[Changes in myocardial damage markers after radiofrequency ablation in patients with arrhythmias]

Klin Lab Diagn. 2002 Jul:(7):3-5.
[Article in Russian]

Abstract

The aim of this study was to evaluate myocardial cell damage after radiofrequency ablation (RFA), one of the most effective methods for the treatment of arrhythmias. Thirty patients aged 30.4 +/- 8.6 years were examined. Biochemical parameters were evaluated repeatedly 6-18 h after RFA. Positive troponin T (Tn-T) test and increased CK-Mb activity (p < 0.22) were observed in 8 patients (group 1), while in group II Tn-T test was negative. Biochemical findings in group I correlated with the results of ECG body surface mapping (STT) (negative area), duration and number of RFA lesions. Myocardial damage was detected using 3 cardiac markers: myo/CK-Mb and Tn-T. These testing should be carried out in due time repeatedly, in order to catch the STT maps and biochemical parameters were in high correlation after RFA. Presumably, T-wave abnormalities in Tn-T-negative group after RFA were due to the cardiac memory phenomenon. Myo/CK-Mb after RFA in Tn-T-positive group coincided with that in acute myocardial infarction. Hence, myocardial damage after RFA can be confirmed by the Tn-T test, which is helpful in the differential diagnosis of minor myocardial damage and cardiac memory phenomenon.

Publication types

  • English Abstract

MeSH terms

  • Adult
  • Catheter Ablation / adverse effects*
  • Creatine Kinase / blood*
  • Creatine Kinase, MB Form
  • Electrocardiography
  • Heart / physiopathology
  • Humans
  • Isoenzymes / blood*
  • Myocardium / metabolism*
  • Myoglobin / analysis*
  • Tachycardia, Paroxysmal / diagnosis
  • Tachycardia, Paroxysmal / physiopathology
  • Tachycardia, Paroxysmal / surgery*
  • Troponin T / blood*
  • Wolff-Parkinson-White Syndrome / diagnosis
  • Wolff-Parkinson-White Syndrome / physiopathology
  • Wolff-Parkinson-White Syndrome / surgery*

Substances

  • Isoenzymes
  • Myoglobin
  • Troponin T
  • Creatine Kinase
  • Creatine Kinase, MB Form