title: Cardiac biochemical markers after cardioversion of atrial fibrillation or atrial flutter.
abstract: BACKGROUND
  Cardioversion or defibrillation of cardiac arrhythmias is often necessary in acutely ill cardiac patients. The electrical current may cause elevation of biochemical markers used to diagnose acute myocardial infarction. Therefore it is important to find cardiac markers with high specificity for myocardial necrosis. The purpose of this study was to assess the effects of elective cardioversion of atrial fibrillation or flutter on troponin T and I among conventional markers in patients with no evidence of acute ischemia.
  
  
  RESULTS
  Fifty-seven consecutive patients underwent 1 to 4 direct current shocks (mean cumulative energy 407 J, range 100 to 920 J) under general anesthesia. At baseline, all had normal troponin levels; 50 patients (mean age 68 years, range 33 to 84 years) had normal cardiac enzymes and were included in the final analysis. Blood samples were drawn at baseline, and 1 to 2, 6 to 8, and 20 to 24 hours after cardioversion. The troponin levels were unaffected by cardioversion in all patients, whereas creatine kinase and myoglobin increased more than 10-fold. Creatine kinase MB mass and aspartate aminotransferase were above reference limits in 18% and 24% of patients, respectively, 20 to 24 hours after cardioversion. There was a significant association between elevated creatine kinase, myoglobin, and creatine kinase MB levels with cumulated energy delivered as well as when possible confounders such as age and sex were adjusted for. High international normalized ratio with warfarin use was associated with increased levels of creatine kinase, aspartate aminotransferase, lactate dehydrogenase, and myoglobin.
  
  
  CONCLUSIONS
  The increase of conventional biochemical markers after direct current cardioversion is positively associated with cumulative energy delivered and international normalized ratio (INR) values; neither influences levels of the cardiac troponins.
authors.affiliation: Haukeland University Hospital, Bergen, Norway. vike@haukeland.no
authors.forename: K
authors.initials: K
authors.lastname: Vikenes
authors.forename: P
authors.initials: P
authors.lastname: Omvik
authors.forename: M
authors.initials: M
authors.lastname: Farstad
authors.forename: J E
authors.initials: JE
authors.lastname: Nordrehaug
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001281:Atrial Fibrillation / Q000097:blood* / Q000503:physiopathology / Q000628:therapy; D001282:Atrial Flutter / Q000097:blood* / Q000503:physiopathology / Q000628:therapy; D015415:Biomarkers / Q000097:blood; D003402:Creatine Kinase / Q000097:blood*; D004554:Electric Countershock; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D009211:Myoglobin / Q000097:blood*; D011379:Prognosis; D011446:Prospective Studies; D014336:Troponin / Q000097:blood*
chemical_list: D015415:Biomarkers; D009211:Myoglobin; D014336:Troponin; D003402:Creatine Kinase