title: Type of desmin expression in cardiomyocytes - a good marker of heart failure development in idiopathic dilated cardiomyopathy.
abstract: OBJECTIVE
  The aim of this study was to determine whether remodelling of the desmin (DES) cytoskeleton affects myocardial function and whether it could be a useful marker of disease progression in patients with idiopathic dilated cardiomyopathy (IDCM).
  
  
  METHODS
  Endomyocardial biopsy was performed in 195 IDCM patients, and five to six specimens were collected from the left ventricle. DES expression was evaluated using tissue immunostaining and Western blotting. The study population was assigned to four groups according to DES expression type: I, normal DES staining at Z-lines giving a regular pattern of cross-striation (n = 57); IIA, increased DES staining with a regular pattern of cross-striation (n = 40); IIB, increased DES staining with an irregular pattern of cross-striation and/or the presence of aggregates (n = 56); and III, decreased/lack of DES staining (n = 42). Fibrosis, cardiomyocyte hypertrophy and ultrastructure were assessed for the four types of DES expression.
  
  
  RESULTS
  The pathological types of DES expression (IIB or III) were associated with pathological changes in mitochondria and the contractile apparatus. Cardiomyocyte diameter and level of fibrosis were both significantly affected. DES expression type correlated with NYHA class, left ventricular end-diastolic diameter, left ventricular ejection fraction and the level of N-terminal pro-brain natriuretic protein.
  
  
  CONCLUSIONS
  The type of immunohistochemical DES expression correlated with the level of myocardial injury at the cellular and organ levels. This correlation was similar to that observed between DES expression and the well-established biochemical, echocardiographic and clinical parameters of heart failure (HF). DES expression type could be used as an important diagnostic feature of HF development.
authors.affiliation: Department of Invasive Cardiology, Central Clinical Hospital of Ministry of Internal Affairs and Administration, Warsaw, Poland. a.pawlak1@wp.pl
authors.forename: A
authors.initials: A
authors.lastname: Pawlak
authors.forename: R J
authors.initials: RJ
authors.lastname: Gil
authors.forename: T
authors.initials: T
authors.lastname: Kulawik
authors.forename: M
authors.initials: M
authors.lastname: Pronicki
authors.forename: A
authors.initials: A
authors.lastname: Karkucińska-Więckowska
authors.forename: T
authors.initials: T
authors.lastname: Szymańska-Dębińska
authors.forename: K
authors.initials: K
authors.lastname: Gil
authors.forename: N
authors.initials: N
authors.lastname: Lagwinski
authors.forename: E
authors.initials: E
authors.lastname: Czarnowska
mesh_terms: D015415:Biomarkers / Q000378:metabolism; D001706:Biopsy; D002311:Cardiomyopathy, Dilated / Q000378:metabolism*; D003893:Desmin / Q000378:metabolism*; D003971:Diastole; D004699:Endocardium / Q000473:pathology; D005260:Female; D005355:Fibrosis / Q000473:pathology; D006333:Heart Failure / Q000209:etiology*; D006801:Humans; D007150:Immunohistochemistry; D016014:Linear Models; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D008928:Mitochondria / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D020097:Natriuretic Peptide, Brain / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D013194:Staining and Labeling; D013318:Stroke Volume
chemical_list: D015415:Biomarkers; D003893:Desmin; D010446:Peptide Fragments; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain