ABSTRACT
INTRODUCTION AND OBJECTIVES: Radiofrequency catheter ablation is the curative treatment of choice for many cardiac arrhythmias. After radiofrequency ablation there is always a localized endomyocardial necrosis, which is necessary to eliminate the arrhythmia. The volume of the necrosis may be evaluated by the rise of several biochemical markers, classically CK and CK-MB. However, the sensitivity and specificity of these markers are not optimal and are probably less than ideal for this purpose. Cardiac Troponin I (cTnI) is a newly available biochemical marker available, with a high cardiac specificity. We designed this study in order to determine the value of serum levels of several cardiac markers in patients who underwent radiofrequency catheter ablation and to establish the utility of cTnI. METHODS: We analyzed the data from 51 patients who underwent radiofrequency ablation and from 16 control patients. In respect to the ablation target, we included in the study 14 left accessory pathways, 7 right accessory pathways, 12 atrioventricular nodal reentry tachycardia, 5 ventricular tachycardia and 13 atrial flutter or fibrillation. The levels of CK, CK-MB, cTnI, and myoglobin were compared with clinical findings, ST-T wave abnormalities and the presence of arrhythmias after ablation. To evaluate the diagnostic capability for each biochemical marker we used the ROC curves. RESULTS: A pathological value of cTnI was found in 47 out of 51 (92%) patients in the ablation group. CK-MB had a lower sensitivity (63%). The sensitivity for the other biochemical markers ranged from 30% for CK to 67% for Myoglobin. The area under the ROC curve for cTnI was 0.9375, significantly superior to the other biochemical markers (0.86, 0.76, 0.75 for MB, Myoglobin, CK respectively) (p < 0.05). The lowest cTnI released was found in patients after nodal reentry tachycardia ablation and the highest after atrial flutter ablation. cTnI increased above normal values in 4 patients in the control group (patients who underwent an electrophysiological study without catheter ablation). We found a moderate level of correlation between the number of radiofrequency pulses and cardiac cTnI release (r = 0.69; p < 0.0001). The correlation was different in each target, ranging between r = 0.25 (p = NS, 0.43) for atrial flutter and fibrillation to r = 0.99 (p < 0.0001) for ventricular tachycardia. CONCLUSIONS: cTnI had the greatest sensitivity (92%) for detecting minor myocardial damage. Thus, we can conclude that the serum level of cTnI detects the minor myocardial damage produced by radiofrequency ablation.