Hypertension In Blacks Research Articles

Microalbuminuria in White and Black Hypertensive Nondiabetic Brazilian Patients

Microalbuminuria (MAU) is a predictor of cardiovascular mortality in patients with diabetes mellitus (DM) and hypertension (HTN) and also in an unselected population. The American Diabetes Association (ADA) and the National Kidney Foundation (NKF) define MAU as an albumin/creatinine ratio (ACR) between 30 and 300 μg/mg in both men and women. Aim: To evaluate the possible relationship among MAU, HTN and gender and ethnicity in Brazilian nondiabetic primary hypertensive patients. Design: Population-based study. Participants: Ninety-eight men and women, seventy-two black and twenty-six white nondiabetic primary hypertensive patients aged 20 years or older were selected. Forty healthy individuals, paired according to age, gender, and ethnics were used as controls. Methods: Early-morning midstream urine was used. Urinary albumin was spectrophotometrically measured with Coomassie Brillant Blue G-250. Creatinine was determined by a method based on Jaffe’s reaction. ACR (μg albumin/mg creatinine) was calculated. Data are expressed as medians. Results: ACR level was significantly higher in 98 hypertensive patients (38.00) than in 40 control individuals (23.00) (P < 0.001). ACR level was significantly higher in 48 hypertensive male (46.00) than in 50 hypertensive female (34.00) (P = 0.008). No significant effect of ethnicity on ACR levels between 26 hypertensive Whites (35.50) and 72 hypertensive Blacks (38.00) was observed (P = 0.978). Conclusions: The ACR level, significantly higher in hypertensive patients than in control individuals, supports data from the literature. To our knowledge, this is the first study demonstrating that the ACR level is significantly higher in men than in women. The lack of an ethnicity effect supports what was already asserted, namely, that in Brazil, at an individual level, color, as determined by physical evaluation, is a poor predictor of genomic African ancestry, as estimated by molecular markers.

Clinical Implications

Clinical Implications

Analysis of Recent Papers in Hypertension Initial Combination Therapy Provides More Prompt Blood Pressure Control and Reduces Cardiovascular Events But Remains Underutilized

Analysis of Recent Papers in Hypertension Initial Combination Therapy Provides More Prompt Blood Pressure Control and Reduces Cardiovascular Events But Remains Underutilized

A Consideration of Genetic Mechanisms Behind the Development of Hypertension in Blacks

Hypertension is a more serious disease in blacks. The determinants of the blood pressure (BP) may be uniquely different from those in whites. The characteristic low-renin, salt-sensitive hypertension of blacks is consistent with the kidney reabsorbing additional sodium (Na), which leads to an expanded plasma volume that drives the BP. Mechanisms considered are genetically based. These include: (1) the intra-renal renin-angiotensin system (RAS), one based on molecular variations in angiotensinogen; (2) the Na, K, 2Cl cotransporter (NKCC2) and its regulators in the thick ascending limb, which are associated with a variety of phenotypes consistent with a more active cotransporter in blacks; and (3) the genes for MYH9 and APOL 1, which have been associated with kidney disease in blacks. To achieve a state of hypertension, an increase in Na uptake in proximal nephron regions may require a distal nephron that does not fully adjust due to less than adequate suppression of aldosterone production.

Efficacy/Safety of a Fixed‐Dose Amlodipine/Olmesartan Medoxomil–Based Treatment Regimen in Hypertensive Blacks and Non‐Blacks With Uncontrolled BP on Prior Antihypertensive Monotherapy

