Cardiac troponin T and cardiac enzymes after external transthoracic cardioversion of ventricular arrhythmias in patients with coronary artery disease.

BACKGROUND

Serum levels of cardiac troponins after external cardioversion (ECV) for atrial fibrillation and atrial flutter are widely investigated, and no increases in cardiac troponin T (cTnT) levels have been reported. However, the effect of ECV on cardiac enzyme release may depend on the type of arrhythmias. Furthermore, ventricular tachycardia (VT) or ventricular fibrillation (VF) could cause release of cardiac enzymes after ECV due to underlying myocardial ischemia, myocardial dysfunction, or more pronounced hemodynamic deterioration during arrhythmia.

AIM

The purpose of this study was to determine whether direct current (DC) shock may increase cardiac enzyme levels in patients with coronary artery disease undergoing ECV for VT or VF, so that diagnosis of acute myocardial infarction, which initially presents with VT or VF, can be excluded.

METHOD AND RESULTS

We obtained measurement of cTnT, total creatine kinase (CK), and CK MB isoenzyme (CK-MB) activity before and after ECV in 27 patients (mean +/- SD age, 62 +/- 13 years) with induced VT or VF (22 patients) who required ECV during provocative electrophysiologic testing and who underwent ECV due to VT (5 patients) in the cardiology department. Blood samples were drawn before, and 4 h, 8 h, and 24 h after ECV. The total energy used was 630 +/- 375 J (range, 200 to 1,280 J). CK levels rose to the upper limit of reference range in seven patients (26%), and CK-MB activity was higher than the normal reference range in five patients (19%) after ECV. In contrast, cTnT concentrations remained within the normal range (< 0.1 micro g/L) in all patients. Peak CK and CK-MB activity levels strongly correlated with the total energy delivered.

CONCLUSION

Elevation of cTnT level after an urgent DC shock strongly indicates the diagnosis of acute myocardial infarction presented with life-threatening arrhythmias, rather than myocardial damage caused by ECV.