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Introduction: Black populations may be more likely to have primary aldosteronism (PA) due to adrenal hyperplasia or other forms of adrenal hyperactivity, with suppressed renin levels and high levels of aldosterone, which may contribute to the development of hypertension., Methods: This sub-study involved 35 black men matched for age, gender and race, and aged 20-65 years, living in the North West Province of South Africa. RAAS triple-A analysis was carried out with LC-MS/MS quantification. Blood pressure, electrocardiography and other variables were determined with known methods., Results: Hypertensive subjects with higher aldosterone levels showed an increased aldosterone-angiotensin II ratio (AA2 ratio) compared to the hypertensive subjects with low aldosterone levels (10.2 vs 3.0 pmol/l; p = 0.003). The serum potassium concentration was significantly lower in the high-aldosterone group and the serum sodium-potassium ratio was significantly higher compared to the low-aldosterone group (3.9 vs 4.5, p = 0.016, 34.8 vs 31.8, p = 0.032, respectively). Furthermore, aldosterone was positively associated with both left ventricular hypertrophy (Cornell product) (Spearman R = 0.560; p = 0.037) and kidney function [albumin-to-creatinine ratio (ACR) ] (Spearman R = 0.589, p = 0.021) in the hypertensive high-serum aldosterone group., Conclusions: The AA2 ratio, a novel screening test that is currently being validated for PA case detection, was used to identify a PA-like phenotype in black men. Excess aldosterone was associated with endothelial dysfunction and left ventricular hypertrophy, independent of blood pressure.

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., (Copyright © 2018 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.)

Background The endogenous steroidal inhibitor of sodium-potassium-dependent adenosine triphosphate and natriuretic hormone, marinobufagenin, plays a physiological role in ionic homeostasis. Animal models suggest that elevated marinobufagenin adversely associates with cardiac and renal, structural and functional alterations. It remains uncertain whether marinobufagenin relates to the early stages of target organ damage development, especially in young adults without cardiovascular disease. We therefore explored whether elevated 24-hour urinary marinobufagenin excretion was related to indices of subclinical target organ damage in young healthy adults. Design This cross-sectional study included 711 participants from the African-PREDICT study (black 51%, men 42%, 24.8 ± 3.02 years). Methods We assessed cardiac geometry and function by two-dimensional echocardiography and pulse wave Doppler imaging. 24-Hour urinary marinobufagenin and sodium excretion were measured, and the estimated glomerular filtration rate determined. Results Across marinobufagenin excretion quartiles, left ventricular mass ( P < 0.001), end diastolic volume ( P < 0.001), stroke volume ( P = 0.004) and sodium excretion ( P < 0.001) were higher within the fourth compared with the first quartile. Partial regression analyses indicated that left ventricular mass ( r = 0.08, P = 0.043), end diastolic volume ( r = 0.10, P = 0.010) and stroke volume ( r = 0.09, P = 0.022) were positively related to marinobufagenin excretion. In multivariate-adjusted regression analysis, left ventricular mass associated positively with marinobufagenin excretion only in the highest marinobufagenin excretion quartile (adjusted R 2   = 0.20; β = 0.15; P = 0.043). This relationship between left ventricular mass and marinobufagenin excretion was evident in women (adjusted R 2   = 0.06; β = 0.127; P = 0.015) but not in men (adjusted R 2   = 0.06; β = 0.007; P = 0.92). Conclusions Left ventricular mass positively and independently associates with marinobufagenin excretion in young healthy adults with excessively high marinobufagenin excretion. Women may be more sensitive to the effects of marinobufagenin on early structural cardiac changes.

