title: [Electrical cardioversion and myocardial injury: evaluation by new cardiac injury markers].
abstract: OBJECTIVE
  Evaluate, based on the evolution of new biochemical markers of cardiac damage, if electrical cardioversion (ECV) causes myocardial injury.
  
  
  METHODS
  Seventy-six patients (P) submitted to elective ECV for atrial fibrillation or atrial flutter were evaluated. Creatine phosphokinase (CPK), CK-MB activity, CK-MB mass, myoglobin and cardiac troponin I (cTnI) were measured before, and 6 and 24 hours after ECV.
  
  
  RESULTS
  ECV was successful in 58 P (76.3%). Cumulative energy (CE) was up to 350 joules (J) in 36 P, from 500 to 650 J in 20 P and from 900 to 960 J in 20 P; the mean energy delivered being 493 J (+/- 309). The levels of cTnI remained within normal limits in all 76 P. The increase of cumulative energy led to an elevation of CPK levels (> p value = 0.007), CK-MB activity (> p value = 0.002), CK-MB mass (> p value = 0.03), and myoglobin (> p value = 0.015). A positive correlation between the cumulative energy and CPK peaks was observed (r = 0.660; p < 0.001), CK-MB activity (r = 0.429; p < 0.0001), CK-MB mass (r = 0.265; p = 0.02), and myoglobin (r = 0.684; p < 0.0001), as well as between the number of shocks and the CPK peaks (r = 0.770; p < 0.001), CK-MB activity (r = 0.642; p < 0.0001), CK-MB mass (r = 0.430; p < 0.0001), and myoglobin (r = 0.745; p < 0.0001).
  
  
  CONCLUSIONS
  ECV does not cause myocardial injury detectable by cTnI measurement. Elevations of CPK, CK-MB activity, CK-MB mass and myoglobin result from skeletal muscle injury and are positively correlated with the CE delivered or with the number of shocks.
authors.affiliation: Instituto Dante Pazzanese de Cardiologia, São Paulo, SP. elizabetssantos@cardiol.br
authors.forename: Elizabete Silva dos
authors.initials: ES
authors.lastname: Santos
authors.forename: Marcos Paulo
authors.initials: MP
authors.lastname: Pereira
authors.forename: Luiz
authors.initials: L
authors.lastname: Minuzzo
authors.forename: Dalmo A R
authors.initials: DA
authors.lastname: Moreira
authors.forename: Rui
authors.initials: R
authors.lastname: Ramos
authors.forename: Alvaro
authors.initials: A
authors.lastname: Avezum
authors.forename: Ari
authors.initials: A
authors.lastname: Timerman
authors.forename: Leopoldo S
authors.initials: LS
authors.lastname: Piegas
mesh_terms: D000704:Analysis of Variance; D001281:Atrial Fibrillation / Q000628:therapy; D001282:Atrial Flutter / Q000628:therapy; D015415:Biomarkers / Q000097:blood; D052279:Creatine Kinase, MB Form / Q000097:blood*; D004554:Electric Countershock / Q000009:adverse effects*; D005260:Female; D006335:Heart Injuries / Q000097:blood / Q000209:etiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009211:Myoglobin / Q000097:blood*; D013997:Time Factors; D019210:Troponin I / Q000097:blood*
chemical_list: D015415:Biomarkers; D009211:Myoglobin; D019210:Troponin I; D052279:Creatine Kinase, MB Form