Search

Although chronic kidney disease (CKD) as determined from estimated glomerular filtration rate (eGFR) is recommended for risk prediction by current hypertension guidelines, the equations to derive eGFR may not perform well in black Africans. We compared whether across the adult lifespan, eGFR or CKD are as closely associated with noncardiac arterial vascular events, as carotid intima-media thickness (IMT), in Africa.In 1152 black South Africans [480 with noncardiac arterial events (294 with critical lower limb ischemia, 186 with stroke) of which 37% were premature] and 672 age, sex and ethnicity-matched controls from a randomly selected community sample, we assessed relations between eGFR, CKD or carotid IMT (B-mode ultrasound) and arterial events.From 20 years until old age, with or without adjustments, IMT was increased in those with as compared with without events (P 0.01 at each decade of age). However, at any decade of age across the adult lifespan neither creatinine concentrations, nor eGFR were altered in those with arterial events (P 0.28). Although IMT was strongly and independently associated with the odds of an event [odds ratio per 1 SD (0.171 mm) effect = 2.19, confidence interval = 1.75-2.78, P 0.0001], neither creatinine concentrations (P = 0.89), modification of diet in renal disease-derived (P = 0.07), nor Chronic Kidney Disease Epidemiology Collaboration-derived [odds ratio per 1 SD (22.5 ml/min per 1.73 m) effect = 1.06, confidence interval = 0.89-1.27, P = 0.51] eGFR were independently associated with the odds of an event. Although many with premature events had an increased IMT (63%), few with either premature events (8%) or with events at an older age (21%) had CKD and CKD had a poor performance (0.539 ± 0.011) and low sensitivity (16%) for event detection.In black South Africans, despite carotid IMT strongly associating with noncardiac arterial vascular events (stroke and critical lower limb ischaemia) consistently across the adult lifespan, few with events have CKD and CKD fails to associate with events.

Objective: The age at which arteriosclerosis begins to contribute to events is uncertain. We determined, across the adult lifespan, the extent to which arteriosclerosis-related changes in arterial function occur in those with precipitous arterial events (stroke and critical limb ischemia). Approaches and Results: In 1082 black South Africans (356 with either critical limb ischemia [n=238] or stroke [n=118; 35.4% premature], and 726 age, sex, and ethnicity-matched randomly selected controls), arterial function was evaluated from applanation tonometry and velocity and diameter measurements in the outflow tract. Compared with age- and sex-matched controls, over 10-year increments in age from 20 to 60years, multivariate-adjusted (including steady-state pressures) aortic pulse wave velocity, characteristic impedance (Zc), forward wave pressures (Pf), and early systolic pulse pressure amplification were consistently altered in those with arterial events. Increases in Zc were accounted for by aortic stiffness (no differences in aortic diameter) and Pf by changes in Zc and not aortic flow or wave re-reflection. Multivariate-adjusted pulse wave velocity (7.48±0.30 versus 5.82±0.15 m/s, P P P P P Conclusions: Arteriosclerosis-related changes in arterial function are consistently associated with arterial events beyond risk factors from as early as 20 years of age.

AIM To determine the degree to which an extended time to the peak of the aortic forward wave or early wave reflection time enhance associations between aortic backward wave pressure and hence central aortic pulse pressure (PPc) and left ventricular mass index (LVMI). METHODS In 701 adult participants from a community sample either receiving no antihypertensive therapy or receiving low-dose thiazide diuretic monotherapy for at least a year (the major therapy employed), we assessed aortic haemodynamics (SphygmoCor software and wave separation analysis; AtCor Medical, West Ryder, New South Wales, Australia) and LVMI (echocardiography). RESULTS An interaction between time to the peak of the aortic forward wave and aortic backward wave pressure was independently associated with aortic augmented pressure (P

Although accounting for a striking proportion of obesity effects on blood pressure (BP) in other populations, the extent to which obesity-associated increases in BP are explained by insulin resistance and metabolic changes in populations of African ancestry is uncertain. We determined the contribution of insulin resistance and associated metabolic abnormalities to variations in office or ambulatory BP in a black African community with prevalent obesity and hypertension. In 1225 randomly selected participants of black South African ancestry (age>16years, 43.1% obese, 47.4% abdominal obesity), we assessed adiposity indexes, the homeostasis model of insulin resistance (HOMA-IR) and associated metabolic abnormalities and office or ambulatory (n ​= ​798) BP. In separate models, waist circumference (p ​

Whether excess adiposity, associated metabolic abnormalities or alternative risk factors for left ventricular (LV) diastolic function are modified rather than mediated by geometric LV remodeling, is uncertain.Echocardiographic LV mass index (LVMI), relative wall thickness (RWT) and diastolic function (lateral and septal wall myocardial tissue lengthening at the level of the mitral annulus [e'] [n=430], ratio of early-to-late transmitral blood flow velocity (E/A), and E/e' [n=430]) were determined in 737 randomly recruited participants of a community-based study (43% obese).Independent of LVMI and confounders, indexes of adiposity and the homeostasis model of insulin resistance (HOMA-IR) were independently associated with LV diastolic function (p0.05). In addition, RWT was independently associated with LV diastolic function (p0.002). Importantly, an independent interaction between HOMA-IR and RWT, but not between blood pressure or age and RWT, was related to LV diastolic function (p0.05). This translated into an independent relationship between HOMA-IR and lateral e' (partial r=-0.17, p0.02), septal e' (partial r=-0.14, p=0.05), E/A (partial r=-0.17, p0.005) and E/e' (partial r=0.19, p0.01) in those with RWT above, but a lack of relationship between HOMA-IR and LV diastolic function (p0.59) in those with RWT below the median for the sample. Similarly, HOMA-IR was independently associated with LV diastolic dysfunction in those with RWT above (p0.05) but not below (p0.19) the median for the sample.The relationship between insulin resistance, but not alternative risk factors and LV diastolic function is markedly modified by the presence of a more concentrically remodeled LV.

