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Cardiac troponin T does not increase after electrical cardioversion for atrial fibrillation or atrial flutter
1Department of Cardiology, St Bartholomew's Hospital, West Smithfield, London, UK.
Insights
Electrical cardioversion for atrial fibrillation or flutter does not increase cardiac troponin T levels. This indicates that elevated creatine kinase (CK) after the procedure originates from skeletal muscle, not myocardial injury.
Area of Science:
- Cardiology
- Electrophysiology
- Biomarker Analysis
Background:
- Electrical cardioversion is a common procedure for restoring sinus rhythm in patients with atrial fibrillation or atrial flutter.
- Concerns exist regarding potential myocardial injury following electrical cardioversion, often assessed through cardiac biomarkers.
- Cardiac troponin T is a sensitive and specific marker for myocardial damage.
Purpose of the Study:
- To investigate whether cardiac troponin T levels change after electrical cardioversion in patients with atrial fibrillation or atrial flutter.
- To differentiate the source of elevated creatine kinase (CK) post-cardioversion.
Main Methods:
- Serum levels of creatine kinase (CK), creatine kinase-MB (CKMB), and cardiac troponin T were measured in 15 patients.
- Measurements were taken before, and at 24 and 48 hours after electrical cardioversion.
- Successful cardioversion and procedural parameters (shocks, energy) were recorded.
Main Results:
- Electrical cardioversion was successful in 80% of patients.
- A significant increase in total CK was observed post-cardioversion.
- No patient showed an increase in cardiac troponin T levels.
Conclusions:
- Electrical cardioversion for atrial arrhythmias does not elevate cardiac troponin T.
- The rise in total CK post-cardioversion is attributable to skeletal muscle, not myocardial injury.
- Elevated cardiac troponin T after cardioversion warrants investigation for alternative causes of myocardial damage.
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.