In this secondary analysis of a dose-titration study of patients with hypertension uncontrolled on prior monotherapy, blacks (n=234) and non-blacks (n=765) were switched to amlodipine (AML)/olmesartan medoxomil (OM) 5/20mg, with uptitration every 4weeks to AML/OM 5/40mg and then AML/OM 10/40mg to achieve a seated cuff blood pressure (SeBP) of <120/70mmHg. Hydrochlorothiazide 12.5 and 25mg could be added if SeBP was ≥125/75mmHg. The cumulative proportions of patients achieving systolic SeBP <140mmHg (<130mmHg if diabetic) at 12weeks were 71.6% for blacks and 77.2% for non-blacks. Mean SeBP change from baseline in blacks (mean baseline BP: 153.0/93.7mmHg) ranged from -11.7/-6.1mmHg for AML/OM 5/20mg to -23.6/-12.9mmHg for AML/OM 10/40mg +hydrochlorothiazide 25mg (all P<.0001). Antihypertensive efficacy was maintained throughout the 24-hour dosing interval. An AML/OM-based regimen was effective in blacks with hypertension uncontrolled on prior monotherapy.

Racial differences in the impact of elevated systolic blood pressure on stroke risk.

Between the ages 45 and 65 years, incident stroke is 2 to 3 times more common in blacks than in whites, a difference not explained by traditional stroke risk factors. Stroke risk was assessed in 27 748 black and white participants recruited between 2003 and 2007, who were followed up through 2011, in the REasons for Geographic And Racial Differences in Stroke (REGARDS) study. Racial differences in the impact of systolic blood pressure (SBP) was assessed using proportional hazards models. Racial differences in stroke risk were assessed in strata defined by age (<65 years, 65-74 years, and ≥75 years) and SBP (<120 mm Hg, 120-139 mm Hg, and 140-159 mm Hg). Over 4.5 years of follow-up, 715 incident strokes occurred. A 10-mm Hg difference in SBP was associated with an 8% (95% CI, 0%-16%) increase in stroke risk for whites, but a 24% (95% CI, 14%-35%) increase for blacks (P value for interaction, .02). For participants aged 45 to 64 years (where disparities are greatest), the black to white hazard ratio was 0.87 (95% CI, 0.48-1.57) for normotensive participants, 1.38 (95% CI, 0.94-2.02) for those with prehypertension, and 2.38 (95% CI, 1.19-4.72) for those with stage 1 hypertension. These findings suggest racial differences in the impact of elevated blood pressure on stroke risk. When these racial differences are coupled with the previously documented higher prevalence of hypertension and poorer control of hypertension in blacks, they may account for much of the racial disparity in stroke risk.

Response to "Is High Prorenin Level Related to Relative Aldosterone Excess?"

To the Editor: We would like to thank Dr. Satoh and colleagues for their interest in our recent study titled “Plasma Levels of Prorenin and Renin in Black and Whites: Their Relative Abundance and Associations with Plasma Aldosterone Concentration.”1 We reported that blacks and whites had similar plasma prorenin levels, but that in blacks the plasma renin concentration (PRC) was markedly lower, and prorenin was negatively associated with plasma aldosterone concentration (PAC). In their Letter to the Editor, Dr. Satoh suggested we should further examine the association between prorenin and aldosterone to plasma renin activity ratio (aldosterone/renin ratio, or ARR), for indication that prorenin might have played a role in the relative excess of aldosterone, especially in blacks, who are thought to be more susceptible to a salt-sensitive form of hypertension. We appreciate this suggestion and agree that this is a logical and potentially important question that should be addressed in a follow-up analysis. We reexamined the data as requested. The relationships between prorenin and ARR are presented in Figure 1. Contrary to the letter’s hypothesis, we found prorenin to be negatively associated with ARR in blacks (β = –0.341; P = 0.039), and not associated with ARR in whites (β = 0.180; P = 0.301). Of note, these results essentially mirrored our previous reports on the prorenin-PAC relationships in the two race groups. Careful examination of Figure 1c and Figure 1d of the original report revealed that at any given level of PRC, prorenin was negatively associated with PAC in blacks, and positively associated with PAC in whites. The new analysis reaffirmed this observation. Figure 1. Relationship between plasma prorenin concentration and plasma aldosterone to renin activity ratio in blacks and whites. Abbreviations: PAC, plasma aldosterone concentration; PRA, plasma renin activity. We agree with Dr. Satoh and colleagues that ARR is a useful gauge for salt sensitivity, characterized by inappropriate aldosterone production and unattenuated sodium reabsorption in the presence of volume overload. Previous reports have demonstrated that ARR is higher in hypertensive blacks than in hypertensive whites.2 Our data, showing that ARR levels were marginally higher in young and normotensive blacks (Table 2 of the original paper), suggest that this difference may already be present before hypertension occurs. The new analysis, however, yielded no clear evidence for a prorenin role in aldosterone production, neither in blacks nor whites. In fact, the negative prorenin-ARR association in blacks argues against the hypothesis that prorenin promotes aldosterone production, at least in young and healthy blacks. As we have commented in the original article, this does not exclude the possibility that in some circumstances aldosterone production may become more autonomous to kidney-derived renin; when upregulated (pro)renin receptor (PRR) expression leads to a prorenin-dependent generation of angiotensin II, it is conceivable that aldosterone excess may occur with increased prorenin levels. Although the plausibility of such a hypothesis is supported by the observations that aldosterone elevation is associated with the PRR overexpression in transgenic rats and PRR gene polymorphisms in white males,3,4 the validity of the hypothesis in salt-sensitive blacks remains to be investigated.

