title: Detection of myocardial injury after internal cardioversion for atrial fibrillation.
abstract: BACKGROUND
  Cardiac troponin levels do not rise to marked levels after external cardioversion of atrial fibrillation. Subsequent test discharges during implantation of cardioverter defibrillators may cause an elevation of cardiac troponin levels, but are still controversial.
  
  
  OBJECTIVE
  To determine whether the biomarkers of cardiac injury increase after internal cardioversion (IC) of atrial fibrillation.
  
  
  METHODS
  Forty-four patients with chronic atrial fibrillation were studied (mean age 59 +/-7 years). Electrode catheters were inserted through the femoral vein. One of these was positioned in the lower right atrium. A second defibrillation electrode was placed in the coronary sinus and an additional catheter was positioned in the right ventricular apex in order to obtain satisfactory R wave synchronization and to provide postshock ventricular pacing. The shocks were delivered by external defibrillator. Starting with a test shock of 1 J intensity, the energy was increased in steps (to maximum 15 J) until cardioversion was achieved. At least 1 min was permitted to elapse between unsuccessful defibrillation attempts before the next shock was applied. Blood samples for serum levels of cardiac troponin T, cardiac troponin I, creatine kinase MB and myoglobin were drawn before and 2 h, 4 h, 8 h and 24 h after IC. Each level of biomarker was compared with baseline.
  
  
  RESULTS
  In 40 of 44 patients, IC was successful at a mean cardioversion threshold of 7.6+/-3.3 J. Although the serum levels of these biomarkers tended to rise, marked elevation was not detected in any of samples (P>0.05 for each). There was no correlation between the levels of biomarkers and the number and energy of shocks applied. No severe complications were observed.
  
  
  CONCLUSIONS
  Following uncomplicated IC of atrial fibrillation, cardiac biomarkers do not rise to marked levels, which indicates that significant myocardial injury does not occur by shocks in the usual dosage.
authors.affiliation: Department of Cardiology, Osmangazi University School of Medicine, Eskisehir, Turkey. bgorenek@hotmail.com
authors.forename: B
authors.initials: B
authors.lastname: Gorenek
authors.forename: G
authors.initials: G
authors.lastname: Kudaiberdieva
authors.forename: O
authors.initials: O
authors.lastname: Goktekin
authors.forename: Y
authors.initials: Y
authors.lastname: Cavusoglu
authors.forename: A
authors.initials: A
authors.lastname: Birdane
authors.forename: N
authors.initials: N
authors.lastname: Ata
authors.forename: A
authors.initials: A
authors.lastname: Unalir
authors.forename: B
authors.initials: B
authors.lastname: Timuralp
mesh_terms: D000368:Aged; D001281:Atrial Fibrillation / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D015415:Biomarkers / Q000097:blood; D002908:Chronic Disease; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D004554:Electric Countershock; D005260:Female; D006801:Humans; D007527:Isoenzymes / Q000097:blood; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood / Q000175:diagnosis* / Q000209:etiology*; D009211:Myoglobin / Q000097:blood; D013223:Statistics as Topic; D013318:Stroke Volume / Q000502:physiology; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood; D020107:Troponin T / Q000097:blood
chemical_list: D015415:Biomarkers; D007527:Isoenzymes; D009211:Myoglobin; D019210:Troponin I; D020107:Troponin T; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form