RT Journal Article
SR Electronic
T1 Cardiac troponin T does not increase after electrical cardioversion for atrial fibrillation or atrial flutter
JF Heart
JO Heart
FD BMJ Publishing Group Ltd and British Cardiovascular Society
SP 226
OP 228
DO 10.1136/hrt.80.3.226
VO 80
IS 3
A1 K Greaves
A1 T Crake
YR 1998
UL http://heart.bmj.com/content/80/3/226.abstract
AB Objective To determine whether cardiac troponin T increases after electrical cardioversion in patients with atrial fibrillation or atrial flutter.Design Serum creatine kinase (CK), creatine kinase-MB (CKMB), and cardiac troponin T were measured before, 24 hours, and 48 hours after cardioversion in 15 patients with atrial fibrillation or atrial flutter.Results 12 of the 15 patients (80%) were successfully cardioverted to sinus rhythm. The median number of shocks was three (range one to six), the median cumulative energy 710 J (50 to 1430 J), and the median peak energy 300 J (50 to 360 J). Total CK increased from a baseline median concentration of 92 (45 to 259) to 1324 (96 to 6660) U/l at 24 hours and 1529 (120 to 4774) U/l at 48 hours after cardioversion. There was a small increase in CKMB but the ratio of CKMB to CK did not increase. There was no increase in cardiac troponin T in any patient.Conclusions Following electrical cardioversion of atrial fibrillation or atrial flutter, cardiac troponin T remains unchanged despite a large rise in total CK, indicating that the CK is derived from skeletal muscle and that myocardial injury does not occur. If cardiac troponin T is increased after cardioversion for atrial arrhythmias then other causes of myocardial damage should be sought.