AIMS The role of the adipokine, resistin in mediating increases in aortic stiffness is uncertain. We aimed to determine independent relations between circulating resistin concentrations and aortic pulse wave velocity (PWV) and wave reflection in a community-based sample with a high prevalence of untreated hypertension and obesity. METHODS Plasma resistin, adiponectin, and C-reactive protein concentrations (ELISA); carotid-femoral (aortic) PWV and the aortic reflected wave index (applanation tonometry and SphygmoCor software) were determined in 683 randomly selected participants of African ancestry from SOWETO, South Africa who had never received antihypertensive therapy. RESULTS Resistin concentrations were not independently associated with office or 24-h (n = 492) blood pressure (BP). In a stepwise regression model with BMI included in the model, age (P

Although the adipokine resistin may play a role in heart failure, the mechanisms of this effect are uncertain. Relations with left ventricular mass (LVM) and function are uncertain.In 739 randomly selected participants from a community sample (43.6% obese), we assessed relations between circulating resistin concentrations and LVM index (LVMI), LVM beyond that predicted by stroke work (inappropriate LVMI [LVMinappr]) and systolic and diastolic LV function (echocardiography).Resistin concentrations were not independently associated with blood pressure (BP). However, resistin concentrations were associated with LVMI (partial r=0.12, p0.0005), LVMinappr (partial r=0.18, p0.0001) and LV hypertrophy (partial r=0.13, p0.001) independent of BP, BMI, the homeostasis model of insulin resistance and additional confounders. Independent relations between resistin concentrations and LVMI and LVMinappr persisted with further adjustments for C-reactive protein concentrations. Resistin concentration (partial r=-0.12, p0.002 in all and partial r=-0.15, p0.0005 in untreated) was the only factor independently associated with LV midwall fractional shortening and these relations were enhanced at incremental concentrations of CRP. Resistin was not independently associated with transmitral and myocardial tissue Doppler indices of LV diastolic function.Resistin in-part explains variations in LVM, hypertrophy and myocardial systolic dysfunction, and these effects are independent of insulin resistance and general inflammatory changes.

Although obesity is an independent risk factor for heart failure and even mild-to-moderate forms of obesity are associated with myocardial systolic dysfunction the mechanisms of the myocardial dysfunction have not been identifi ed. We assessed whether dietary-induced obesity is associated with an increased sensitivity of the myocardium to s-adrenergic-induced cardiomyocyte apoptosis or fibrosis. To induce obesity, rats were fed a diet that promotes an increased caloric intake. Adrenergic-induced cardiomyocyte apoptosis was determined by injecting rats for 5 days with isoproterenol (0.01 mg/kg/day for 3 days and 0.02 mg/kg/day for 2 days) and then studying the degree of cardiomyocyte damage using a TUNEL assay and assessing the pathological score. Five months of feeding rats a diet that promoted the development of an increased body weight (Control=481±4.3 g, Diet=550±7.8 g, p‹0.001) and visceral fat content (Control=19.6±0.8 g, Diet=33.0±1.2 g, p‹0.0001), did not alter baseline cardiomyocyte apoptosis. However, 5 days of s-adrenergic activation resulted in an enhanced cardiomyocyte apoptosis in rats receiving the experimental diet as compared to rats receiving a normal diet (p‹0.01). No changes in the myocardial pathological score (fibrosis) were noted. The enhanced adrenergic-induced cardiomyocyte apoptosis in obese rats could not be explained by dietary-induced increases in baseline left ventricular internal diameters, decreases in systolic function (endocardial or midwall fractional shortening) or differences in the response of the heart to adrenergic-induced increases in inotropic or chronotropic function. In conclusion, the present study suggests that obesity may contribute to myocardial dysfunction by increasing the sensitivity of the myocardium to adrenergic-induced cardiomyocyte damage.

AIMS We determined the extent to which relationships between nurse-derived blood pressures (BPs) and cardiovascular damage may be attributed to isolated increases in in-office SBP independent of ambulatory BP. METHODS In 750 participants from a community sample, nurse-derived office BP, ambulatory BP, carotid-femoral pulse wave velocity (PWV; applanation tonometry and SphygmoCor software; n=662), and left ventricular mass indexed to height (LVMI; echocardiography; n=463) were determined. RESULTS Nurse-derived office BP was associated with organ changes independent of 24-h BP (LVMI; partial r=0.15, P

AIM: To assess the impact of obesity on the validity and performance of electrocardiographic criteria for the detection of left ventricular hypertrophy (LVH) in a group of participants of black African ancestry with a high prevalence of obesity. METHODS: Electrocardiographic voltage criteria for the detection of echocardiographic LVH [left ventricular mass index (LVMI) >51 g/m²·⁷] were evaluated in 661 participants from a community sample of black African ancestry (43% obese). RESULTS: BMI was inversely associated with Sokolow-Lyon voltages (partial r= -0.27, P < 0.0001) and no BMI-Cornell voltage relations were noted (P = 0.21). BMI was associated with voltage criteria that incorporate only limb lead recordings (r = 0.17-0.23), but these relations were weaker than BMI-LVMI relations (r = 0.36, P < 0.01 and P < 0.0001 for comparisons of r values). All electrocardiographic criteria were as strongly related to blood pressure as LVMI. Sokolow-Lyon voltage-LVMI relations were noted only after adjustments for BMI (P < 0.02) and Sokolow-Lyon voltages showed no performance for LVH detection. Cornell voltages showed significant performance in nonobese [area under receiver operating curve (AUC) = 0.67 ± 0.04, P < 0.0005], but not in obese (AUC = 0.56 ± 0.04, P = 0.08). Electrocardiographic criteria which employ limb-lead recordings only (e.g. RaVL) showed better performance in nonobese than in obese (AUC = 0.75 ± 0.04 and 0.59 ± 0.04, respectively, P < 0.005 for comparison) and markedly reduced specificity for LVH detection in obese (76%) than in nonobese (92%, P < 0.0001) despite similar sensitivities (32 vs. 29%). CONCLUSION: In groups of black African ancestry, obesity contributes to a poor validity and performance of all voltage criteria for the detection of LVH. None of the current criteria are recommended for use in obesity.

In high-Na + , low-K + diets, which suppress renin release in salt-sensitive groups, the mechanisms maintaining increases in renin-angiotensin-aldosterone system activation downstream from renin and renin-angiotensin-aldosterone system–induced effects on blood pressure (BP) are uncertain. Whether circulating angiotensinogen concentrations (AGT) or its determinants may contribute to maintaining serum aldosterone concentrations (aldosterone) and increases in BP on high-Na + , low-K + diets was evaluated in 579 participants of a community sample of African ancestry. Plasma renin concentrations were inversely related to BP ( P + /K + , P + /K + was independently associated with aldosterone ( P P + /K + at or more than the median for the sample, AGT was positively associated with aldosterone ( P P + /K + less than the median for the sample. Standardized β-coefficients (slopes) of AGT-aldosterone and AGT-SBP relationships were greater in participants with urinary Na + /K + at or more than the median (AGT-aldosterone=0.30±0.06, AGT-SBP=0.16±0.05) compared with those with urinary Na + /K + less than the median (AGT-aldosterone=−0.04±0.06; AGT-SBP=−0.03±0.05; P + /K + at or more than the median for the sample was equivalent to the relationship between body mass index and BP. In conclusion, in participants of African ancestry, in the presence of high-Na + , low-K + diets, which suppress renin release, renin-angiotensin-aldosterone system activation and its impact on BP are maintained in part by AGT.

