THE ASSOCIATION OF HYPERTENSION AND OBESITY: WHAT IMPACT ON THE LONGITUDINAL SYSTOLIC FUNCTION OF THE LEFT VENTRICLE

Abstract

Objective: Hypertension and obesity are well known each result in heart failure with preserved ejection fraction. Indeed, there is ample evidence that the accumulation of adipose tissue in obese subjects negatively affects the left atrial and ventricular structure, as well as diastolic and systolic function. Predisposing factors for heart failure with preserved LVEF are advanced age, hypertension, diabetes, dyslipidemia and obesity. The development of the 2D strain has made it possible to make an early diagnosis of ventricular dysfunction in patients with cardiovascular risk factors. Design and method: This work consists of performing in a series of 128 hypertensive patients divided into two subgroups: 58 obese patients and 70 patients with normal BMI. A complete cardiographic echo study was performed in both subgroups, including LVEF by Simpson biplane method, calculation of indexed left ventricular mass and parietal relative thickness, analysis of diastolic function and finally study of longitudinal LV deformation by speckle tracking technique. Results: We note in this work that dyslipidemia and diabetes were significantly more prevalent in the HTA+obesity arm. The average blood pressure figures were slightly higher in the HTA+obesity arm. LVH was clearly predominant in the HTA+obesity arm with a more consequent decrease in the longitudinal contraction index. In obese hypertensive patients, LVH was most often concentric (53.4%). An increase in filling pressures was found in 11 obese hypertensive patients compared to only 4 non-obese hypertensive patients (p = 0.0001), with a good correlation with the decrease in GLS. These results suggest that increased BMI is closely associated with atrioventricular interaction in patients with hypertension, with a perfect correlation with impairment of longitudinal systolic function and diastolic function compared to the control group. Conclusions: Although the pathophysiological mechanism behind obesity is disputed, several possible explanations have been proposed: obesity has been considered a state of chronic volume overload, increased blood volume, neurohormonal activation, thus increasing oxidative stress. Therefore, obesity is associated with mild ventricular dilation (eccentric remodeling). However, this finding is in contrast to other studies that associate obesity with a concentric rather than eccentric remodeling of the LV.