title: Integrated backscatter as a fibrosis marker in the metabolic syndrome: association with biochemical evidence of fibrosis and left ventricular dysfunction.
abstract: OBJECTIVE
  Myocardial fibrosis is an important contributor to heterogeneity of left ventricular (LV) dysfunction in the metabolic syndrome (MS). Comparison of strain with calibrated integrated backscatter (cIB) and serological fibrosis markers could provide a means to understand the association of cardiac function with markers of fibrosis.
  
  
  RESULTS
  We studied 172 patients with MS (age 50 ± 13 years) and 61 healthy controls in a prospective, cross-sectional study. Echocardiographic evaluation included myocardial velocities and deformation, and calibrated cIB. Procollagen type III amino-terminal propeptide (PIIINP) and procollagen type I carboxy-terminal propeptide (PICP) were measured from serum. MS patients demonstrated LV systolic and diastolic function, and myocardial echodensity disturbances, as well as elevated serum PIIINP and PICP levels. For most functional variables, calibrated cIB in the basal septum was the strongest determinant of impaired LV performance, independent of higher procollagen levels, LV mass index, age, body mass index, creatinine level, and C-reactive protein. Patients with increased abdominal fat deposit (assessed by the waist-to-hip ratio) presented higher levels of procollagen peptides and septal calibrated cIB, and with more profound LV dysfunction as indicated by lower myocardial deformation and early diastolic velocity, and higher E/e'.
  
  
  CONCLUSIONS
  Myocardial echodensity is a stronger correlate of LV systolic and diastolic dysfunction in MS, than circulating procollagen peptides. Both fibrosis and LV function abnormalities are increased at a higher waist-to-hip ratio, which might provide a rationale for the implementation of intensified therapy in this subset of patients.
authors.affiliation: Department of Cardiology, Wroclaw Medical University, Borowska 213, Wroclaw, Poland.
authors.forename: Wojciech
authors.initials: W
authors.lastname: Kosmala
authors.forename: Monika
authors.initials: M
authors.lastname: Przewlocka-Kosmala
authors.forename: Anna
authors.initials: A
authors.lastname: Wojnalowicz
authors.forename: Andrzej
authors.initials: A
authors.lastname: Mysiak
authors.forename: Thomas H
authors.initials: TH
authors.lastname: Marwick
mesh_terms: D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D003404:Creatinine / Q000097:blood; D003430:Cross-Sectional Studies; D015150:Echocardiography, Doppler / Q000379:methods*; D005260:Female; D005355:Fibrosis; D006801:Humans; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology; D010446:Peptide Fragments / Q000097:blood; D011347:Procollagen / Q000097:blood; D011446:Prospective Studies; D012044:Regression Analysis; D018487:Ventricular Dysfunction, Left / Q000097:blood* / Q000000981:diagnostic imaging* / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D010446:Peptide Fragments; D011347:Procollagen; C041876:procollagen Type III-N-terminal peptide; C042813:procollagen type I carboxy terminal peptide; D002097:C-Reactive Protein; D003404:Creatinine