Introduction: Blood pressure (BP) control in people of African descent is poor, largely because of a lack of treatment. Although the requirements for immediate initiation of antihypertensive drug therapy are defined by global cardiovascular risk, the global cardiovascular risk profiles of untreated hypertensives at a community level are uncertain. Aim: To identify the distribution of global cardiovascular risk profiles of untreated hypertensives in an urban, developing community of African descent in South Africa. Methods: As part of the African Programme on Genes in Hypertension, we assessed nurse-derived clinic BP (the mean of five standardised BP values obtained according to guidelines), current antihypertensive therapy, and total cardiovascular risk in 1 029 participants older than 16 years of age from randomly selected nuclear families from the South West Township of Gauteng (SOWETO). Results: Approximately 46% of participants had systolic/diastolic BP values ≥ 140/90 mmHg and ∼23% of participants were hypertensives not receiving antihypertensive medication. Approximately 12% of untreated hypertensives had a high added risk and ∼18% a very high added risk (6.7% of the total sample). In untreated hypertensives, in contrast to the absence of severe hypertension and diabetes mellitus in those with lower risk profiles, a high cardiovascular risk profile in this group was characterised by severe hypertension in ∼52% and diabetes mellitus in ∼33%. Based on a high added risk carrying at least a 20% chance and a very high added risk at least a 30% chance of a cardiovascular event in 10 years, this translates into 1 740 events per 100 000 of the population within 10 years, events that could be prevented through antihypertensive drug therapy. Conclusions: In an urban, developing community of African ancestry, a significant proportion (6.7%) of people may have untreated hypertension and a global cardiovascular risk profile that suggests a need for antihypertensive drug therapy. Cardiovascular risk in this group is driven largely by the presence of severe hypertension or diabetes mellitus.

BACKGROUND As groups of African descent may have higher nocturnal blood pressure (BP) for a given day BP than other ethnic groups, we ascertained whether this translates into differences in conventional (CBP) and 24-h ambulatory (ABP) BP control at a community level. METHODS Ambulatory 24-h, day and night BP (model 90207; SpaceLabs, Issaquah, WA) and CBP (mean of five values) control rates were determined in 689 randomly selected participants (>1 6 years) of African ancestry in South Africa.Target organ effects were determined from urinary microalbumin-to-creatinine ratios (ACR) and aortic pulse wave velocity (PWV, applanation tonometry). RESULTS Of the participants 45.7% were hypertensive and 22.6% were receiving antihypertensive medication. More participants had uncontrolled BP at night (34.0%) than during the day (22.6%, P < 0.0001). Uncontrolled CBP was noted in 37.2% of participants, while a much lower proportion had uncontrolled ABP (24.1 %) (P < 0.0001). Marked differences in the proportion of hypertensive participants with uncontrolled CBP and ABP were noted (treated: CBP = 62.2%, ABP = 33.3%, P < 0.0001; all: CBP = 81.3%, ABP = 44 . 4% , P < 0.0001 ).These differences were accounted for by a high prevalence of isolated increases in CBP (white-coat effects) (treated = 35.9%; all = 39.4%). Indeed, after censoring data from participants with white-coat effects, similar CBP and ABP control rates were noted. Participants with white-coat effects had similar ACR and PWV values as participants with normal ABP and CBP. CONCLUSIONS In communities of African descent, despite worse BP control at night than during the day, a high prevalence of white-coat effects translates into a striking underestimation of BP control in hypertensives when employing CBP rather than ABP measurements.

Objectives As the impact of mild smoking on blood pressure (BP) is uncertain, we assessed the relationship between predominantly mild current smoking and out-of-office BP and the effect of angiotensin-converting enzyme (ACE) genotype on this relationship in a community sample of black African ancestry. Methods In 689 participants randomly recruited from an urban, developing community of black African descent, we assessed smoking habits, out-of-office (24-h), and in-office conventional and central (applanation tonometry) BP, and ACE insertion (I)/deletion (D) variant genotype. Results A total of 14.5% (n = 100) were current smokers, the majority being mild (72%, 7.4 ± 4.6 cigarettes/day). Despite current smokers having only modest increases in in-office (P

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 participants16 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 level6.1%; 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 (p0.05 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, p0.0001) 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.

We explored whether dietary-induced obesity hastens the transition from concentric left ventricular (LV) hypertrophy to pump dysfunction in spontaneously hypertensive rats (SHRs) and the mechanisms thereof. After feeding rats a diet for 4 to 5 months, obesity was induced in SHRs and Wistar-Kyoto (WKY) control rats. Obesity was not associated with abnormal blood glucose control (glycosylated hemoglobin) or with increases in systolic blood pressure. However, in SHRs, but not in WKY rats, obesity was associated with a reduced LV chamber systolic function, as determined by echocardiography, and in isolated perfused heart studies. A marked increase in LV end diastolic diameter and a right shift in the LV diastolic pressure-volume relation were noted in obese SHRs but not in obese WKY rats. Moreover, LV intrinsic myocardial systolic function, as determined from the slope of the linearized LV systolic stress-strain relationship (LV myocardial end systolic elastance), was markedly reduced in obese as compared with lean SHRs, whereas LV myocardial end systolic elastance was maintained in obese WKY rats. Obesity increased LV weight, cardiomyocyte width, cardiomyocyte apoptosis (TUNEL), the activity of myocardial matrix metalloproteinases (zymography), and serum leptin concentrations in SHRs but not in WKY rats. In conclusion, SHRs are susceptible to the adverse effects of dietary-induced obesity on the heart, an effect that hastens the progression from concentric LV hypertrophy to pump dysfunction independent of blood pressure changes or alterations in glycosylated hemoglobin. This effect may be mediated through a proclivity of SHRs to developing both obesity-induced effects on cardiomyocyte apoptosis and activation of myocardial collagenases through leptin resistance and obesity-induced hypertrophy.