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., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Background: Blood pressure variability ratio (BPVR)(derived from within-subject SD of 24-hour ambulatory blood pressure [BP]) predicts all-cause mortality independent of BP and has a similar prognostic ability to ambulatory arterial stiffness (AASI). Whether BPVR, and AASI, offer prognostic information beyond measurements of arterial stiffness at a given pressure, as indexed by pulse wave velocity (PWV), is not known., Methods: We assessed whether BPVR and AASI were associated with indices of subclinical organ damage (TOD) [estimated glomerular filtration rate (eGFR), left ventricular mass index, early-to-late transmitral velocity (E/A), carotid intima-media thickness (IMT)] independent of BP, and whether BPVR-TOD and AASI-TOD relations were independent of PWV (applanation tonometry) in 772 randomly selected participants from an urban, developing community. AASI was derived from 24-hour diastolic BP vs. systolic BP standard linear regression., Results: On bivariate analyses, BPVR, AASI, and PWV were correlated with all indices of TOD (P < 0.0005). However, after adjustments for potential confounders including age and 24-hour mean BP, BPVR, and PWV (P < 0.005 to P < 0.0001), but not AASI (P > 0.25), were independently associated with eGFR, but not other indices of TOD. Importantly, the BPVR-eGFR relation was independent of BP variability (P < 0.005) and PWV (P < 0.001)., Conclusions: BPVR was negatively associated with eGFR independent of mean BP, BP variability, and PWV. Therefore, in the prediction of cardiovascular risk, measurements of arterial stiffening (BPVR) may provide information beyond the impact of arterial stiffness., (© American Journal of Hypertension, Ltd 2017. All rights reserved. For Permissions, please email: journals.permissions@oup.com)

A decreased aortic-to-brachial pulse pressure (PP) amplification, which is independently associated with cardiovascular outcomes, may index several aortic functional changes. However, that aortic functional change most likely to account for this effect is uncertain. In 706 randomly selected community participants of African ancestry with a mean age of 44.4 ± 18.2 years, we assessed aortic function using radial applanation tonometry and SphygmoCor software (including forward [Pf] and backward [Pb] wave separation analysis assuming a triangular flow waveform) and left ventricular mass index (LVMI) (echocardiography). In multivariate models with the inclusion of brachial PP, 1/PP amplification (partial r = 0.12, P < .005), reflected wave pressures (partial r = 0.09, P < .05), and aortic pulse wave velocity (PWV; partial r = 0.09, P < .05) were independently associated with LVMI. Similarly, in multivariate models with the inclusion of brachial PP, 1/PP amplification (P < .005), the reflected wave pressure (P < .01), and aortic PWV (P < .01) were independently associated with LVH. With adjustments for reflected wave pressures, the brachial PP-independent relationships between 1/PP amplification and LVMI or LVH were abolished (P > .08 for both). However, adjustments for PWV failed to modify brachial PP-independent relations between 1/PP amplification and LVMI or LVH. Similar results were noted when brachial systolic blood pressure rather than PP was included in regression models and in sensitivity analysis conducted in participants not receiving antihypertensive therapy. In conclusion, the independent relations between the reciprocal of aortic-to-brachial PP amplification and LVMI or LVH in a largely young to middle-aged sample are accounted for by variations in backward wave pressures rather than aortic stiffness., (Copyright © 2017 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Background: Electrocardiographic (ECG) QRS voltages used to generate criteria for left ventricular hypertrophy (LVH) detection are considerably attenuated by obesity. This effect renders the utility of ECG criteria to detect LVH in obese individuals of African ancestry to be of limited value., Hypothesis: A novel approach to correcting QRS voltages for the attenuating effect of body mass index (BMI) will improve the ability of ECG criteria to detect LVH in a group of African descent., Methods: Left ventricular mass was determined from echocardiography in 661 randomly selected participants (43.0% obese) of black African ancestry in South Africa., Results: As compared with Cornell and Sokolow-Lyon voltage criteria, BMI best correlated with RaVL , Gubner-Ungerleider, and Lewis QRS complex voltages, but these relations were noted only in those with BMI <29 kg/m(2) . Correcting RaVL and Lewis voltages by the difference in the slope of BMI-voltage relations in those with BMI <29 kg/m(2) vs those with BMI ≥29 kg/m(2) showed the greatest performance for LVH detection (uncorrected RaVL : 0.695 ± 0.025, corrected RaVL : 0.733 ± 0.022; P < 0.0001), and also increased the sensitivity (uncorrected RaVL : 30.6%, corrected RaVL : 42.4%; P < 0.0005) with no significant change in specificity (uncorrected RaVL : 86.3%, corrected RaVL : 83.0%; P = 0.28)., Conclusions: We offer a novel approach to correcting ECG voltages for the attenuating effects of obesity in individuals of African ancestry, and this improves the performance and sensitivity for LVH detection., (© 2016 Wiley Periodicals, Inc.)