Definition and Prevalence of Salt Sensitivity and Salt-sensitive Hypertension

High salt intake is associated with significantly increased risk of stroke and total cardiovascular disease. Reduction in habitual dietary salt intake of 6 g/day decreases systolic and diastolic BP, but not in all hypertensive subjects. Salt sensitivity is defined as the tendency for BP to fall during dietary salt restriction and rise during salt supplementation. Salt sensitivity is diagnosed by a low and high salt diet protocol or a rapid sodium, volume expansion and contraction protocol. Prevalence of salt sensitivity ranged from 30 to 60% in hypertensive subjects and from 15 to 46% in normotensive subjects. Salt sensitivity is more frequently found in hypertensive subjects, blacks, aged people, and women.

Salt-Sensitive Hypertension and Cardiac Hypertrophy in Transgenic Mice Expressing a Corin Variant Identified in Blacks

Blacks represent a high-risk population for salt-sensitive hypertension and heart disease, but the underlying mechanism remains unclear. Corin is a cardiac protease that regulates blood pressure by activating natriuretic peptides. A corin gene variant (T555I/Q568P) was identified in blacks with hypertension and cardiac hypertrophy. In this study, we tested the hypothesis that the corin variant contributes to the hypertensive and cardiac hypertrophic phenotype in vivo. Transgenic mice were generated to express wild-type (WT) or T555I/Q568P variant corin in the heart under the control of α-myosin heavy chain promoter. The mice were crossed into a corin knockout (KO) background to create KO/TgWT and KO/TgV mice that expressed WT or variant corin, respectively, in the heart. Functional studies showed that KO/TgV mice had significantly higher levels of proatrial natriuretic peptide in the heart compared with that in control KO/TgWT mice, indicating that the corin variant was defective in processing natriuretic peptides in vivo. By radiotelemetry, corin KO/TgV mice were found to have hypertension that was sensitive to dietary salt loading. The mice also developed cardiac hypertrophy at 12 to 14 months of age when fed a normal salt diet or at a younger age when fed a high-salt diet. The phenotype of salt-sensitive hypertension and cardiac hypertrophy in KO/TgV mice closely resembles the pathological findings in blacks who carry the corin variant. The results indicate that corin defects may represent an important mechanism in salt-sensitive hypertension and cardiac hypertrophy in blacks.

