title: Leptin, a novel predictor of lung function in heart failure.
abstract: BACKGROUND
  Leptin is a protein hormone produced by adipose tissue. Leptin has proinflammatory properties and is usually elevated in patients with chronic heart failure. We assessed if serum leptin relates to the loss in lung function in noncachectic patients with chronic heart failure.
  
  
  METHODS
  One hundred thirty-five consecutively eligible non-Hispanic white subjects (age, 24 to 79 years; 85 men and 50 women) with a diagnosis of stable systolic heart failure were recruited prospectively, along with 106 matched control subjects. FVC, FEV(1), and single-breath diffusing capacity of the lung for carbon monoxide (DLco) were measured by spirometry. Plasma leptin was measured by radioimmunoassay. Multiple linear regression was applied.
  
  
  RESULTS
  The relationships of FEV(1), FVC, and DLco with leptin differed significantly between heart failure and control subjects after controlling for age, sex, percentage of body fat, and ejection fraction. In heart failure, leptin was as an independent predictor of FVC values (additional R(2) = 0.05, p < 0.0001), FEV(1) values (additional R(2) = 0.05, p < 0.0001), and DLco values (additional R(2) = 0.14, p < 0.0001). In a final multiple regression model predicting lung function in heart failure, the independent effect of leptin was significant after further adjustments.
  
  
  CONCLUSIONS
  The predictive information provided by leptin is additive to that provided by measures of body fat in heart failure patients, especially for DLco. Leptin may play a role in the impairment of lung function in subjects with heart failure.
authors.affiliation: Atherosclerosis Research Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Justo
authors.initials: J
authors.lastname: Sierra-Johnson
authors.affiliation: Division of Cardiovascular Diseases, Department of Internal Medicine, and the Division of Biostatistics, Department of Health Sciences Research, Mayo Clinic and Foundation, Rochester MN.
authors.forename: Abel
authors.initials: A
authors.lastname: Romero-Corral
authors.affiliation: Division of Cardiovascular Diseases, Department of Internal Medicine, and the Division of Biostatistics, Department of Health Sciences Research, Mayo Clinic and Foundation, Rochester MN.
authors.forename: Virend K
authors.initials: VK
authors.lastname: Somers
authors.affiliation: Division of Cardiovascular Diseases, Department of Internal Medicine, and the Division of Biostatistics, Department of Health Sciences Research, Mayo Clinic and Foundation, Rochester MN.
authors.forename: Lyle J
authors.initials: LJ
authors.lastname: Olson
authors.affiliation: Division of Cardiovascular Diseases, Department of Internal Medicine, and the Division of Biostatistics, Department of Health Sciences Research, Mayo Clinic and Foundation, Rochester MN. Electronic address: johnson.bruce@mayo.edu.
authors.forename: Bruce D
authors.initials: BD
authors.lastname: Johnson
mesh_terms: D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D006333:Heart Failure / Q000097:blood* / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D020738:Leptin / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D011446:Prospective Studies; D011653:Pulmonary Diffusing Capacity / Q000502:physiology; D012307:Risk Factors; D014797:Vital Capacity / Q000502:physiology
chemical_list: D020738:Leptin