AIM To determine whether high-quality nurse-recorded auscultatory blood pressure (BP) values obtained at a single visit predict cardiovascular target organ changes as closely as ambulatory BP measurements. METHODS In a randomly selected population sample (n = 458, 21% receiving antihypertensive treatment; approximately 40% hypertensive), we compared high-quality single visit nurse-recorded auscultatory BP values to same-day 24-h ambulatory BP in their ability to predict multiple target organ changes [left ventricular mass index (LVMI), left ventricle (LV) mean wall thickness (MWT), early-to-late transmitral velocity ratios (E/A), (echocardiography); log of urinary albumin-to-creatinine ratios (log ACR) (24-h urine samples); large artery dysfunction [carotid-femoral pulse wave velocity (PWV) and central augmentation index (Alc) (applanation tonometry)]. RESULTS Nurse-recorded systolic BP (SBP) measurements obtained at a single visit were as closely associated with LVMI (r = 0.44), LV MWT (r = 0.44), E/A (r = -0.55), log ACR (r = 0.20), PWV (r = 0.62) and AIc (r = 0.41) (P < 0.0001 for all relations) as was 24-h SBP (LVMI; r = 0.33, LV MWT; r = 0.37, E/A; r = -0.35, log ACR; r = 0.24, PWV; r = 0.41, and AIc; r = 0.18, P < 0.001 for all relations) and either day or night SBP. On multivariate regression analysis with both nurse-recorded SBP and 24-h SBP in the same model, nurse-recorded SBP was independently associated with LVMI (P = 0.006), LV MWT (P = 0.03), E/A (P < 0.02), PWV (P < 0.0001) and AIc (P = 0.0002), and 24-h SBP was independently and positively associated with log ACR (P < 0.005), and PWV (P = 0.01). CONCLUSION One or more, high-quality single visit nurse-recorded auscultatory BP measurements may be equally as effective as ambulatory BP in predicting target organ damage in a population sample of African ancestry.

BACKGROUND As it is uncertain whether excess adiposity promotes primarily concentric or eccentric left ventricular hypertrophy (LVH), we aimed to determine at a population level, the independent relationship between waist circumference (WC) and LV geometric changes and the potential hemodynamic mechanisms thereof. METHODS We assessed the relations between WC and LV end-diastolic diameter (EDD), LV mean wall thickness (MWT = posterior + septal wall thickness/2), LV relative wall thickness (RWT = MWT/EDD), LV mass index (LVMI), concentric LVH (LVMI > 51 g/m2.7 and RWT > 0.45), eccentric LVH (LVMI > 51 g/m2.7 and RWT 0.45), in 309 never treated for hypertension, randomly recruited adult participants with a high prevalence of excess adiposity ( approximately 25% overweight; 38% obese). Pulse-wave analysis was performed to determine central artery blood pressures (BPs). Two hundred and thirty-one participants had high-quality ambulatory BP monitoring. RESULTS Approximately 7% of participants had concentric LVH, approximately 16% concentric LV remodeling, and approximately 15% eccentric LVH. After adjustments for potential confounders including conventional systolic BP (SBP), WC was related to MWT (partial r = 0.23, P = 0.0001), RWT (partial r = 0.13, P = 0.03), concentric LVH (P < 0.04), concentric LV remodeling (P = 0.02), but not with EDD or eccentric LVH (P = 0.91). Similar outcomes were noted after adjustments for central or 24-h SBP, and for conventional, central, or 24-h pulse pressure. Separate analysis in normotensive subjects revealed similar outcomes. CONCLUSIONS In a population sample with a high prevalence of obesity, excess adiposity promotes concentric, rather than eccentric LV geometric changes, effects which are independent of conventional, central artery or 24-h BP measured on a single occasion.

BACKGROUND We aimed to clarify whether age influences the independent relationship between adiposity and pulse-wave velocity (PWV). METHODS We explored the effect of age on the independent relationships between indexes of central adiposity (waist circumference (WC) and waist-to-hip ratio (WHR)) and carotid-femoral PWV, central augmentation index (AIc), or pressure wave amplification assessed from applanation tonometry measurements obtained at the radial, carotid, and femoral arteries in 508 randomly selected subjects >16 years of age in a population sample of African ancestry with a high prevalence of excess adiposity ( approximately 63% overweight or obese). RESULTS In women a strong interaction between age and either WC or WHR was associated with logPWV independent of confounders and the individual terms (r = 0.68, P < 0.0001). This translated into a markedly greater increase in logPWV with increases in either WC or WHR in women older than the median age as compared to women younger (slopes of WC-logPWV relationships = 0.0031 +/- 0.0009 vs. -0.0007 +/- 0.0007, P < 0.002). In women older than the median age for the group, a one s.d. increase in WC (12.8 cm) translated into a 0.70 m/s increase in PWV as compared to a 0.14 m/s decrease in PWV for each one s.d. increase in WC (13.0 cm) in women younger than the median age (P < 0.001). No index of adiposity was independently associated with the log of AIc or aortic-brachial wave amplification. CONCLUSION In women of African ancestry, a greater independent effect of adiposity on PWV is noted in older as compared to younger women.

AIM: The relationship between waist circumference (WC) and conventional blood pressure (BP) is independent of other clinical indices of adiposity. As ambulatory BP may offer more prognostic information than conventional BP, we aimed to identify whether indices of central adiposity are associated with ambulatory BP independent of other indices of adiposity. METHODS: The relationship between indices of adiposity [WC, waist-to-hip ratio, body mass index (BMI) or skin-fold thickness] and ambulatory or conventional BP was determined in 300 randomly selected individuals of African descent living in an urban developing community in South Africa. Relationships were determined with multiple indices of adiposity in the same regression model and after adjusting for age, gender, alcohol and tobacco intake, the presence or absence of diabetes mellitus or inappropriate blood glucose control [haemoglobin A1c (HbA1c)], antihypertensive therapy and menopausal status. RESULTS: Sixty-five per cent of participants were overweight or obese. With respect to the relationships between indices of adiposity, BMI and WC showed the strongest correlation (r=0.84, P

AIMS To determine whether brachial blood pressure (BP)-independent relations between aortic pressure and cardiovascular damage are better explained by reflected (backward) (Pb) or forward (Pf) wave pressure effects. METHODS In 1174 participants from a community of African ancestry, we assessed central aortic pulse pressure (PPc), Pb, and Pf (radial applanation tonometry, SphygmoCor) as well as left ventricular mass index (LVMI) (n = 786), aortic pulse wave velocity (PWV) (n = 1019), carotid intima-media thickness (IMT) (n = 578), transmitral early-to-late left ventricular diastolic velocity (E/A) (n = 779) and estimated glomerular filtration rate (eGFR) (n = 1174). RESULTS Independent of mean arterial pressure and confounders, PPc, and both Pb and Pf were associated with end-organ measures or damage (P