Factors Associated With Medication Adherence in Hypertensive Blacks

Rates of medication adherence are low among hypertensive blacks despite numerous interventions to increase their adherence. The aim of the study was to conduct a systematic review of the literature to understand the factors associated with medication adherence in hypertensive blacks. A systematic computer search of qualitative and quantitative studies that examined factors associated with medication adherence in hypertensive blacks from 1966 to 2010 was performed. Studies were excluded if medication adherence was not either the primary or secondary outcome variable. Studies (n = 18) were cross-sectional or qualitative, measured adherence via self-report, and conducted in low-income blacks. Factors that were associated with medication adherence were self-efficacy, depression, patient-provider communication, and healthcare system related. Findings from existing studies should be interpreted with caution because of their methodological limitations. Longitudinal studies with heterogeneous samples of hypertensive blacks are imperative so that targeted interventions can be developed for this vulnerable population. Even though there are methodological limitations associated with existing studies, clinicians may want to consider some of the factors that were associated with medication adherence in this systematic review as they provide care for hypertensive blacks. Given that self-efficacy and patient-provider communication are modifiable factors, they can be the focus of interventions to increase medication adherence. Finally, clinicians may want to screen their hypertensive patients for depression and treat, if necessary.

Hypertension in the US Black Population: Risk Factors, Complications, and Potential Impact of Central Aortic Pressure on Effective Treatment

The identification of specific factors that contribute to hypertension development and progression among blacks in the US is the focus of much ongoing research. The purpose of this paper is to review these factors and discuss how they present unique opportunities for improving the management of hypertension in this difficult-to-treat population. We searched the published literature for articles discussing the risk factors for hypertension and cardiovascular disease in blacks; the target-organ damage and cardiovascular complications associated with hypertension in this difficult-to-treat population; and the role of central blood pressure in predicting cardiovascular events. The prevalence of hypertension is higher in blacks than in other race/ethnic groups, with environmental and genetic risk factors likely playing an important role. The cardiovascular and renal consequences of hypertension (eg, left ventricular hypertrophy and renal failure) are also greater in blacks relative to their white counterparts. Preliminary data suggest that central blood pressure may be higher in blacks than in whites and has the potential for greater prognostic capability relative to peripheral blood pressure. There is an urgent need to successfully control hypertension in the black population. Although data are limited in blacks, evidence suggests that central blood pressure warrants more continued assessment in future clinical studies.

Rotating night shift work and disparate hypertension risk in African-Americans.

Hypertension disproportionally affects black compared with white Americans, even after accounting for known risk factors. Circadian disruption as encountered by rotating night shift workers has been associated with an increased risk for hypertension. Because blood pressure responds differently to sleep alterations in blacks compared with whites, we hypothesized that rotating night shift work may be a stronger risk factor for hypertension among blacks. We prospectively examined the association between rotating night shift work and the risk of hypertension in 1510 black and 94 142 white female participants of the Nurses' Health Study II who were nonhypertensive at baseline in 1991. We used Cox proportional hazards models to control for potential confounders. During 16 years of follow-up (1991-2007), we identified 580 incident cases of hypertension in blacks and 23 360 cases in whites. In blacks, the multivariable hazard ratio for incident hypertension among women who worked rotating night shift for more than 12 months in the previous 2 years was 1.81 [95% confidence interval (CI) 1.14-2.87], compared with those working none. By contrast, in whites, we observed no increase in risk (hazard ratio 0.99, 95% CI 0.93-1.06). The association between shift work and hypertension varied significantly by race (P interaction = 0.01). In secondary analyses, the multivariable hazard ratio for incident hypertension in black women who ever performed rotating night shift work was 1.46 (95% CI 1.07-1.99), compared with those never working rotating night shifts. In whites, there was no increase in risk (hazard ratio 0.97, 95% CI 0.93-1.01) (P interaction < 0.01). Rotating night shift work is independently associated with an increased risk of hypertension in blacks but not in whites.

Unraveling the Mechanism of Renin-Angiotensin- Aldosterone System Activation and Target Organ Damage in Hypertensive Blacks

See related article, pp 62–69 The International Society on Hypertension in Blacks consensus statement in 2010 noted that, in the setting of high dietary sodium intake, hypertensive blacks have particularly impressive responses to renin-angiotensin-aldosterone system (RAAS) blockade.1 The statement went on to point out that the excessive target-organ damage (TOD) in hypertensive blacks can be attributed to RAAS activation. Although a normal-to-“high-renin” hypertensive state is most prevalent, the classic hypertension literature has categorized blacks as typically having a “low-renin” state.2 There is somewhat of a paradox in the observation that blacks, despite having a low-renin state, have high serum aldosterone concentrations.3 Blacks experience disproportionately higher rates of hypertension-related TOD compared with whites.4 The mediators of the higher rates of TOD noted in blacks are most likely directly attributed to high levels of downstream mediators of the RAAS, such as aldosterone and angiotensin II. The mechanism by which a low-renin state can be associated with such an apparently active RAAS is not clearly defined. The article by Michel et al,5 in this issue of Hypertension , addresses the mechanism by which RAAS activation affects blood pressure (BP) …

