Left Ventricular Morphology and Function in Normotensive, Metabolically Healthy Obese Individuals without Fatty Liver Disease.

Abstract

Background: Obesity is one of the major risk factors for the development of heart failure (HF), although the exact underlying mechanism remains unclear. In the clinical setting, assessing the impact of obesity on the cardiovascular system is difficult due to comorbidities.

Objectives: The purpose of this study was to evaluate an independent influence of obesity on the left ventricular (LV) morphology and function. To eliminate hemodynamic and metabolic confounders, we performed an echocardiographic evaluation of severely obese but normotensive and metabolically healthy patients without fatty liver disease.

Methods: The patients were retrospectively selected from the cohort of 180 consecutive obese patients systematically evaluated with transthoracic echocardiography before bariatric surgery. Finally, 25 obese subjects, predominantly females, were evaluated with transthoracic echocardiography. Inclusion criteria were defined as absence of diabetes, hypertension, and hyperlipidemia, no use of medications and no hepatic steatosis on liver biopsy. They were matched with a control group of healthy subjects with normal body mass index.

Results: In obese patients, LV hypertrophy (LVH) (expressed as LV mass indexed for height in meters2.7) was significantly more frequent in the obese group (48 vs. 0%, p < 0.001). LV longitudinal systolic function measured by mitral annular systolic velocity was significantly lower in the obese group (S' 8.5 vs. 9.7 cm/s, p = 0.002). All studied indices of the LV diastolic function (E/A, mean E' and E/E' ratio) were impaired in obese subjects, even after adjustment for systolic blood pressure and heart rate (E/A 1.31 vs. 1.64, p < 0.001, E' mean 11 vs. 14.8 cm/s, p < 0.001, E/E' 7.5 vs. 6.4, p = 0.002 for obese vs. controls, respectively).

Conclusions: LVH is significantly more common, and LV diastolic and longitudinal systolic function is significantly impaired in young, metabolically healthy, normotensive, severely obese individuals without fatty liver disease when compared to age and sex-matched lean subjects. These abnormalities may represent the independent effect of the obesity on the heart, which may contribute to the development the obesity-related HF in later life.