Although several characteristics of aortic function, which are largely determined by age, predict outcomes beyond brachial blood pressure (BP), the extent to which brachial BP control accounts for age-related variations in aortic function is uncertain. We aimed to determine the extent to which brachial BP control in the general population (systolic/diastolic BP140/90 mm Hg) accounts for age-related aortic hemodynamic changes across the adult lifespan.Central aortic pulse pressure (PPc), backward wave pressure (Pb), pulse wave velocity (PWV), and PP amplification (PPamp) (applanation tonometry and SphygmoCor software) were determined in 1,185 participants from a community sample (age16 years; 36.4% uncontrolled BP).With adjustments for distending pressure (mean arterial pressure, MAP), no increases in PPc, Pb, or PWV and decreases in PPamp were noted in those with an uncontrolled brachial BP younger than 50 years. In those older than 50 years with an uncontrolled brachial BP, MAP-adjusted aortic hemodynamic variables were only modestly different to those with a controlled brachial BP (PPc, 46±14 vs. 42±15 mm Hg, P0.02, Pb, 23±8 vs. 21±8 mm Hg, PWV, 8.42±3.21 vs. 8.19±3.37 m/second, PPamp, 1.21±0.17 vs. 1.21±0.14). Nonetheless, with adjustments for MAP, marked age-related increases in PPc, Pb, and PWV and decreases in PPamp were noted in those with uncontrolled and controlled brachial BP across the adult lifespan (P0.0001).Brachial BP control in the general population fails to account for most distending pressure-independent, age-related changes in aortic hemodynamics across the adult lifespan.

As acknowledged by all guidelines, left ventricular hypertrophy (LVH) is a major risk factor for cardiovascular events independent of conventional risk factors and coronary artery disease. In addition, compared to a normal LV geometry, concentric LV remodeling (an increased relative wall thickness (RWT) without an increase in LV mass (LVM)) is associated with a worse prognosis.1–4 Although LVM rather than concentric LV remodeling predicts incident heart failure,3 concentric LV remodeling without LVH is associated with the development of diastolic dysfunction, and concentric rather than eccentric LVH is associated with greater increases in indices of LV filling pressures.5 Thus, the extent of concentric LV remodeling may determine whether progression from LVH to heart failure with a preserved rather than reduced systolic chamber function occurs. The factors that determine LV remodeling are therefore of considerable interest. Although the impact of age, sex, blood pressure, and obesity on LV geometric remodeling has been well described, there is nevertheless uncertainty as to the role of genetic factors independent of LVM, a major determinant of LV wall thickness, and a change that itself is well recognized as being inherited.6–14 Compared to age-, and sex-matched controls, siblings of those with LVH have a greater risk of concentric, but not eccentric LVH.9 However, in that study,9 whether siblings were also at risk for concentric LV remodeling is uncertain and hence LVM may have made a major contribution to the inheritance of concentric LVH. Moreover, in the Framingham Heart Study, the risk for concentric LV remodeling was only modestly increased in related compared to unrelated individuals, whereas the risk for concentric LVH was markedly augmented.15 Hence, again, LVM may have been the major determinant of the inheritance of LV remodeling. Although alternative studies indicate that RWT is indeed inherited,10–12,16 none of these studies reported on the inheritance of RWT independent of LVM. To address the aforementioned uncertainty as to the extent to which genetic factors contribute toward concentric LV remodeling beyond LVM, in the present study, we aimed to evaluate the intrafamilial aggregation and heritability of RWT independent of LVM and additional confounders. We hypothesized that RWT would show intrafamilial aggregation and heritability independent of LVM and additional confounders.

To determine whether blood pressure (BP) or an excess adiposity, both frequently observed comorbidities that independently relate to left ventricular diastolic dysfunction (LVDD), have a greater impact on LVDD at a community level.We assessed the relative independent impact of an excess adiposity versus BP on indices of LVDD as determined from the ratios of early-to-late transmitral blood flow velocity (E/A) and E/the mean of lateral and septal wall myocardial tissue lengthening at the level of the mitral annulus (e'; (E/e') in 417 randomly recruited participants of a community-based study with a high prevalence of excess adiposity (43% obese and 25% morbidly obese).In multivariate adjusted models, including adjustments for appropriate BP values (SBP for E/e' and DBP for E/A), waist circumference was independently associated with E/A (partial r = -0.12, P 0.02) and E/e' (partial r = 0.15, P 0.005). In contrast, BMI was independently associated with E/e' (partial r = 0.11, P 0.05), but not E/A (partial r = -0.09, P = 0.08). In multivariate models, SBP had a greater impact on E/e' (standardized β-coefficient = 0.32 ± 0.05, P 0.0001) than did waist circumference (standardized β-coefficient = 0.16 ± 0.05, P 0.005; P 0.05 for comparison), whereas DBP had a similar impact on E/A (standardized β-coefficient = -0.10 ± 0.03, P 0.005) as did waist circumference (standardized β-coefficient = -0.10 ± 0.04, P 0.05). Importantly, whereas SBP was the main factor independently associated with an increased E/e' (≥10) (P 0.0005), waist circumference was not independently associated with either a decreased E/A (≤0.75) (P = 0.82) or an increased E/e' (≥10; P = 0.15).In a community sample with a high prevalence of excess adiposity, BP exceeds obesity as the most important modifiable risk factor for LVDD. These data suggest that in communities with a high prevalence of obesity, if weight loss programmes fail to produce sustainable target body weights, rigorous BP management to lower than normal thresholds may be sufficient to prevent LVDD.

An inability to show consistent relationships between gene variants and blood pressure (BP) may be confounded by the use of office BP measurement. Whether the difference between office BP and day BP (office-day) is genetically predetermined is unknown. We therefore aimed to determine the intrafamilial aggregation and heritability of office-day BP.Nurse-derived office BP (mean of 5 measurements according to guidelines) and 24-h ambulatory BP were determined for 592 participants from 198 families (67 spouse pairs, 361 parent-child pairs, and 169 sibling-sibling pairs), with 12 families having three generations, from an urban developing community of black Africans. Heritability estimates were determined using SAGE software.With adjustments for confounders, office systolic BP (SBP) (h=0.35±0.09, P0.0001) showed comparable heritability estimates to 24-h SBP (h=0.33±0.09, P0.0001). Similarly, with adjustments for confounders, office diastolic BP (DBP) (h=0.37±0.09, P0.0001) showed comparable heritability estimates as 24-h DBP (h=0.35±0.09, P0.0001). However, multivariate adjusted heritability estimates of day SBP (h=0.29±0.09, P0.0001) and DBP (h=0.33±0.09, P0.0001) were not diminished by further adjustments for office SBP (h=0.42±0.09, P0.0001) or DBP (h=0.34±0.09, P0.0001). Further, independent of confounders, office-day BP showed significant intrafamilial aggregation and heritability (SBP: h=0.51±0.10, P0.0001; DBP: h=0.37±0.09, P0.0001), effects that persisted with further adjustments for office, day, or day-night BP (P0.0005 for SBP and DBP).Although office and ambulatory BP may show similar heritability estimates, genetic associations with carefully determined office BP measurements may be confounded by the heritability of office-day BP differences.

