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.
Highlights
In this mini-review we will examine the impact of obesity in the hypertensive population, focusing on the common cardiovascular changes and interaction, leading to considerations on sex difference and body composition and potential influence on management (Fig. 1).Obesity as a comorbidity in arterial hypertension More than 80% of hypertensive patients present with additional risk factors, including glucose intolerance, hyperinsulinemia, lipid disordersThere is strong evidence that the prevalence of hypertension increases sharply with increasing body weight [2]
Abnormal conditions associated with cardiovascular modifications in obesity Hemodynamic load Two conditions are frequent in obesity, potentially helping explaining the prevalent concentric left ventricular (LV) geometry: severe obstructive sleep apnea (OSA) and masked hypertension
Adipose mass and LV geometry We studied the effect of fat mass in a special sub-population of obese individuals exhibiting a relative deficiency of fat-free mass and a consequent excess of adipose mass [54], a condition that is sometimes defined as ≪sarcopenic obesity≫ [57]
Summary
In this mini-review we will examine the impact of obesity in the hypertensive population, focusing on the common cardiovascular changes and interaction, leading to considerations on sex difference and body composition and potential influence on management (Fig. 1).Obesity as a comorbidity in arterial hypertension More than 80% of hypertensive patients present with additional risk factors, including glucose intolerance, hyperinsulinemia, lipid disorders (reduced HDL-cholesterol and increased LDL-cholesterol and triglycerides)There is strong evidence that the prevalence of hypertension increases sharply with increasing body weight [2]. In the young obese offspring participants of the Strong Heart Family Study cohort [18], prevalence of occasional high BP was low (10% in the obese sub-population), clear-cut LV hypertrophy (LVH) was progressively greater in overweight and obese adolescents compared to normal-weight individuals, paralleling the magnitude of adipose mass (Fig. 2). The increase in relative wall thickness (the most used index of concentricity) and LV mass is typically associated with evidence of subclinical LV systolic dysfunction, especially when hypertension coexists, such as depressed midwall shortening, abnormal reduced tissue myocardial velocities, strain and strain rate [30, 31].
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