Low-grade inflammation has been correlated with risk factors of cardiovascular diseases (CVD). Whether the pro-inflammatory and thrombotic ratio (fibrosis) may contribute to CVD is not known. We therefore aimed to assess whether Cornell Product left ventricular hypertrophy (LVH) is associated with fibrosis and coronary perfusion (silent ischemia) in a bi-ethnic male cohort from South Africa. A cross sectional study was conducted including 165 African and Caucasian men between the ages of 20-65. Fasting blood samples were obtained to measure fibrinogen, C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor (TNF-α). Ambulatory blood pressure, ECG and 12 lead ECG measures were obtained to determine silent ischemic events (ST events) and LVH, respectively. Africans revealed more silent ischemia, higher 24 h blood pressure, inflammatory, coagulation as well as fibrosis levels than Caucasians. In a low-grade inflammatory state (CRP > 3 mg/l), Africans revealed higher fibrosis (p ≤ 0.01) values, but lower IL-6 and TNF-α values than Caucasians. Linear regression analyses in several models demonstrated positive associations between silent ischemia and fibrosis [Adj. R(2) 0.23; ß 0.35 (95% CI 0.13, 0.58), p ≤ 0.01]. In a low-grade inflammatory state (CRP>3mg/l), fibrinogen predicted AV-block in African men [OR 3.38 (95% CI 2.24, 4.53); p = 0.04]. Low-grade inflammation may induce AV-block through mechanisms involving fibrosis and ischemia to increase the burden on the heart in African men.

Background: Whether left ventricular (LV) geometric remodeling, as indexed by relative wall thickness (RWT), aggregates in families and is inherited independent of LV mass (LVM) and additional confounders is uncertain., Methods: We determined whether RWT as assessed from 2D targeted M-mode echocardiography shows intrafamilial aggregation and heritability independent of LVM in 181 nuclear families (73 spouse pairs, 403 parent-child pairs, and 177 sibling-sibling pairs) with 16 families including 3 generations from an urban developing community of black Africans. Intrafamilial aggregation and heritability estimates (S.A.G.E. software) were assessed independent of confounders, including central aortic systolic blood pressure (SBPc) (radial applanation tonometry and SphygmoCor software)., Results: Independent of confounders including SBPc, LV RWT was correlated in parent-child (r = 0.32, P < 0.0001) and sibling-sibling (r = 0.29, P < 0.0001), but not in spouse (r = 0.11, P = 0.33) pairs. The relationships between parent-child (r = 0.28, P < 0.0001) and sibling-sibling (r = 0.24, P < 0.001) pairs persisted with further adjustments for LVM or LVM indexed to height(2.7) (LVMI). Similarly, independent of confounders, LV RWT showed significant heritability (h(2) ± SEM = 0.56 ± 0.09, P < 0.0001) and this persisted with further adjustments for LVM (h(2) ± SEM = 0.48 ± 0.09, P < 0.0001) or LVMI (h(2) ± SEM = 0.49 ± 0.09, P < 0.0001)., Conclusions: In a group of African ancestry, independent of LVM, LV geometric remodeling shows significant intrafamilial aggregation and heritability. Genetic factors may in-part determine the LV geometric remodeling process independent of the extent of cardiac hypertrophy., (© American Journal of Hypertension, Ltd 2014. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Background: Hypertension and vascular hyperresponsiveness have been associated with structural wall abnormalities in black Africans. Whether low grade inflammation would have an additive effect is uncertain. Therefore, a novel investigation aimed to assess whether inflammation and pressure overload would have an additive association with ECG left ventricular hypertrophy (LVH)., Methods: We included 75 African and 87 Caucasian males. Ambulatory blood pressure monitoring was done in the working week. A resting 12-lead ECG recording was used for the determination of LVH with the Cornell product formula. Fasting blood samples were obtained for high sensitivity C-reactive protein (hs-CRP) analyses after a controlled overnight stay. Men were stratified into low (≤3 mg/L) and high (>3 mg/L) hs-CRP groups., Results: African men revealed higher ambulatory blood pressure levels compared to Caucasian men independent of hs-CRP levels after adjustment for age, physical activity, cotinine, log γ-GT and body surface area. In forward stepwise linear regression analyses, SBP was positively associated with ECG LVH in all Africans. Considering low grade inflammatory status (>3 mg/L hs-CRP), SBP [Adj R(2)=0.49 (β=0.99, 0.45, 1.44), p≤0.01] and pulse pressure [Adj R(2)=0.61 (β=0.0.34, 0.88), p≤0.01] respectively, predicted ECG LVH in African but not in Caucasian men., Conclusions: Hyperdynamic blood pressure and inflammation acted in tandem as possible promoting factors to structural wall abnormalities in African men., (Copyright © 2013 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.)