Although the circulating renin–angiotensin system (RAS) is suppressed in salt-sensitive populations, the role of the intrarenal RAS in blood pressure (BP) control in these groups independent of the circulating RAS is uncertain. We evaluated the relationship between 24-hour urinary angiotensinogen excretion and either office (mean of 5 measurements; n=425) or 24-hour ambulatory (n=340) BP independent of the circulating RAS in a community-based sample of African descent that had never received antihypertensive drug therapy. Circulating RAS activity was determined from plasma renin and angiotensinogen and serum aldosterone concentrations. Urinary angiotensinogen to creatinine ratio (angiotensinogen/creat) was correlated with plasma angiotensinogen concentrations ( P r =0.16; P r =0.07; P =0.14) was not independently associated with office systolic BP. Urinary angiotensinogen/creat was also associated with 24-hour systolic BP (partial r =0.11; P + /K + , or 24-hour urinary Na + excretion rates ( P P P =0.01) systolic BP. In conclusion, independent of the systemic RAS, including plasma angiotensinogen concentrations, urinary angiotensinogen excretion is associated with BP in a salt-sensitive, low-renin group of African descent. These data lend further support for a role of the RAS in BP control in salt-sensitive groups of African ancestry.

AIMS To determine whether SBP or DBP is best associated with different components of left ventricular diastolic dysfunction. METHODS In 241 randomly selected participants, echocardiographic left ventricular diastolic function was assessed from early-to-atrial (E/A) transmitral velocity and E/e' where e' represents myocardial tissue lengthening velocity in early diastole as measured at the mitral annulus. Relationships between diastolic function and blood pressure (BP) were assessed from brachial and central aortic (radial applanation tonometry and SphygmoCor software) measurements. RESULTS Independent of confounders, brachial DBP (partial r = -0.21, P

Whether routine clinical parameters associated with left ventricular mass (LVM) enhance the performance of electrocardiographic (ECG) criteria for LV hypertrophy (LVH) detection and hence modify overall cardiovascular risk stratification is unknown. An approach to echocardiographic LVH detection was identified from ECG criteria and clinical variables [age, body mass index (BMI), systolic blood pressure (SBP) and estimated glomerular filtration rate] associated with LVM in 621 participants of African ancestry. Performance (area under the receiver operating curve) and classification accuracy for LVH detection and the impact on cardiovascular risk stratification were determined. Compared to Cornell criteria alone, the combined use of Cornell criteria and clinical variables increased the performance (p

Background. Primary healthcare is the foundation of a country’s healthcare system. Without an efficient and cost-effective programme, the level of healthcare offered across all levels of health management is adversely affected. Objective. To analyse the effectiveness of the management of hypertension and diabetes mellitus (DM) among two distinct patient populations, one with significant cardiovascular risk factors and the other without. Method. We performed a case control study of a high-risk group of patients presenting with chronic critical limb ischaemia (CLI) to the Divisions of Vascular Surgery at Charlotte Maxeke Johannesburg Academic Hospital and Chris Hani Baragwanath Academic Hospital, and a randomly selected group of ‘healthy’ community participants from Johannesburg’s South Western Townships (Soweto). Results. We assessed 217 patients with CLI and 1 030 participants from the community. We assessed the number of patients who were not achieving their therapeuatic targets, among those known to be hypertensive (CLI: 44.7%; community: 59.9%) and diabetic (CLI: 83.5%; community: 66%). Undiagnosed diabetes affected 10.8% of patients with CLI and 11% of the community sample. Conclusion. Traditional vascular risk factors are managed poorly at both primary healthcare and at tertiary care levels. There is a need to identify factors that will address this issue.

Whether independent relationships between white coat effects (office minus day (office-day blood pressure (BP))) and organ damage or arterial stiffness may be explained by associations with an attenuated nocturnal BP dipping, has not been determined.In 750 participants from a sample of African ancestry, office and 24-hour BP, carotid-femoral pulse wave velocity (PWV) (applanation tonometry and SphygmoCor software) (n = 662), and left ventricular mass indexed to height(2.7) (LVMI) (echocardiography) (n = 463) were determined.Office-day systolic BP (SBP) was correlated with day minus night (day-night) SBP, percentage night divided by day (night/day) SBP, and night SBP (P0.0005), and these relationships persisted with adjustments for confounders, including day SBP (P0.005). With adjustments for 24-hour SBP and additional confounders, office-day SBP was associated with LVMI (P0.01) and PWV (P0.0001). With adjustments for day SBP and additional confounders, day-night SBP, percentage night/day SBP, and night SBP were related to PWV (P0.05) but not to LVMI (P0.44). The relationships between office-day SBP and LVMI or PWV persisted with adjustments for either day-night or percentage night/day SBP (LVMI: P = 0.01; PWV: P0.0001) or night SBP (LVMI: P0.01; PWV: P = 0.0001), and in product of coefficient mediation analysis with appropriate adjustments, neither indexes of nocturnal BP dipping nor nocturnal BP per se contributed toward the impact of office-day BP on LVMI or PWV (P0.09).In a group of African ancestry, although white coat effects are independently associated with an attenuated nocturnal decrease in SBP, neither decreased BP dipping nor nocturnal BP contribute toward the independent relationships between white coat effects and LVMI or arterial stiffness.

