title: Marked elevation of myocardial trace elements in idiopathic dilated cardiomyopathy compared with secondary cardiac dysfunction.
abstract: OBJECTIVE
  We sought to investigate the possible pathogenetic role of myocardial trace elements (TE) in patients with various forms of cardiac failure.
  
  
  BACKGROUND
  Both myocardial TE accumulation and deficiency have been associated with the development of heart failure indistinguishable from an idiopathic dilated cardiomyopathy.
  
  
  METHODS
  Myocardial and muscular content of 32 TE has been assessed in biopsy samples of 13 patients (pts) with clinical, hemodynamic and histologic diagnosis of idiopathic dilated cardiomyopathy (IDCM), all without past or current exposure to TE. One muscular and one left ventricular (LV) endomyocardial specimen from each patient, drawn with metal contamination-free technique, were analyzed by neutron activation analysis and compared with 1) similar surgical samples from patients with valvular (12 pts) and ischemic (13 pts) heart disease comparable for age and degree of LV dysfunction; 2) papillary and skeletal muscle surgical biopsies from 10 pts with mitral stenosis and normal LV function, and 3) LV endomyocardial biopsies from four normal subjects.
  
  
  RESULTS
  A large increase (>10,000 times for mercury and antimony) of TE concentration has been observed in myocardial but not in muscular samples in all pts with IDCM. Patients with secondary cardiac dysfunction had mild increase (< or = 5 times) of myocardial TE and normal muscular TE. In particular, in pts with IDCM mean mercury concentration was 22,000 times (178,400 ng/g vs. 8 ng/g), antimony 12,000 times (19,260 ng/g vs. 1.5 ng/g), gold 11 times (26 ng/g vs. 2.3 ng/g), chromium 13 times (2,300 ng/g vs. 177 ng/g) and cobalt 4 times (86,5 ng/g vs. 20 ng/g) higher than in control subjects.
  
  
  CONCLUSIONS
  A large, significant increase of myocardial TE is present in IDCM but not in secondary cardiac dysfunction. The increased concentration of TE in pts with IDCM may adversely affect mitochondrial activity and myocardial metabolism and worsen cellular function.
authors.affiliation: Department of Cardiology, Catholic University, Rome, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Frustaci
authors.forename: N
authors.initials: N
authors.lastname: Magnavita
authors.forename: C
authors.initials: C
authors.lastname: Chimenti
authors.forename: M
authors.initials: M
authors.lastname: Caldarulo
authors.forename: E
authors.initials: E
authors.lastname: Sabbioni
authors.forename: R
authors.initials: R
authors.lastname: Pietra
authors.forename: C
authors.initials: C
authors.lastname: Cellini
authors.forename: G F
authors.initials: GF
authors.lastname: Possati
authors.forename: A
authors.initials: A
authors.lastname: Maseri
mesh_terms: D000328:Adult; D000368:Aged; D001706:Biopsy; D002311:Cardiomyopathy, Dilated / Q000097:blood* / Q000473:pathology; D004699:Endocardium / Q000378:metabolism / Q000473:pathology; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000473:pathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D012307:Risk Factors; D014131:Trace Elements / Q000097:blood*; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000473:pathology
chemical_list: D014131:Trace Elements