Prevalence and Significance of Sickle Cell Trait in Nigerian Patients with Essential Hypertension

Dr Sagir G. Ahmed, Department of Haematology Aminu Kano Teaching Hospital PMB 3452, Kano Kano State, Nigeria. +2348034418015 drsagirahmed@yahoo.com Abstract lifestyle and nutritional culture of the Africans are Global epidemiology shows that hypertension becoming increasingly westernized over time and is severer, commoner and occurs at relatively younger might be partly responsible for rising incidence of nonage in the black Africans in comparison to the whites. communicable diseases, including hypertension, in Since sickle cell trait (SCT) was associated with Africa. This is consistent with the finding of higher hyperviscosity, we hypothesize that SCT is a possible prevalence of hypertension in urban populations in 1 risk factor for hypertension in blacks and it might be Nigeria . Moreover, the prevalence of adult partly responsible for the high prevalence and severity hypertension appears to be rising as previous studies of hypertension in blacks. Hence, we studied reported prevalence rates of about 12% in 1992, 20% in 1, 2, 3 haematological parameters and prevalence of SCT in 1999 and up to 36% in a more recent study in 2008 . hypertensive patients and evaluated the impact of SCT Global epidemiology had shown that hypertension is on response to anti-hypertensive therapy as seen in severer, commoner and occurs at relatively younger 4, 5, Aminu Kano Teaching Hospital, Nigeria. age in the black Africans than in the white Europeans 6 The hypertensive patients had WBC and . 9 9 platelet counts of 5.8 x10 /L and 225 x10 /L that did not Individuals with sickle cell trait (SCT) have significantly differ from the corresponding values of red cells with Hb AS genotype that contain about 40% 9 9 7 6.2 x10 /L and 235 x10 /L seen among the HbS and 60% HbA . The abundance of HbA prevents 7 normotensive controls (p>0.05), but the hypertensive sickling under physiological conditions . The patients had a haematocrit of 0.37L/L that was frequency of SCT is up to 20-25% in West Africa significantly lower than the value of 0.44L/L seen including Nigeria, and the frequency has reached among the normotensive controls (p 0.05). Hypertensive patients with SCT had black Africans with normal Hb AA genotype . mean systolic and diastolic pressures of 158 and 95 Haemorheological studies had revealed that systemic mm Hg that were significantly higher than the arterial blood pressure is generally influenced by corresponding values of 145 and 86 mm Hg seen in vascular peripheral resistance, which is in turn affected 12, 13 patients with Hb AA genotype (p<0.05). These by blood viscosity . We therefore hypothesize that results suggest that SCT was not a risk factor for SCT genotype is a possible risk factor for essential hypertension but it was associated with poor hypertension in blacks and it might be partly response to anti-hypertensive therapy in affected responsible for the high prevalence and severity of patients. Hence hypertensive patients with SCT hypertension in the black race. If our hypothesis is need closer monitoring during therapy. correct, we predicted that: 1 The prevalence of SCT among black patients

Relation of obesity to circulating B-type natriuretic peptide concentrations in blacks: the Jackson Heart Study.

