title: Biochemical markers and cardiac troponin I release after radiofrequency catheter ablation: approach to size of necrosis.
abstract: BACKGROUND
  We designed this study to determine the value of serum levels of several cardiac markers in patients who underwent radiofrequency ablation and to establish the utility of cardiac troponin I (cTnI). After radiofrequency ablation there is always a small localized endomyocardial necrosis. The volume of the necrosis may be estimated by the rise of several biochemical marker levels, classically creatinine kinase (CK) and CK-MB. cTnI is a newly available biochemical marker with a high cardiac specificity.
  
  
  RESULTS
  We analyzed the data from 51 patients who underwent radiofrequency ablation and from 16 control patients who underwent an electrophysiologic study without ablation. The levels of CK, CK-MB mass, cTnI, and myoglobin were compared with clinical findings, ST-T wave abnormalities, and the presence of arrhythmias. The study shows that there is a higher release of cTnI compared with the standard markers CK, CK-MB, and myoglobin. A pathologic value of cTnI was found in 92% of the patients of the ablation group. CK-MB had a lower sensitivity (63%). The area under the receiver operating characteristic curve for cTnI was 0.9375, significantly superior to the other biochemical markers (P <.05). We found a moderate level of correlation between the number of radiofrequency pulses and cardiac cTnI release (r = 0.69, P <.0001).
  
  
  CONCLUSIONS
  The serum level of cTnI detects the minor myocardial damage produced by radiofrequency ablation. This would be useful information to have in patients who might have the potential for other ischemic events. The other biochemical or ablation parameters usually reported, including the radiofrequency ablation parameters, have no good correlation with the size of the myocardial necrosis. Therefore we suggest that monitoring of cTnI is the best way to detect and quantify the size of myocardial necrosis created by radiofrequency ablation.
authors.affiliation: Arrhythmia Unit and Clinical Biochemistry Department, Ramón y Cajal Hospital, Department of Medicine, Alcalá University. Madrid, Spain.
authors.forename: A H
authors.initials: AH
authors.lastname: Madrid
authors.forename: J M
authors.initials: JM
authors.lastname: del Rey
authors.forename: J
authors.initials: J
authors.lastname: Rubí
authors.forename: J
authors.initials: J
authors.lastname: Ortega
authors.forename: J M
authors.initials: JM
authors.lastname: González Rebollo
authors.forename: J G
authors.initials: JG
authors.lastname: Seara
authors.forename: E
authors.initials: E
authors.lastname: Ripoll
authors.forename: C
authors.initials: C
authors.lastname: Moro
mesh_terms: D000328:Adult; D001145:Arrhythmias, Cardiac / Q000097:blood* / Q000473:pathology / Q000628:therapy*; D015415:Biomarkers / Q000097:blood; D017115:Catheter Ablation; D003402:Creatine Kinase / Q000097:blood; D005260:Female; D006801:Humans; D007527:Isoenzymes; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D011446:Prospective Studies; D019210:Troponin I / Q000097:blood*
chemical_list: D015415:Biomarkers; D007527:Isoenzymes; D019210:Troponin I; D003402:Creatine Kinase