title: Cardiac beta1-adrenoceptor autoantibodies in human heart disease: rationale and design of the Etiology, Titre-Course, and Survival (ETiCS) Study.
abstract: OBJECTIVE
  Evidence for a pathophysiologic relevance of autoimmunity in human heart disease has substantially increased over the past years. Conformational autoantibodies stimulating the cardiac beta1-adrenoceptor (beta1-aabs) are considered of importance in heart failure development and clinical pilot studies have shown their prognostic significance in human 'idiopathic' cardiomyopathy.
  
  
  METHODS
  We recently developed a novel highly sensitive fluorescence-based functional assay to detect stimulating beta1-aabs. We will use this method to assess Etiology, Titre-Course, and effect on Survival (ETiCS) of beta1-aabs in a prospective multicentre study with serial follow-up of patients after a first acute myocarditis or myocardial infarction. Several European core laboratories will jointly study the hypothesis that both disorders may trigger autoimmune reactions leading to the generation of beta1-aabs and/or other heart-directed aabs. Further, sera from healthy controls and well-characterized patient cohorts with dilated, ischaemic, or hypertensive cardiomyopathy will be analysed retrospectively for beta1-aab prevalence, incidence, persistence, and/or clearance.
  
  
  CONCLUSIONS
  ETiCS is so far the largest clinical diagnostic study projected to address cardiac autoimmunity. It attempts to unravel the pathophysiology of cardiac autoantibody formation and persistence/clearance. ETiCS will enhance current knowledge on autoimmunity in human heart disease and promote endeavours to develop novel therapies targeting cardiac aabs.
authors.affiliation: Department of Internal Medicine I, Centre of Cardiovascular Medicine, University of Würzburg, University Hospital Würzburg, Klinikstrasse 6-8, 97070 Würzburg, Germany.
authors.forename: Nikolas
authors.initials: N
authors.lastname: Deubner
authors.forename: Dominik
authors.initials: D
authors.lastname: Berliner
authors.forename: Angela
authors.initials: A
authors.lastname: Schlipp
authors.forename: Götz
authors.initials: G
authors.lastname: Gelbrich
authors.forename: Alida L P
authors.initials: AL
authors.lastname: Caforio
authors.forename: Stephan B
authors.initials: SB
authors.lastname: Felix
authors.forename: Michael
authors.initials: M
authors.lastname: Fu
authors.forename: Hugo
authors.initials: H
authors.lastname: Katus
authors.forename: Christiane E
authors.initials: CE
authors.lastname: Angermann
authors.forename: Martin J
authors.initials: MJ
authors.lastname: Lohse
authors.forename: Georg
authors.initials: G
authors.lastname: Ertl
authors.forename: Stefan
authors.initials: S
authors.lastname: Störk
authors.forename: Roland
authors.initials: R
authors.lastname: Jahns
mesh_terms: D000918:Antibody Specificity / Q000276:immunology; D001323:Autoantibodies / Q000276:immunology*; D015551:Autoimmunity / Q000276:immunology*; D002311:Cardiomyopathy, Dilated / Q000276:immunology*; D006801:Humans; D007118:Immunoassay / Q000379:methods; D015337:Multicenter Studies as Topic; D009203:Myocardial Infarction / Q000276:immunology*; D009205:Myocarditis / Q000276:immunology*; D009206:Myocardium / Q000276:immunology*; D018579:Patient Selection; D018342:Receptors, Adrenergic, beta-1 / Q000276:immunology*; D012107:Research Design
chemical_list: D001323:Autoantibodies; D018342:Receptors, Adrenergic, beta-1