title: [External and internal electrical cardioversion: comparative, prospective evaluation of cell damage by means of troponin I].
abstract: OBJECTIVE
  In this study we measured the concentrations of cardiac troponin I (cTnI) and several biochemical markers of myocardial damage after elective external cardioversion or internal cardioversion by specific catheters or automatic defibrillators.
  
  
  METHODS
  Biochemical markers were analyzed prospectively for 30 consecutive patients after electrical cardioversion. Concentrations of cTnI, myoglobin, creatine kinase (CK), CK-MB and the MB/CK ratio were determined in samples before cardioversion and 2, 8 and 24 h later. The shock energy ranged from 50 to 360 joules (235 106 joules) in external cardioversions and from 3 to 37 joules (15 8 joules) in internal cardioversions.
  
  
  RESULTS
  We detected abnormal concentrations of CK, myoglobin, CK-MB and MB/CK in 33% of the patients after external cardioversion. The concentrations of cTnI remained within normal limits at all times, with no elevations detected. Whereas no abnormal concentration of any biochemical marker was detected in any patient who required internal cardioversion for atrial fibrillation, two patients who underwent external cardioversion from an automatic defibrillator did have abnormal concentrations of CK-MB, myoglobin, and even of cTnI.
  
  
  CONCLUSIONS
  The concentration of cTnI remained below the detection limit after external cardioversion, even though the other more non-specific markers changed. No enzyme alteration was detected in patients who underwent internal cardioversion of atrial fibrillation.
authors.affiliation: Servicios de Bioquímica Clínica, Hospital Ramón y Cajal, Universidad de Alcalá, Madrid, Spain.
authors.forename: José M
authors.initials: JM
authors.lastname: del Rey Sánchez
authors.forename: Antonio
authors.initials: A
authors.lastname: Hernández Madrid
authors.forename: José M
authors.initials: JM
authors.lastname: González Rebollo
authors.forename: Gonzalo
authors.initials: G
authors.lastname: Peña Pérez
authors.forename: Aníbal
authors.initials: A
authors.lastname: Rodríguez
authors.forename: Detelina
authors.initials: D
authors.lastname: Savova
authors.forename: Lucas
authors.initials: L
authors.lastname: Cano Calabria
authors.forename: Pedro
authors.initials: P
authors.lastname: Cabeza
authors.forename: José D
authors.initials: JD
authors.lastname: Cascón Pérez
authors.forename: Manuel
authors.initials: M
authors.lastname: Gómez Bueno
authors.forename: José
authors.initials: J
authors.lastname: Mercader
authors.forename: Eduardo
authors.initials: E
authors.lastname: Ripoll
authors.forename: Concepción
authors.initials: C
authors.lastname: Moro
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001281:Atrial Fibrillation / Q000628:therapy*; D015415:Biomarkers / Q000097:blood; D009202:Cardiomyopathies / Q000097:blood / Q000209:etiology* / Q000473:pathology*; D004554:Electric Countershock / Q000009:adverse effects* / Q000379:methods*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D019210:Troponin I / Q000097:blood*
chemical_list: D015415:Biomarkers; D019210:Troponin I