Lower plasma B-type natriuretic peptide (BNP) concentrations in obese individuals ("natriuretic handicap") may play a role in the pathogenesis of obesity-related hypertension. Whether this phenomenon may contribute to hypertension in blacks is unknown. We tested the hypothesis that body mass index is inversely related to BNP concentrations in blacks. We examined the relation of plasma BNP to body mass index in 3742 Jackson Heart Study participants (mean age, 55 ± 13; 62% women) without heart failure using multivariable linear and logistic regression, adjusting for clinical and echocardiographic covariates. The multivariable-adjusted mean BNP was higher for lean participants compared with obese participants in both normotensive (P<0.0001) and hypertensive (P<0.0012) groups. In sex-specific analyses, the adjusted mean BNP was higher in lean hypertensive individuals compared with obese hypertensive individuals for both men (20.5 versus 10.9 pg/mL, respectively; P=0.0009) and women (20.0 versus 13.8 pg/mL; P=0.011). The differences between lean and obese participants were more pronounced in normotensive participants (men, 9.0 versus 4.4 pg/mL; P<0.0001; women, 12.8 versus 8.4 pg/mL; P=0.0005). For both hypertensive and normotensive individuals in the pooled sample, multivariable-adjusted BNP was significantly related to both continuous body mass index (P<0.05 and P<0.0001, respectively) and categorical body mass index (P for trend <0.006 and <0.0001, respectively). Our cross-sectional study of a large community-based sample of blacks demonstrates that higher body mass index is associated with lower circulating BNP concentrations, thereby extending the concept of a natriuretic handicap in obese individuals observed in non-Hispanic whites to this high-risk population.

Trends in Mortality From All Causes and Cardiovascular Disease Among Hypertensive and Nonhypertensive Adults in the United States

Little is known about trends in the mortality rate among people with hypertension in the United States. The objective of the present study was to examine the change in the all-cause mortality rate among people with and without hypertension in the United States and whether any such changes differed by sex or race. Data from 10 852 participants aged 25 to 74 years of the National Health and Nutrition Examination Survey (NHANES) I Epidemiological Follow-Up Study (1971 to 1975) and of 12 420 participants of the NHANES III Linked Mortality Study (1988 to 1994) were used. The mean follow-up times were 17.5 and 14.2 years, respectively. In each cohort, the mortality rate was higher among hypertensive adults than nonhypertensive adults, among hypertensive men than hypertensive women, and among hypertensive blacks than hypertensive whites. Among all hypertensive participants, the age-adjusted mortality rate was 18.8 per 1000 person-years for NHANES I and 14.3 for NHANES III (13.3 and 9.1 per 1000 person-years for nonhypertensive participants, respectively). The reduction among hypertensive men (7.7 per 1000 person-years; 95 confidence interval, 5.2 to 10.2) exceeded that among hypertensive women (1.9 per 1000 person-years; 95 confidence interval, [-0.4 to 4.2]) (P<0.001), and the reduction among hypertensive blacks (5.4 per 1000 person-years; 95 confidence interval, [0.6 to 10.1]) exceeded that among hypertensive whites (4.4 per 1000 person-years; 95 confidence interval, [2.2 to 6.5]) (P=0.707). The mortality rate decreased among hypertensive adults, but the mortality gap between adults with and without hypertension remained relatively constant. Efforts are needed to accelerate the decrease in the mortality rate among hypertensive adults.

Why Do Black Americans Have Higher Prevalence of Hypertension?

See related article, pp 383–389 Studies have consistently reported a higher prevalence of hypertension in blacks than in whites, a main reason for the higher incidence of cardiovascular disease in blacks.1 The long list of putative causes for this higher prevalence suggests that the real reasons are still unknown. Biological differences in the mechanisms of blood pressure control or in the environment and habits of whites and blacks are among the potential causes. The higher prevalence of hypertension in blacks living in the United States instead of Africa2 demonstrates that environmental and behavioral characteristics are the more likely reasons for the higher prevalence in blacks living in the United States. They could act directly or by triggering mechanisms of blood pressure increase that are dormant in blacks living in Africa. Kaplan and Victor3 listed 18 genotypes and intermediate phenotypes that were implicated with an increase of blood pressure in blacks. A higher sensitivity to alcohol could be added to that list.4 Some of these mechanisms, such as a higher renal retention of sodium by blacks, are attractive. The “slavery hypertension hypothesis” states that the higher prevalence of hypertension among blacks could have resulted from an enhanced ability to conserve salt by slaves, protecting them from fatal salt-depletive diseases during the stormy Atlantic passage, such as diarrhea and vomiting.5 This condition would induce hypertension when they and their descendants consumed the much higher sodium content in American compared with African foods. This hypothesis …