Although in cross-sectional studies left ventricular mass (LVM), which exceeds that predicted by workload (inappropriate LVM [LVM(inappr)]) but not absolute LVM or LVM index (LVMI), is inversely related to LV ejection fraction (EF), whether on-treatment decreases in LVM(inappr) (%observed/predicted LVM) account for increases in EF beyond LVM or LVMI is unclear. Echocardiography was performed in 168 mild-to-moderate hypertensives treated for 4 months. Although in patients with an LVMI >51 g/m(2.7) (n=112; change in LVMI, -13.7±14.0 g/m(2.7); P<0.0001) but not in patients with an LVMI ≤51 g/m(2.7) (n=56; change in LVMI, 1.3±9.3 g/m(2.7)) LVMI decreased with treatment, treatment failed to increase EF in either group (1.2±10.8% and 2.7±10.7%, respectively). In contrast, in patients with inappropriate LV hypertrophy (LVM(inappr) >150%; n=33) LVM(inappr) decreased (-32±27%; P<0.0001) and EF increased (5.0±10.3%; P<0.05) after treatment, whereas in patients with an LVM(inappr) ≤150% (n=135), neither LVM(inappr) (-0.5±23%) nor EF (0.9±10.3%) changed with therapy. With adjustments for circumferential LV wall stress and other confounders, whereas on-treatment decreases in LVM or LVMI were weakly related to an attenuated EF (partial r=0.17; P<0.05), on-treatment decreases in LVM(inappr) were strongly related to increases in EF even after further adjustments for LVM or LVMI (partial r=-0.63 [CI, -0.71 to -0.52]; P<0.0001). In conclusion, decreases in LVM(inappr) are strongly related to on-treatment increases in EF beyond changes in LVM and LVMI. LV hypertrophy can, therefore, be viewed as a compensatory change that preserves EF, but when in excess of that predicted by stroke work, it can be viewed as a pathophysiological process accounting for a reduced EF.

AIM. Research has shown a significant relationship between hypertension and attenuated baroreceptor sensitivity (BRS), which in turn reflects alterations of autonomic control of the cardiovascular system. The objective of this study was to compare the BRS of African and Caucasian men and determine possible associations with blood pressure and left ventricular hypertrophy. MATERIALS AND METHODS. Participants included African (n = 82) and Caucasian (n = 100) male teachers, aged between 20 and 65 years, recruited in the North-West Province, South Africa. Ambulatory blood pressure monitoring was conducted for a 22-23-h period and, thereafter, cardiovascular parameters were recorded with a Finometer and 12-lead ECG during rest and while challenging the cardiovascular system with the cold pressor and Stroop color?word conflict tests. Spontaneous BRS was calculated as well as the Cornell product [marker of left ventricular hypertrophy (LVH)]. RESULTS. The African men had significantly lower BRS stress responses. Attenuated BRS coupled to an ?-adrenergic response pattern predicted elevation of blood pressure in the African men. BRS reduction did not prove to be a significant predictor of LVH. CONCLUSION. Lower BRS, especially during stress, may pose a significant health threat for African men regarding earlier development or promotion of α -adrenergic-driven hypertension and greater risk for cardiovascular disease.

