title: Evidence of cardiac myolysis in severe nonischemic heart failure and the potential role of increased wall strain.
abstract: BACKGROUND
  Myocyte death could play a role in heart failure (HF) irrespective of the presence of coronary artery disease. The study aimed to assess this hypothesis by use of the cardiac troponin I (cTnI) assay.
  
  
  RESULTS
  Seventy-one patients with nonischemic HF, New York Heart Association (NYHA) class II-IV, with a normal coronary angiogram and after exclusion of myocardiopathies were evaluated in the study. The control group included 9 healthy subjects and 15 patients hospitalized for severe noncardiac dyspnea. Cardiac TnI concentrations were determined at admission with a research reagent (cTnIus) characterized by a detection limit of 0.026 ng/mL and a high analytic sensitivity of 0.002 ng/mL. cTnIus levels were more than 0.026 ng/mL in 19 HF patients, ranging between 0.027 and 0.463 ng/mL, whereas no cTnIus level was detectable in the control group. With use of a reference assay, only 2 HF patients had abnormal cTnI values. Severe HF was observed in 17 of these 19 patients, assessed by NYHA class IV or by the presence of pulmonary edema. Patients with an increased cTnIus level had a more restrictive mitral Doppler pattern (P <.001) and a more distinctive left ventricular (LV) concentric remodeling (P <.0001), whereas LV ejection fraction was similar in both HF groups. The increased cTnIus level was also associated with a LV wall strain biologic marker (ie, an increased brain natriuretic peptide plasma level) (P <.001).
  
  
  CONCLUSIONS
  cTnI assay is a promising biochemical method for detecting cardiac myolysis in HF, independent of the presence of coronary artery disease. This subtle myolysis could be in part related to the severely increased LV wall strain.
authors.affiliation: Department of Cardiology, Beaujon Hospital, 100 Bd Gal Leclerc, 92110 Clichy, France.
authors.forename: D
authors.initials: D
authors.lastname: Logeart
authors.forename: P
authors.initials: P
authors.lastname: Beyne
authors.forename: C
authors.initials: C
authors.lastname: Cusson
authors.forename: M
authors.initials: M
authors.lastname: Tokmakova
authors.forename: M
authors.initials: M
authors.lastname: Leban
authors.forename: C
authors.initials: C
authors.lastname: Guiti
authors.forename: P
authors.initials: P
authors.lastname: Bourgoin
authors.forename: A C
authors.initials: AC
authors.lastname: Solal
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D016923:Cell Death; D018450:Disease Progression; D015150:Echocardiography, Doppler; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D015592:Immunoradiometric Assay; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D020097:Natriuretic Peptide, Brain / Q000097:blood; D012720:Severity of Illness Index; D019210:Troponin I / Q000097:blood*; D016277:Ventricular Function, Left
chemical_list: D015415:Biomarkers; D019210:Troponin I; D020097:Natriuretic Peptide, Brain