K. Greaves et T. Crake, CARDIAC TROPONIN-T DOES NOT INCREASE AFTER ELECTRICAL CARDIOVERSION FOR ATRIAL-FIBRILLATION OR ATRIAL-FLUTTER, HEART, 80(3), 1998, pp. 226-228
Objective-To determine whether cardiac troponin T increases after elec
trical cardioversion in patients with atrial fibrillation or atrial fl
utter. Design-Serum creatine kinase (CK), creatine kinase-MB (CKMB), a
nd cardiac troponin T were measured before, 24 hours, and 48 hours aft
er cardioversion in 15 patients with atrial fibrillation or atrial flu
tter. Results-12 of the 15 patients (80%) were successfully cardiovert
ed to sinus rhythm. The median number of shocks was three (range one t
o six), the median cumulative energy 710 J (50 to 1430 J), and the med
ian peak energy 300 J (50 to 360 J). Total CK increased from a baselin
e median concentration of 92 (45 to 259) to 1324 (96 to 6660) U/l at 2
4 hours and 1529 (120 to 4774) U/l at 48 hours after cardioversion. Th
ere was a small increase in CKMB but the ratio of CKMB to CK did not i
ncrease. There was no increase in cardiac troponin T in any patient. C
onclusions-Following electrical cardioversion of atrial fibrillation o
r atrial flutter, cardiac troponin T remains unchanged despite a large
rise in total CK, indicating that the CK is derived from skeletal mus
cle and that myocardial injury does not occur. If cardiac troponin T i
s increased after cardioversion for atrial arrhythmias then other caus
es of myocardial damage should be sought.