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

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Abstract

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/m2]. LV hypertrophy (LV mass ≥51 g/m2.7), 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 (β = 0.29, p = 0.02), and a negative one with stress-adjusted mid-wall fractional shortening (β = −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.

Section snippets

Subjects

From November 2010 to December 2012 a total of 121 consecutive patients with morbid obesity (mean age 43 ± 13 years, 35% men, 43.9 ± 7 kg/m2) were referred to the Unit of Internal Medicine, Angiology and Atherosclerosis of Perugia University for a comprehensive cardiovascular and metabolic assessment. All of them were potential candidates for bariatric surgery according to the National Institutes of Health Consensus Development criteria [16].

We excluded from the study patients with known

Results

Clinical, anthropometric and echocardiographic characteristics of the study population (n = 80) are reported in Table 1. Fifty-three patients (66%) had a BMI above 40 kg/m2, and 43 (54%) were hypertensive. Average systolic/diastolic BP was 136/84 ± 18/11 mmHg. A sizeable proportion of the population (64%) had HOMA-IR values ≥2.6.

Discussion

Results from our study show that in a population of middle-aged subjects with morbid obesity, pericardial and epicardial fat thicknesses at echocardiography were differently related to measures of adiposity, insulin sensitivity and measures of cardiac structure and function. While both epicardial and pericardial fat thicknesses were associated with BMI and waist circumference, only pericardial fat thickness showed a relationship with insulin resistance. The relationship of pericardial fat

Funding source

None.

Potential conflict of interest

None.

References (38)

  • M. Chinali et al.

    Impact of obesity on cardiac geometry and function in a population of adolescents: the Strong Heart Study

    J Am Coll Cardiol

    (2006)
  • T. Owan et al.

    Favorable changes in cardiac geometry and function following gastric bypass surgery: 2-year follow-up in the Utah obesity study

    J Am Coll Cardiol

    (2011)
  • R. Sicari et al.

    Pericardial rather than epicardial fat is a cardiometabolic risk marker: an MRI vs echo study

    J Am Soc Echocardiogr

    (2011)
  • A. Celentano et al.

    Inappropriate left ventricular mass in normotensive and hypertensive patients

    Am J Cardiol

    (2001)
  • Health, United States

    (2010)
  • T. Pischon et al.

    General and abdominal adiposity and risk of death in Europe

    N Engl J Med

    (2008)
  • K.A. Britton et al.

    Ectopic fat depots and cardiovascular disease

    Circulation

    (2011)
  • S.R. Preis et al.

    Abdominal subcutaneous and visceral adipose tissue and insulin resistance in the Framingham heart study

    Obesity (Silver Spring)

    (2010)
  • B. Gaborit et al.

    Assessment of epicardial fat volume and myocardial triglyceride content in severely obese subjects: relationship to metabolic profile, cardiac function and visceral fat

    Int J Obes (Lond)

    (2012)
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