title: Coronary endothelial dysfunction and myocardial cell damage in chronic stable idiopathic dilated cardiomyopathy.
abstract: Impairment of endothelium-dependent vasodilatation in response to acetylcholine reflects an abnormal endothelial function. Labelled indium-111 monoclonal antimyosin antibodies enable detection of myocardial cell damage. We analysed whether endothelial dysfunction correlates with myocardial antimyosin uptake in a selected group of patients with idiopathic dilated cardiomyopathy.
  
  
  METHODS
  Twenty-two consecutive patients with chronic stable idiopathic dilated cardiomyopathy (18 males and four females) were included. The duration of heart failure symptoms was 46+/-34 months. At inclusion, the functional class of New York Heart Association was 2.1+/-0.7. Endothelial function was evaluated using intracoronary graded concentrations of acetylcholine. Vasomotor responses of the left anterior descending coronary artery were measured by quantitative coronary analysis. Myocardial uptake of antimyosin antibodies was quantified by means of a heart-to-lung ratio (HLR).
  
  
  RESULTS
  Eighteen patients showed endothelial dysfunction (82%) and the remaining four patients showed a normal endothelial function. There were no statistically significant differences between patients with and without endothelial dysfunction in relation to clinical, echocardiographic and hemodynamic parameters. In addition, these variables did not correlate with the magnitude of the vasomotor response to acetylcholine. Eighteen patients (82%) showed abnormal antimyosin uptake; 15 of them (83%) showed endothelial dysfunction. The global mean HLR of antimyosin uptake was 1.73+/-0.24. The coronary vasomotor response to acetylcholine correlated with the intensity of uptake of antimyosin antibodies (r=-0.45, P<0.04).
  
  
  CONCLUSIONS
  Coronary endothelial dysfunction and myocardial antimyosin uptake was found in a high percentage of patients with chronic stable idiopathic dilated cardiomyopathy. The abnormal vasomotor response seems to be related to the degree of myocardial damage.
authors.affiliation: Hemodynamic Unit, Hospital de la Santa Creu i Sant Pau, Sant Antoni M. Claret 167, 08025 Barcelona, Spain. 18461vmc@comb.es
authors.forename: Vicens
authors.initials: V
authors.lastname: Martí
authors.forename: Rosa
authors.initials: R
authors.lastname: Aymat
authors.forename: Manel
authors.initials: M
authors.lastname: Ballester
authors.forename: Joan
authors.initials: J
authors.lastname: García
authors.forename: Ignasi
authors.initials: I
authors.lastname: Carrió
authors.forename: Josep M
authors.initials: JM
authors.lastname: Augé
mesh_terms: D000911:Antibodies, Monoclonal; D002311:Cardiomyopathy, Dilated / Q000000981:diagnostic imaging*; D002908:Chronic Disease; D017023:Coronary Angiography; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging* / Q000503:physiopathology; D005260:Female; D006321:Heart / Q000000981:diagnostic imaging*; D006439:Hemodynamics; D006801:Humans; D007205:Indium Radioisotopes; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D009942:Organometallic Compounds; D011877:Radionuclide Imaging
chemical_list: D000911:Antibodies, Monoclonal; D007205:Indium Radioisotopes; D009942:Organometallic Compounds; C058899:imciromab pentetate