AIM To evaluate whether the relationship between early glomerular dysfunction and left-ventricular mass (LVM) occurs in a community sample and whether this relationship depends on haemodynamic factors. METHODS In 621 randomly selected participants from a community sample (332 were normotensive), estimated glomerular filtration rate (eGFR), LVM and dimensions were determined using echocardiography, and aortic blood pressure (BP) assessed from applanation tonometry and SphygmoCor software. Aortic pulse wave velocity (PWV) and high-quality 24-h BP values were available from 554 and 437 participants, respectively. RESULTS With adjustments for confounders (including clinic SBP), eGFR was associated with LVM index (LVMI) and LVM in excess of that predicted from stroke work (inappropriate LVM, LVMinappr) in all participants (LVMI: partial r = -0.18, P

AIMS We sought to determine whether within normal/high-normal blood pressure (BP) ranges (120-139/80-89 mmHg), aortic BP may further refine BP-related cardiovascular risk assessment, as determined from target organ changes. METHODS In 1169 participants from a community sample of African ancestry, 319 (27%) of whom had a normal/high-normal BP, aortic BP was determined using radial applanation tonometry and SphygmoCor software, and target organ changes assessed from carotid-femoral pulse wave velocity (PWV) (n = 1025), estimated glomerular filtration rate (eGFR) (n = 944), and left ventricular mass indexed to height (LVMI) (n = 690). RESULTS Normal versus high-normal BP categories failed to differentiate between those participants with a BP above optimal values with versus without multivariate-adjusted target organ changes. However, in those with a normal/high-normal BP with aortic SBP values that were less than 95% confidence interval of healthy participants with optimal BP values (45% of those with a normal/high-normal BP), no unadjusted or multivariate adjusted target organ changes were noted. In contrast, those with a normal/high-normal BP with aortic SBP values that exceeded optimal thresholds, demonstrated unadjusted and multivariate adjusted increases in PWV and LVMI and decreases in eGFR (P

AIM We determined whether left ventricular hypertrophy (LVH) which exceeds that predicted from workload [inappropriate LV mass (LVM(inappr))] is associated with reduced left ventricle (LV) systolic chamber function independent of and more closely than absolute or indexed left ventricular mass (LVM). METHODS In 626 randomly selected adult participants from a community sample of black Africans, using echocardiography we assessed absolute LVM, LVM indexed to height(2.7) (LVMI), LVM(inappr), LV wall stress, ejection fraction, and midwall fractional shortening (FSmid). LVM(inappr) was determined as percentage of observed/predicted LVM. Predicted LVM was calculated from a previously validated formula that incorporates stroke work. LVMI(inappr) more than 150% was considered to be inappropriate LVH. This threshold was identified from the upper 95% confidence interval for LVMI(inappr) determined in 140 healthy participants. RESULTS A total of 21.7% of participants had LVH (LVMI > 51 g/m(2.7)) and 18.5% had inappropriate LVH. With adjustments for LV stress and other confounders there was a strong inverse relationship between LVM(inappr) and ejection fraction (partial r = -0.41, P

AIM To compare the intra-familial aggregation and heritability of central (aortic) (PPc) versus peripheral (brachial) (PPp) pulse pressure after imputing pretreatment blood pressures (BPs) in treated participants in a community of black African ancestry. METHODS Central PPc [generalized transfer function (GTF) and radial P2-derived] was determined with applanation tonometry at the radial artery (SphygmoCor software) in 946 participants from 258 families with 23 families including three generations from an urban developing community of black Africans. In the 24.1% of participants receiving antihypertensive treatment, pretreatment brachial BP was imputed from published overall averaged effects of therapy grouped by class and dose, specific for groups of black African descent. From these data PPc was estimated from proportionate differences in central aortic and brachial PP. Heritability estimates were determined from SAGE software. Echocardiography was evaluated in 507 participants in order to determine stroke volume. RESULTS With adjustments for confounders, parent-child (P

Central aortic blood pressure (BP; BPc) predicts outcomes beyond brachial BP. In this regard, the application of a generalized transfer function (GTF) to radial pulse waves for the derivation of BPc is an easy and reproducible measurement technique. However, the use of the GTF may not be appropriate in all circumstances. Although the peak of the second shoulder of the radial waveform (P2) is closely associated with BPc, and, hence, BPc may be assessed without the need for a GTF, whether P2-derived BPc is associated with adverse cardiovascular changes independent of brachial BP is uncertain. Thus, P2- and GTF-derived aortic BPs were assessed using applanation tonometry and SphygmoCor software. Left ventricular mass was indexed for height 1.7 (n=678) and carotid intima-media thickness (IMT; n=462) was determined using echocardiography and vascular ultrasound. With adjustments for nurse-derived brachial pulse pressure (PP), P2-derived central PP was independently associated with left ventricular mass indexed for height 1.7 (partial r =0.18; P r =0.40; P 1.7 : partial r =0.17, P r =0.37, P r =−0.21 to 0.05). Twenty-four–hour, day, and night PP-target organ relations did not survive adjustments for nurse-derived brachial BP. In conclusion, central PP derived from P2, which does not require a GTF, is associated with cardiovascular target organ changes independent of brachial BP. Thus, when assessing adverse cardiovascular effects of aortic BP independent of brachial BP, P2-derived measures may complement GTF-derived measures of aortic BP.

Background: The extent to which Human Immunodeficiency Virus (HIV) is associated with increases in carotid Intima-Media Thickness (IMT) independent of conventional cardiovascular risk factors is unclear. Hence, we evaluated whether independent of conventional risk factors, an increased carotid IMT occurs in African HIV infected patients with chronic Critical Limb Ischemia (CLI). Methods: Carotid IMT was measured in 217 sequentially recruited patients with CLI, 25 of whom were HIV positive and in 430 randomly selected controls from a community sample. Results: As compared to HIV negative patients with CLI, HIV positive patients were younger (49 ± 10 vs. 64 ± 11 years, p

BACKGROUND: As the independent relationship between C-reactive protein (CRP) concentrations and central aortic blood pressures (BP) in populations with high CRP concentrations is uncertain, we aimed to evaluate this question in a community sample, 57% with CRP concentrations >3 mg/l (high cardiovascular risk). METHODS: Central aortic hemodynamics (applanation tonometry, SphygmoCor software) and serum ultrasensitive-CRP concentrations were assessed in 836 randomly recruited participants from an urban developing community of African ancestry. RESULTS: Log CRP was strongly correlated with age, steady-state pressures (indexed by mean arterial pressure (MAP)), indexes of adiposity, central systolic BP (SBPc), central pulse pressure (PPc), the augmented (reflected) (AP) and forward (P1) pressure wave components of PPc, aortic pulse wave velocity (PWV), and the effective reflecting distance (ERD) (P < 0.0001 for all). Moreover, before adjustments SBPc, PPc, AP, P1, PWV, and ERD increased incrementally across low, moderate and high risk categories of CRP (P < 0.0001). However, in multivariate models with adjustments for confounders, no independent association between CRP and SBPc, PPc, AP, P1, PWV, or ERD was noted (P > 0.10 for all) and multivariate adjusted central hemodynamic variables were similar in participants with low, moderate, or high risk CRP concentrations. The lack of independent relationship between CRP concentrations and central aortic hemodynamics was reproduced in normotensives, hypertensives, men, women, lean and overweight/obese participants, and in participants lesser or ≥ 60 years of age. CONCLUSION: Even in communities with prevalent high CRP concentrations, low-grade inflammation as indexed by CRP, does not independently account for increases in aortic PP, the component waves, or the determinants of PPc.