Genetic Variation in NCAM1 Contributes to Left Ventricular Wall Thickness in Hypertensive Families

Left ventricular (LV) mass and related phenotypes are heritable, important predictors of cardiovascular disease, particularly in hypertensive individuals. Identify genetic predictors of echocardiographic phenotypes in hypertensive families. A multistage genome-wide association study (GWAS) was conducted in hypertensive-ascertained black families (HyperGEN, stage I; GENOA, stage II); findings were replicated in HyperGEN white families (stage III). Echocardiograms were collected using a common protocol, and participants were genotyped with the Affymetrix Genome-Wide Human SNP 6.0 Array. The following were analyzed using mixed models adjusted for ancestry: in stages I and II, 1258 and 989 blacks, respectively; and in stage III, 1316 whites. Phenotypes included LV mass, LV internal dimension (LVID), wall thicknesses (posterior [PWT] and intraventricular septum [IVST]), and relative wall thickness (RWT). In stage I, 5 single nucleotide polymorphisms (SNPs) had P≤10(-6). In stage II, 1 SNP (rs1436109; NCAM1 intron 1) replicated with the same phenotype (PWT, P=0.025) in addition to RWT (P=0.032). In stage III, rs1436109 was associated with RWT (P=5.47×10(-4)) and LVID (P=1.86×10(-4)). Fisher combined probability value for all stages was RWT=3.80×10(-9), PWT=3.12×10(-7), IVST=8.69×10(-7), LV mass=2.52×10(-3), and LVID=4.80×10(-4). This GWAS conducted in hypertensive families identified a variant in NCAM1 associated with LV wall thickness and RWT. NCAM is upregulated during the remodeling period of hypertrophy to heart failure in Dahl salt-sensitive rats. Our initial screening in hypertensive blacks may have provided the context for this novel locus.

Treating the Black Hypertensive in 2010: Achieve Lower Targets While Awaiting More Definitive Evidence

Treating the Black Hypertensive in 2010: Achieve Lower Targets While Awaiting More Definitive Evidence

Serum Lipids and Lipoproteins Levels and Selected Trace Metals In Newly Diagnosed Hypertensive Nigerians

There have been several reports on the role of macronutrients in the pathogenesis of high blood pressure (HBP), however, reports on the relationship between micronutrients and trace metals are few, especially in blacks. This study aim to determine the serum levels of trace metals and correlate same with serum levels of lipoproteins (an established marker of HBP) in newly diagnosed hypertensives (NDH) A total of 50 NDH subjects (24 males and 26 females) attending Ladoke Akintola University of Technology Teaching Hospital, Osogbo were randomly selected and recruited after obtaining their informed consent. 62 consenting healthy individuals (28 males and 34 females) were recruited from member of staff as controls. Fasting blood samples were collected from subjects and controls using appropriate techniques. Serum Total cholesterol (Tc), triglycerides (TG), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) were estimated using commercially available kit from Randox Laboratory. Trace metals (Selenium(Se), Zinc(Zn), Cobalt(Co) and Copper(Cu)) were analyzed using flame atomic absorption spectrophotometry. Data obtained were analyzed with the aid of SPSS statistical package version 18.0. Serum Tc and LDL-Chol were higher in subjects (5.69 ±1.40 and 3.85±0.94) mmol/l than in controls (4.53±1.30 and 2.56±1.38) mmol/l, p 0.05. Serum Tg were almost similar Preamong subjects and controls 1.40±0.21 vs 1.34±0.67mmol/l, p > 0.05. Reduced levels of Se and Zn were found in NDH (8.55±5.61, 70.44±28.48μg/dl) compared with controls (21.75±7.30, 120.15±25.76μg/dl), p Key words: lipids, lipoproteins, micronutrients, newly diagnosed black hypertensives.