Cardiac troponin I after external electrical cardioversion for atrial fibrillation as a marker of myocardial injury--a preliminary report.

BACKGROUND It is uncertain whether external electrical cardioversion (CV) of atrial fibrillation (AF) can cause myocardial injury identifiable by troponin I (cTnI). AIM To examine whether external CV of AF can cause cTnI rise as measured with high-sensitivity assay, and to identify factors determining this elevation. METHODS Patients with non-valvular AF selected for CV were included. Exclusion criteria were myocardial ischaemia, elevated D-dimer, heart and renal failure. Patients underwent monophasic or biphasic CV. Troponin I was measured before, and 6 and 12 hours after the procedure with TNI-ADV assay; NT-proBNP was measured before CV. Echocardiography was performed in all patients. RESULTS Twenty-two patients were examined. Troponin I 6 and 12 hours after CV [0.04 ng/ml (0.00-0.30), 0.04 ng/ml (0.00-0.13)] was significantly higher than before [0.017 pg/ml (0.00-0.08)] (p=0.01, p=0.02). Only in one patient did cTnI exceed the cut-off for myocardial infarction after 6 hours (>0.16 ng/ml) with subsequent normalisation after 12 hours. Left ventricular end-diastolic dimension (LVEDD) was significantly higher and ejection fraction lower in the group with cTnI rise in comparison with the group with no cTnI elevation (54,2+/-6,3 vs. 47,6+/-5,7 mm, p=0,02; 56,2+/-8,9 vs. 63,2+/-7,1%, p=0,05). LVEDD=53 mm had 75% sensitivity and 72% specificity for predicting cTnI elevation after CV. Age, gender, AF duration, type of CV, energy, left atrial dimension, baseline cTnI and NT-proBNP were not predictive of cTnI increase. CONCLUSIONS Cardioversion can lead to mild but significant cTnI rise as measured with a high-sensitivity assay. The influence of CV on cTnI elevation appears to be more pronounced in patients with relatively large LVEDD.