Obesity and hypertensive heart disease: focus on body composition and sex differences

Abstract

There is evidence that hypertension is frequently associated with overweight/obesity even in kids and adolescents. Either conditions influence development of left ventricular (LV) hypertrophy (LVH), through different biological and hemodynamic mechanisms: obesity is conventionally thought to elicit a coherent growth of LV chamber dimensions and myocardial wall thickness (eccentric LV geometry), whereas a more accentuated increase in wall-thickness (concentric LV geometry) is attributed to hypertension. While during youth these differences are visible, proportion of LV concentric geometry, the most harmful LV geometric pattern, sharply raises in obese individuals during middle age, and becomes the most frequent geometric patterns among obese-hypertensive individuals. Two conditions with elevated hemodynamic impact, severe obstructive sleep apnea and masked hypertension contribute to the development of such a geometric pattern, but non-hemodynamic factors, and specifically body composition, also influence prevalence of concentric LV geometry. Contrasting a general belief, it has been observed that adipose mass strongly influences LV mass, particularly in women, especially when fat-free mass is relatively deficient. Thus, though blood pressure control is mandatory for prevention and reduction of LVH in obese hypertensive patients, without reduction of visceral adiposity regression of LVH is difficult. Future researches should be addressed on (1) assessing whether LVH resulting from alteration of body composition carries the same prognosis as pressure overload LVH; (2) defining tissue characterization of the hypertrophic heart in obese-hypertensive patients; (3) evaluating whether assessment of hemodynamic loading conditions and biological markers can help defining management of the association of obesity with hypertension.

Keywords: Body composition; Hypertension; Left ventricular mass; Obesity.

Fig. 1

Physiologic changes promoting common cardiovascular modifications in obesity and hypertension. OSA obstructive sleep apnea, LV left ventricular

Fig. 2

Systolic blood pressure (BP, a), adipose mass (b), left ventricular (LV) diastolic diameter (c) and prevalence of LV hypertrophy (d) in normal weight (n = 114), overweight (n = 113) and obese adolescents (n = 223). Note that prevalence of LV hypertrophy follows the excess of adipose mass, more than BP or LV chamber dimension. Adapted from Ref. 12. Asterisk significant vs normal weight subgroup; dagger significant vs overweight subgroup

Fig. 3

Relative contribution of parameters associated with variance of LV mass index, by standardized β-coefficients obtained by multiple linear regression analysis in the cohort of the Strong Heart Study. Adipose mass together with waist-to-hip ratio exhibit significant association with LV mass index variance only in women. From Ref. [50]

Fig. 4

Prevalence of single components of metabolic syndrome (MetS), according to the NCEP-ATPIII definition, in the participants in the HyprGEN study (from Ref. 47). Columns represents the prevalence in the sub-population without MetS (white) or with present MetS (grey) or with diagnosis of MetS, partially controlled by treatment of single components. Prevalence of all risk factors is significantly reduced in the managed MetS sub-group (0.05 < p < 0.0001), except central fat. LV hypertrophy is not influenced by the control of those risk factors, including hypertension