Limited contribution of insulin resistance and metabolic parameters to obesity-associated increases in ambulatory blood pressure in a black African community.

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 â€‹= â€‹798) BP. In separate models, waist circumference (p â€‹< â€‹0.0005-<0.0001) and HOMA-IR (p â€‹< â€‹0.51-0.005), were independently associated with office, 24 â€‹h, day or night systolic (SBP) or diastolic (DBP) BP. However, whilst a one standard deviation increase in waist circumference translated into a 1.47-3.08 â€‹mm Hg increased in office, 24-h SBP or DBP, in mediation analysis HOMA-IR accounted for only 0.12-0.30 â€‹mm Hg of the impact of a one standard deviation effect of waist circumference on office, and 24-h SBP and 0.003-0.17 â€‹mm Hg of the impact of a one standard deviation effect of waist circumference on office and 24-h DBP. In conclusion, in a black African community, insulin resistance accounts for a negligible proportion of the impact of obesity on office or ambulatory BP.

The relationship between blood pressure and left ventricular mass index depends on an excess adiposity.

AIM: To determine whether blood pressure (BP)-LVM relationships depend in-part on the influence of an excess adiposity and whether this translates into a greater effect of hypertension on LVM in obese as compared with lean people. METHODS: In 399 randomly recruited participants from a general population with a high prevalence of excess adiposity ( approximately 68%), we assessed whether the relationships between conventional blood pressure (BP) and LVM indexed for height (LVMI) (determined from echocardiography) are influenced by adiposity. We confirmed these outcomes using 24-h ambulatory measurements in 297 participants; and carotid-femoral pulse wave velocity (PWV) (applanation tonometry) in 328 participants and from plasma leptin concentrations, we assessed whether leptin could mediate this effect. RESULTS: After adjustments for appropriate confounders, including the individual terms for adiposity and BP, interactions between adiposity indices (either waist circumference or the mean of subscapular and triceps skin-fold thickness) and either conventional systolic BP (SBP), 24-h SBP, PWV, conventional pulse pressure (PP), or 24-h PP were independently associated with LVMI (P < 0.001 for interactions). The adiposity index-haemodynamic interaction translated into a steeper slope of the BP-LVMI and PWV-LVMI relations in obese as compared with lean participants. Every one SD increase in conventional SBP ( approximately 22 mmHg) was associated with a 1.61 g/m increase in LVMI in participants with a normal waist circumference, in comparison to a 5.24 g/m increase in LVMI in those with an increased waist circumference (P < 0.0001). Furthermore, the adiposity index-haemodynamic interaction resulted in an increased LVMI in never-treated hypertensives with central obesity (LVMI, normotensives = 45.6 g/m, hypertensives = 51.0 g/m, P < 0.02), but not in participants with a normal waist circumference (LVMI, normotensives = 43.4 g/m, hypertensives = 45.0 g/m). Significant plasma leptin concentration-haemodynamic interactions were also associated with LVMI independent of confounders and adiposity indices, an effect that translated into a steeper slope of the haemodynamic factor-LVMI relations in participants with a plasma leptin concentration above as compared with those below the median for the group. CONCLUSION: Adiposity-induced increases in LVM reflect an enhanced effect of BP on LV growth, an effect that may be mediated by leptin. This translates into an impact of never-treated hypertension on LVMI in centrally obese, but not in lean people in groups of African descent in South Africa.

Gender-specific brachial artery blood pressure-independent relationship between pulse wave velocity and left ventricular mass index in a group 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.