The prognostic significance of blood pressure (BP) variability has lately enjoyed considerable attention. The need for early markers of cardiovascular dysfunction is imperative in black South Africans who have a significant risk for cardiovascular disease. We therefore compared 24-h BP variability with various traditional and advanced BP measurements, regarding their association with sub-clinical organ damage in black and white South Africans. The study included 409 African and Caucasian teachers aged 25-60 yrs. We measured office BP, 1-min continuous (finger) BP, ambulatory BP, BP reactivity and determined weighted 24-h BP variability. Albumin-to-creatinine ratio, Cornell product and carotid cross-sectional wall area (CSWA) were measures of organ damage. Africans had higher 24-h BP, BP variability, BP reactivity and sub-clinical organ damage (P<0.001). Correlations of BP variability with organ damage were overall weak when compared with other BP measurements. In normotensive groups, we found an independent association of 24-h systolic BP (SBP) variability with Cornell product only in Africans (r=0.37; P=0.01), confirmed in multiple regression models, with 24-h SBP included in the model. Only in hypertensive Caucasians, a significant correlation between CSWA and 24-h SBP variability was evident (r=0.30; P=0.01), although CSWA indicated stronger correlations with office or 24-h SBP than 24-h SBP variability. To conclude, 24-h SBP variability could potentially be an effective measure for the early detection of normotensive Africans at increased risk for the development of cardiovascular complications. Its usefulness based on associations with target organ damage in hypertensive groups seems to be less than traditional office or 24-h BP measurements.

The relative independent contribution of excess adiposity, as indexed by measures of central, general, or peripheral adiposity, toward abnormal cardiac diastolic chamber function at a community level is unclear. In 377 randomly selected participants >16 years old from a community sample with a high prevalence of excess adiposity ( approximately 25% overweight and approximately 43% obese), we assessed the independent contribution of the indexes of adiposity to the variation in early-to-late (atrial) transmitral velocity (E/A). After adjustments for a number of confounders, including age, gender, pulse rate, conventional diastolic (or systolic) blood pressure, antihypertensive treatment, left ventricular mass index, and the presence of diabetes mellitus or a hemoglobin A1c level >6.1%; waist circumference was an independent predictor of a reduced E/A (p = 0.0038). Body mass index (p = 0.07), waist-to-hip ratio (p = 0.23), and skinfold thickness (p = 0.37) were not independently associated with E/A, whereas waist circumference was independently associated with E/A, even after adjustments for other adiposity indexes, including body mass index (p <0.05 to 0.005). In contrast to the effects on diastolic function, the waist circumference did not correlate with the left ventricular ejection fraction (p = 0.23). The independent relation between the waist circumference and E/A (standardized beta coefficient -0.14 +/- 0.05, p = 0.0038) was second only to age (standardized beta coefficient -0.57 +/- 0.05, p <0.0001) and similar to blood pressure (standardized beta coefficient -0.11 +/- 0.04, p = 0.0075) in the magnitude of the independent effect on E/A. The inclusion of the relative wall thickness rather than the left ventricular mass index in the regression equation produced similar outcomes. The exclusion of the left ventricular mass index and relative wall thickness from the regression equations or the inclusion of carotid-femoral pulse wave velocity or 24-hour blood pressure as confounders failed to modify the relation between waist circumference and E/A. In conclusion, the waist circumference was second only to age in the impact on an independent association with E/A in a population sample with a high prevalence of excess adiposity. This effect was not accounted for by left ventricular hypertrophy or remodeling, the 24-hour blood pressure, or arterial stiffness.

