title: Gene expression profiling from endomyocardial biopsy tissue allows distinction between subentities of dilated cardiomyopathy.
abstract: OBJECTIVE
  Expression profile analysis using endomyocardial biopsy specimens from patients with cardiomyopathies promises to improve the differential diagnosis of heart failure.
  
  
  METHODS
  In this study, left ventricular endomyocardial biopsy specimens were obtained from 50 patients and histopathologically classified according to the World Heart Federation Task Force criteria as having dilated cardiomyopathy (n = 17), inflammatory cardiomyopathy (n = 11), myocarditis (n = 15), or pericarditis (n = 7). Microarrays were performed by hybridization of synthesized complementary DNA against a Lab-Arraytor60-combi microarray (SIRS-Lab, Jena, Switzerland). Differentially expressed genes were clustered hierarchically according to their variation in hybridization signals.
  
  
  RESULTS
  In samples from patients with dilated cardiomyopathy, two different types of gene expression profiles were distinguishable. One pattern was unique for dilated cardiomyopathy and inflammatory cardiomyopathy, respectively, and the other more closely resembled that seen in samples from inflammatory heart disease. Additionally, we confirmed the microarray data by showing that dilated cardiomyopathy is associated with a reduced myocardial toll-like receptor 9 expression that resulted from progressive loss of functional cardiomyocytes. Taken together, our data demonstrate the utility and validity of microarrays from endomyocardial biopsy specimens in detecting subentities of dilated cardiomyopathy that do not differ histopathologically, but transcriptionally, from each other. The gene expression profile observed in one subgroup of patients with dilated cardiomyopathy is indicative of ongoing immune activation, albeit infiltrating immunocompetent cells were not detected histopathologically.
  
  
  CONCLUSIONS
  Thus, our transcriptional data indicate that dilated cardiomyopathy constitutes a heterogeneous disease with an broad overlap to inflammatory heart disease.
authors.affiliation: Department of Cardiology, University of Marburg, Baldingerstrasse, Marburg, Germany.
authors.forename: Volker
authors.initials: V
authors.lastname: Ruppert
authors.forename: Thomas
authors.initials: T
authors.lastname: Meyer
authors.forename: Sabine
authors.initials: S
authors.lastname: Pankuweit
authors.forename: Eva
authors.initials: E
authors.lastname: Möller
authors.forename: Reinhard C
authors.initials: RC
authors.lastname: Funck
authors.forename: Wolfram
authors.initials: W
authors.lastname: Grimm
authors.forename: Bernhard
authors.initials: B
authors.lastname: Maisch
mesh_terms: D000328:Adult; D001707:Biopsy, Needle; D017252:CD3 Complex / Q000032:analysis; D015704:CD4 Antigens / Q000032:analysis*; D002311:Cardiomyopathy, Dilated / Q000175:diagnosis / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D003937:Diagnosis, Differential; D005260:Female; D020869:Gene Expression Profiling; D006333:Heart Failure / Q000209:etiology; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009205:Myocarditis / Q000175:diagnosis / Q000235:genetics; D010493:Pericarditis / Q000175:diagnosis / Q000235:genetics; D010496:Pericardium / Q000378:metabolism / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology; D051217:Toll-Like Receptor 9 / Q000096:biosynthesis / Q000235:genetics
chemical_list: D017252:CD3 Complex; D015704:CD4 Antigens; D051217:Toll-Like Receptor 9