in Blacks?

See related article, pp 220–226 Treatment-naive masked hypertension has been defined as discordant in-office normotension (<140/<90 mm Hg) versus out-of-office hypertension (≥135/85 mm Hg) for either home blood pressure (BP) monitoring (HBPM) or ambulatory BP monitoring (ABPM) of daytime ABPM (≥135/85 mm Hg), night-time ABPM (≥120/70 mm Hg), 24-hour ABPM (≥130/80 mm Hg), or a combination of these out-of-office BP subtypes. Masked hypertension may be a precursor of sustained hypertension, remain masked hypertension for a prolonged period of time, and occasionally revert to normotension.1 However, there are at least 5 other aspects of masked hypertension of clinical importance: (1) it has been considered an intermediate phenotype between sustained normotension and sustained hypertension, which most frequently arises from antecedent high-normal BP (130–139/85–89 mm Hg), less frequently from antecedent normal BP (120–129/80–84 mm Hg); and least frequently from antecedent optimal BP (<120/<80 mm Hg)1 (note that normal and high-normal BP when combined are called prehypertension); (2) it frequently is associated with hypertensive target organ damage even without progressing to hypertension, perhaps because of increased pressure burden in daily life, and despite a long-dormant period before transitioning to sustained hypertension1; (3) it has been associated with many cardiometabolic abnormalities, including obesity, metabolic syndrome, diabetes mellitus, obstructive sleep apnea, and chronic renal disease1; (4) it frequently has been associated with nocturnal hypertension and impaired nocturnal dipping of BP—a particularly high-risk phenotype2; and (5) there is an especially high prevalence of masked hypertension in people of African descent, approaching 30% to 50% in some series.3–6 It is with this background that the present investigators used ABPM to define …