Cardiac dysfunction is highly prevalent in dialysis patients in the developed world, and is a major cause of morbidity and mortality. The relative impact of pre-existing cardiac disease and dialysis/uremia on cardiovascular morbidity are not clear. We conducted a retrospective, cross-sectional analysis of cardiac function and mortality in 202 incident and prevalent dialysis patients over an 18-month period in a population with a low prevalence of cardiovascular disease at dialysis initiation. Systolic dysfunction was defined as an ejection fraction (EF) of <50%. Left ventricular hypertrophy (LVH) was determined by echocardiography or electrocardiogram. Clinical data was collected by chart review. Ninety-nine percent of patients were black, with a mean age of 41.7 +/- 10.1 years, and median follow up 28 months (range 1-216 months). Echocardiograms were available in 132 patients. Seventy-seven patients received hemodialysis, and 55 received peritoneal dialysis. Mean EF was 63.2 +/- 11.1. EF was not lower in patients with greater duration of dialysis, although LVH tended to increase (not statistically significant). In 39 patients who died during the study period, cardiac function was not different from survivors, and no patient died of ischemic heart disease or heart failure. In conclusion, in a population of patients with a low prevalence of cardiovascular disease at dialysis initiation, cardiac function appears preserved over time, and cardiac morbidity and mortality are low. This finding suggests that dialysis and uremia per se, in the absence of pre-existing cardiac disease, may not be major contributors to cardiovascular morbidity.

Aim: As it is uncertain whether arterial stiffness is related to left ventricular mass and left ventricle mean wall thickness independent of blood pressure measured at the brachial artery, we aimed to ascertain this effect in never-treated participants with a high prevalence of risk factors for large artery dysfunction., Methods: The conventional and ambulatory blood pressure-independent relations between indices of large artery function and either left ventricular mass or mean wall thickness were determined in 309 never-treated randomly recruited South Africans of African ancestry with prevalent risk factors for large artery changes [24% were hypertensive, 63% were overweight/obese, and 17% had diabetes mellitus or abnormal blood glucose control (glycosylated hemoglobin A1c > 6.1%)]. Large artery function was assessed from applanation tonometry performed at the carotid, radial and femoral arteries and central augmentation index and aortic pulse wave velocity (carotid femoral pulse wave velocity) derived from these measures. Left ventricular mass indexed for height (left ventricular mass index) and mean wall thickness were determined using echocardiography., Results: Pulse wave velocity was associated with left ventricular mass index (r = 0.67, P < 0.0001) and mean wall thickness (r = 0.61, P < 0.0001) in women, but not in men (r = 0.04-0.08) (P < 0.0001 for the interaction between pulse wave velocity and gender). On multivariate analysis with appropriate adjustments including either conventional systolic blood pressure, pulse pressure or mean arterial pressure, pulse wave velocity was independently associated with left ventricular mass index (partial r = 0.25, P < 0.005 after adjustments for systolic blood pressure) and with mean wall thickness (partial r = 0.17, P < 0.05 after adjustments for systolic blood pressure) in women, but not in men. With the inclusion of 24-h ambulatory rather than conventional systolic blood pressure, pulse pressure or mean arterial pressure in the regression equation, pulse wave velocity was similarly independently associated with left ventricular mass index (partial r = 0.39, P < 0.001 after adjustments for 24-h systolic blood pressure) and mean wall thickness (partial r = 0.33, P < 0.003 after adjustments for 24-h systolic blood pressure) in women, but not in men. Central augmentation index was not independently associated with left ventricular mass index or mean wall thickness. In women, the contribution of pulse wave velocity to left ventricular mass index or mean wall thickness independent of systolic blood pressure (standardized beta-coefficient for left ventricular mass index=0.37 +/- 0.13, P < 0.005) was equivalent to the contribution of systolic blood pressure (standardized beta-coefficient for left ventricular mass index = 0.38 +/- 0.13, P < 0.005). Moreover, after adjusting for clinic or ambulatory systolic blood pressure and other confounders, in women every one standard deviation increase in pulse wave velocity (2.1 m/s) translated into a 4.3 or 6.2 g/m increase in left ventricular mass index, respectively., Conclusion: Arterial stiffness is associated with left ventricular mass index and left ventricle wall thickness independent of conventional or ambulatory blood pressure and additional confounders in a never-treated population sample of women, but not men, of African ancestry with prevalent risk factors for large artery dysfunction.

