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.

Insulin Resistance the Hinge Between Hypertension and Type 2 Diabetes

“…Experimental data suggest that insulin might be involved in the pathogenesis of both the concentric and eccentric patterns of LVH. Stimulation of myocardial cell growth and activation of the sympathetic nervous system might preferentially lead to concentric LV hypertrophy through a direct trophic effect and pressure overload, whereas sodium and water retention could lead to eccentric LV hypertrophy through volume overload [58]. The direct effect of insulin on myocardial cell growth could be mediated, at least in part, by the IGF-1 receptors [59].…”

Diabetes, body fat, skeletal muscle, and hypertension: The ominous chiasmus?

“…In addition to genetic and environmental factors known to play a role in the development of hypertension, body weight and obesity are highly correlated with hypertension; indeed, there is robust evidence that the prevalence of hypertension increases sharply with increasing body weight . Importantly, obesity has been shown to shift the secretory profile of the adipose tissue, which in turn contributes to the dysregulation of blood pressure; these phenomena occur through both direct actions of circulating adipokines on the vasculature and indirect actions via other systems, including the renal, central, and peripheral nervous system.…”

Joint influences of obesity, diabetes, and hypertension on indices of ventricular remodeling: Findings from the community-based Framingham Heart Study

“…Obesity, diabetes mellitus, and arterial hypertension are important independent risk factors for heart failure [1][2][3]. Accordingly, distinct forms of obesity cardiomyopathy [4][5][6][7][8], diabetic cardiomyopathy [9][10][11][12][13], and hypertensive heart disease [14][15][16][17] have been well described.…”