PMID- 11174339
OWN - NLM
STAT- MEDLINE
DCOM- 20010329
LR  - 20161124
IS  - 0002-8703 (Print)
IS  - 0002-8703 (Linking)
VI  - 141
IP  - 2
DP  - 2001 Feb
TI  - Evidence of cardiac myolysis in severe nonischemic heart failure and the 
      potential role of increased wall strain.
PG  - 247-53
AB  - 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. METHODS AND 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.
FAU - Logeart, D
AU  - Logeart D
AD  - Department of Cardiology, Beaujon Hospital, 100 Bd Gal Leclerc, 92110 Clichy, 
      France.
FAU - Beyne, P
AU  - Beyne P
FAU - Cusson, C
AU  - Cusson C
FAU - Tokmakova, M
AU  - Tokmakova M
FAU - Leban, M
AU  - Leban M
FAU - Guiti, C
AU  - Guiti C
FAU - Bourgoin, P
AU  - Bourgoin P
FAU - Solal, A C
AU  - Solal AC
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am Heart J
JT  - American heart journal
JID - 0370465
RN  - 0 (Biomarkers)
RN  - 0 (Troponin I)
RN  - 114471-18-0 (Natriuretic Peptide, Brain)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Biomarkers/blood
MH  - Cell Death
MH  - Disease Progression
MH  - Echocardiography, Doppler
MH  - Female
MH  - Heart Failure/*blood/diagnostic imaging/pathology/physiopathology
MH  - Heart Ventricles/diagnostic imaging/metabolism/physiopathology
MH  - Humans
MH  - Immunoradiometric Assay
MH  - Male
MH  - Middle Aged
MH  - Myocardium/*metabolism/pathology
MH  - Natriuretic Peptide, Brain/blood
MH  - Severity of Illness Index
MH  - Troponin I/*blood
MH  - Ventricular Function, Left
EDAT- 2001/02/15 11:00
MHDA- 2001/04/03 10:01
CRDT- 2001/02/15 11:00
PHST- 2001/02/15 11:00 [pubmed]
PHST- 2001/04/03 10:01 [medline]
PHST- 2001/02/15 11:00 [entrez]
AID - S0002-8703(01)10833-1 [pii]
AID - 10.1067/mhj.2001.111767 [doi]
PST - ppublish
SO  - Am Heart J. 2001 Feb;141(2):247-53. doi: 10.1067/mhj.2001.111767.