Although central pulse pressure (PPc) is strongly related to central mean arterial pressure (MAPc), PPc predicts cardiovascular outcomes beyond MAPc. Whether modifiable risk factors for hypertension contribute to PPc and its determinants, independent of MAPc, is uncertain. In 635 randomly recruited participants, we assessed the independent relationship between 24-hour urinary sodium (Na + ) or potassium (K + ) excretion and brachial artery PP (in office or 24-hour; n=487), PPc, the forward (P1) and augmented (Paug) pressure wave components of PPc, central augmentation index, and determinants of central pressure waves, including aortic pulse wave velocity, effective reflecting distance, and reflective wave transit time. Central dynamics were determined using applanation tonometry of the carotid, femoral, and radial arteries. With adjustments for potential confounders, urinary Na + /K + was independently associated with in-office, central, and 24-hour PP, as well as Paug, P1, and central augmentation index ( P P + /K + was independently associated with PPc, 24-hour PP, Paug, P1, and central augmentation index ( P P =0.005) but not with in-office PP, pulse wave velocity, effective reflecting distance, or reflective wave transit time. In conclusion, in a population of African ancestry, urinary salt excretion is independently related to central and 24-hour PP independent of MAPc or diastolic BP, effects that are attributed to increases in both P1 and Paug but not to pulse wave velocity. Hence, modifying salt intake could influence cardiovascular risk through effects on 24-hour and central PPs, as well as P1 and Paug, independent of steady-state pressure (MAP or diastolic BP) or pulse wave velocity.

AIM We sought to determine whether prehypertension (BP = 120-139/80-89 mmHg) is associated with target organ changes independent of confounders. METHODS In 771 participants from a population sample of African ancestry, approximately 46% of whom had hypertension, and approximately 30% prehypertension, organ damage was assessed from echocardiography (left ventricular mass indexed to height2.7, the mean of posterior and septal wall thickness and early-to-late transmitral velocity), 24-h urine samples (urinary albumin-to-creatinine ratio), serum creatinine concentrations, and carotid-femoral pulse wave velocity. Ambulatory blood pressure values that met with prespecified quality control criteria were available in 539 participants. RESULTS A greater proportion of hypertensives (P < 0.0001) but not prehypertensives had elevated 24-h blood pressure values as compared with participants with optimal blood pressure values. Before adjustment for confounders, hypertension was associated with all target organ changes (P < 0.0001), and after adjustment, an independent association was noted between hypertension and all target organ changes (P < 0.05-0.005) except albumin-to-creatinine ratio or serum creatinine concentrations. Before adjustment, prehypertension was associated with left ventricular mass indexed to height2.7, mean wall thickness, pulse wave velocity, and early-to-late transmitral velocity (P < 0.05-0.001), but not with other target organ changes. After adjustment, however, prehypertension was not independently associated with target organ changes. Other factors independently associated with target organ changes were age (all target organs), waist circumference (left ventricular mass indexed to height2.7 and early-to-late transmitral velocity) and diabetes mellitus (albumin-to-creatinine ratio and pulse wave velocity). Interactions between prehypertension and any of the alternative risk factors were not independent predictors of target organ changes. CONCLUSION Although associated with it, prehypertension is not an independent predictor of organ damage in young-to-middle-aged persons of African ancestry.

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.

levels. The group underwent extensive hemodynamic profiling after at least 20 minutes of supine rest, including standard office brachial BP (Omron Hem-705CP) and central BP (radial tonometry with generalized transfer function, SphygmoCor). Central (heart-femoral) and peripheral (brachialankle) PWV were determined by Colin VP 2000. Strength of association was determined by Pearson correlations. Results: Means (ranges) in 78 subjects (44M, 34 F) were: age 55 (19-91) years, weight 84 (48-130) kg, height 167 (140-188) cm. Peripheral BP values (mmHg) were: systolic (S)BP 139 (100-192), diastolic (D)BP 80 (55-132), mean arterial pressure (MAP) 108 (76-162), pulse pressure (PP) 60 (35115). Corresponding central BP values were: SBP 132 (88-195), PP 52 (23-119), radial second systolic peak (P2) 131 (82-203), MAP 103 (75168). Central and peripheral PWV were: hfPWV 1182 (569-2038) and baPWV 1507 (893-3206) cm/sec. Central augmentation index values were: 139 (81-246) %. Table 1 shows correlation coefficients between BP and PWV; baPWVand hfPWV were also strongly correlated (r1⁄4.732). Conclusion: Central and peripheral PWV values are highly correlated with both central and peripheral BP values and to a lesser degree with augmentation index. There were slightly stronger associations between peripheral than central BP and PWV. These findings demonstrate the tight association between a single casual office BP and corresponding PWV values, indicating that SBP and PWV convey similar information.

levels. The group underwent extensive hemodynamic profiling after at least 20 minutes of supine rest, including standard office brachial BP (Omron Hem-705CP) and central BP (radial tonometry with generalized transfer function, SphygmoCor). Central (heart-femoral) and peripheral (brachialankle) PWV were determined by Colin VP 2000. Strength of association was determined by Pearson correlations. Results: Means (ranges) in 78 subjects (44M, 34 F) were: age 55 (19-91) years, weight 84 (48-130) kg, height 167 (140-188) cm. Peripheral BP values (mmHg) were: systolic (S)BP 139 (100-192), diastolic (D)BP 80 (55-132), mean arterial pressure (MAP) 108 (76-162), pulse pressure (PP) 60 (35115). Corresponding central BP values were: SBP 132 (88-195), PP 52 (23-119), radial second systolic peak (P2) 131 (82-203), MAP 103 (75168). Central and peripheral PWV were: hfPWV 1182 (569-2038) and baPWV 1507 (893-3206) cm/sec. Central augmentation index values were: 139 (81-246) %. Table 1 shows correlation coefficients between BP and PWV; baPWVand hfPWV were also strongly correlated (r1⁄4.732). Conclusion: Central and peripheral PWV values are highly correlated with both central and peripheral BP values and to a lesser degree with augmentation index. There were slightly stronger associations between peripheral than central BP and PWV. These findings demonstrate the tight association between a single casual office BP and corresponding PWV values, indicating that SBP and PWV convey similar information.