title: Left ventricular function impairment in patients with normal-weight obesity: contribution of abdominal fat deposition, profibrotic state, reduced insulin sensitivity, and proinflammatory activation.
abstract: BACKGROUND
  Obesity predisposes to left ventricular (LV) dysfunction and heart failure; however, the risk of these complications has not been assessed in patients with a normal body mass index (BMI) but increased body fat content (normal-weight obesity, NWO). We hypothesized that LV performance in NWO may be impaired and sought to investigate potential contributors to cardiac functional abnormalities.
  
  
  RESULTS
  One hundred sixty-eight subjects (age, 38±7 years) with BMI <25kg/m(2) and no history of any disease affecting the myocardium were classified on the basis of body fat content into 2 groups: with NWO and without NWO. Echocardiographic indices of LV systolic and diastolic function, including myocardial velocities and deformation, serological fibrosis markers, indicators of proinflammatory activation, and metabolic control, were evaluated. Subjects with NWO demonstrated impaired LV systolic and diastolic function, increased fibrosis intensity (assessed by procollagen type I carboxy-terminal propeptide [PICP]), impaired insulin sensitivity, and increased proinflammatory activation as compared with individuals with normal body fat. The independent correlates of LV systolic and diastolic function variables were as follows: for strain, IL-18 (β=-0.17, P<0.006), C-reactive protein (β=-0.20, P<0.002) and abdominal fat deposit (β=-0.20, P<0.003); for tissue S velocity, PICP (β=-0.21, P<0.002) and abdominal fat deposit (β=-0.43, P<0.0001); for tissue E velocity, abdominal fat deposit (β=-0.30, P<0.0001), PICP (β=-0.31, P<0.0001) and homeostasis model assessment of insulin resistance index (HOMA IR; β=-0.20, P<0.002); and for E/e'-PICP, IL-18 (both β=0.18, P<0.01) and HOMA IR (β=0.16, P<0.04).
  
  
  CONCLUSIONS
  In patients with NWO, subclinical disturbances of LV function are independently associated with the extent of abdominal fat deposit, profibrotic state (as reflected by circulating PICP), reduced insulin sensitivity, and proinflammatory activation.
authors.affiliation: Departments of Cardiology and Endocrinology, Wroclaw Medical University, Wroclaw, Poland. wojciech.kosmala@am.wroc.pl
authors.forename: Wojciech
authors.initials: W
authors.lastname: Kosmala
authors.forename: Diana
authors.initials: D
authors.lastname: Jedrzejuk
authors.forename: Roksolana
authors.initials: R
authors.lastname: Derzhko
authors.forename: Monika
authors.initials: M
authors.lastname: Przewlocka-Kosmala
authors.forename: Andrzej
authors.initials: A
authors.lastname: Mysiak
authors.forename: Grazyna
authors.initials: G
authors.lastname: Bednarek-Tupikowska
mesh_terms: D050153:Abdominal Fat / Q000473:pathology*; D000328:Adult; D015415:Biomarkers / Q000097:blood; D015992:Body Mass Index; D002097:C-Reactive Protein; D018618:Echocardiography, Doppler, Color / Q000379:methods; D005260:Female; D005355:Fibrosis; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology*; D006801:Humans; D056865:Ideal Body Weight; D007249:Inflammation / Q000097:blood / Q000150:complications* / Q000473:pathology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008297:Male; D009765:Obesity / Q000097:blood / Q000150:complications* / Q000473:pathology; D011446:Prospective Studies; D015203:Reproducibility of Results; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology*
chemical_list: D015415:Biomarkers; D007328:Insulin; D002097:C-Reactive Protein