Pericardial fat, insulin resistance, and left ventricular structure and function in morbid obesity

Background and aim: Morbid obesity is often accompanied by insulin resistance and increased ectopic fat surrounding the heart. We evaluated the relation of epicardial and pericardial fat with insulin resistance and left ventricular (LV) structure and function. Methods and results: Epicardial and pericardial fat thicknesses were determined at 2-dimensional echocardiography in 80 morbid obese subjects [age 42 +/- 12 years, 31% men, body mass index (BMI) 44.4 +/- 7 kg/m(2)]. LV hypertrophy (LV mass >= 51 g/m(2.7)), inappropriately high LV mass for a given cardiac workload (observed vs predicted LV mass >128%), and stress-adjusted LV mid-wall fractional shortening were determined. Pericardial and epicardial fat thicknesses had direct associations with BMI (r = 0.40 and 0.45, both p < 0.01) and waist circumference (r = 0.37 and 0.45, both p < 0.01). Pericardial (partial r = 0.35, p < 0.01), but not epicardial fat thickness (partial r = 0.05, p = n.s.), was correlated with homeostasis model assessment-insulin resistance after adjustment for BMI. Pericardial fat also had a strong negative correlation with mid-wall fractional shortening (p = 0.01) and a positive one with inappropriately high LV mass (p < 0.01), while no such relation was found for epicardial fat (both p = n.s.). Independently of age, male sex, BMI, and anti-hypertensive treatment, pericardial fat thickness had an independent positive association with inappropriately high LV mass (beta = 0.29, p = 0.02), and a negative one with stress-adjusted mid-wall fractional shortening (beta = -0.26, p = 0.04). Conclusions: Pericardial fat thickness is associated with insulin resistance, inappropriately high LV mass, and LV systolic dysfunction in obese individuals. Findings from this study confirm the existence of a connection between insulin resistance, cardiac ectopic fat deposition and cardiac dysfunction in morbid obesity. (C) 2013 Elsevier B. V. All rights reserved.