Introduction: In South Africa a cluster of cardiovascular diseases accounts for 17% of all deaths. It is also predicted that South Africa will face an epidemic of chronic kidney disease due to obesity, type 2 diabetes and hypertension. It is important to estimate the burden of underlying cardiovascular and renal disease in South Africa., Objectives: The primary objective of the study was to establish the prevalence of left ventricular hypertrophy by ECG criteria, and micro- and macroalbuminuria in mild, moderate and severe hypertensive groups. The secondary objective was to establish the prevalence of left ventricular hypertrophy and micro- and macroalbuminuria in hypertensive patients with underlying type 2 diabetes., Methods: Patients > or = 35 years with essential hypertension with or without type 2 diabetes were recruited from 100 general practices throughout South Africa. BP, weight, height, waist circumference and urinary albumin/creatinine ratio were measured, and an ECG was performed. The Sokolow-Lyon and Cornell criteria were used for estimation of left ventricular hypertrophy. An overall prevalence rate was determined using weights from the severity category distribution inside the study population., Results: One thousand and ninety-one patients were available for analysis. There were 530 (48.5%) males and 561 (51.5%) females, 691 (63.3%) whites, 162 (14.8%) blacks, 150 (13.7%) Asians and 88 (8.1%) Coloureds. Of the patients, 10.9% had newly diagnosed hypertension, 20% had type 2 diabetes, and 38.1% mild, 32.1% moderate and 30.6% severe hypertension. The prevalence of left ventricular hypertrophy in the sample weighted to the hypertensive population over the age of 35 years with access to medical aids was 18.9%. Relative to white ethnicity, black ethnicity (OR 2, p = 0.03), and relative to mild hypertension, moderate (OR 2.2, p = 0.05) and severe hypertension (OR 4.9, p < 0.0001) were independent predictors of left ventricular hypertrophy. The overall prevalence of micro- and macroalbuminuria in the weighted sample was 21.3 and 4.1%, respectively. In the diabetics the prevalence of microalbuminuria was 32.3% and macroalbuminuria 10.4%, respectively. The independent predictors of microalbuminuria or worse were severe hypertension (OR 2.9, p < 0.0001), type 2 diabetes (OR 2.5, p < 0.002), and Asian ethnic group (OR 2, p = 0.02)., Conclusions: The study, based on a convenience sample of hypertensives from private practices in South Africa showed that the prevalence of left ventricular hypertrophy and microalbuminuria or worse was 18.9 and 25.4%, respectively.

Background: In a single-center study, we compared to what extent changes in conventional and ambulatory blood pressure (BP) predicted regression of left ventricular mass (LVM) index in response to antihypertensive treatment in previously untreated and treated patients with sustained hypertension., Methods and Results: We enrolled 173 black African patients who, off treatment, had a daytime diastolic BP ranging from 90 to 114 mm Hg. Antihypertensive drugs were titrated and combined to reduce the daytime diastolic BP below 90 mm Hg. Echocardiograms were obtained at baseline and follow-up. Mean systolic/diastolic clinic BP, 24-hour BP, and LVM index were similar in previously untreated (n=64) and previously treated (n=109) patients and averaged 171/102 mm Hg, 151/97 mm Hg, and 118 g/m2, respectively. At 4 months, these values had decreased (P<0.001) by 26/12 mm Hg, 23/14 mm Hg, and 14 g/m2 in previously untreated patients and by 22/9 mm Hg, 21/13 mm Hg, and 19 g/m2 in previously treated patients. In the previously untreated patients, the regression in LVM index correlated to a similar degree (P=0.09) with the decreases in the conventional (r=0.34; P=0.005) and the 24-hour (r=0.26; P=0.04) systolic BP. In the previously treated patients, the corresponding correlations were 0.02 (P=0.82) and -0.10 (P=0.32), respectively. Compared with the 24-hour systolic BP, automated oscillometric measurements of systolic BP obtained at the clinic yielded similar results., Conclusions: In previously untreated patients with sustained hypertension followed at a single center, reductions in clinic and ambulatory systolic pressure in response to antihypertensive treatment equally predicted the regression in LVM index.