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

Abstract

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.