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Absence of significant myocardial injury following elective direct current cardioversion for atrial fibrillation
Ronstan Lobo1, Roger D White1,2, Leslie J Donato3
1Department of Cardiovascular Disease, Mayo Clinic, Rochester, Minnesota.
Insights
Direct current (DC) cardioversion for arrhythmias causes minor troponin changes in most patients. Myocardial injury from DC cardioversion is rare, occurring in only 2% of cases studied.
Area of Science:
- Cardiology
- Electrophysiology
- Biomarkers
Background:
- Direct current (DC) cardioversion is a standard procedure for terminating cardiac arrhythmias.
- Current guidelines suggest cardioversion may cause myocardial injury.
Purpose of the Study:
- To investigate whether external DC cardioversion leads to myocardial injury.
- To assess myocardial injury using serial measurements of high-sensitivity cardiac troponin T (hs-cTnT) and high-sensitivity cardiac troponin I (hs-cTnI).
Main Methods:
- Prospective study of patients undergoing elective external DC cardioversion for atrial fibrillation.
- hs-cTnT and hs-cTnI levels measured before and at least 6 hours after cardioversion.
- Myocardial injury defined by significant changes in both hs-cTnT and hs-cTnI.
Main Results:
- 98 subjects analyzed; median cumulative energy 121.9 J, with 23.5% receiving ≥300 J.
- Small, statistically significant increases observed in both hs-cTnT and hs-cTnI post-cardioversion (P < .001).
- Only 2% of patients met the criteria for myocardial injury, irrespective of shock energy or baseline levels.
Conclusions:
- DC cardioversion causes minimal, statistically significant troponin level changes in a small percentage of patients.
- Myocardial injury directly attributable to elective cardioversion is uncommon.
- Marked troponin elevations post-cardioversion warrant investigation for alternative causes of myocardial injury.
Background:
Direct current (DC) cardioversion is used to terminate cardiac arrhythmias. Current guidelines list cardioversion as a cause of myocardial injury.
Objective:
This study determined whether external DC cardioversion results in myocardial injury measured by serial changes in high-sensitivity cardiac troponin T (hs-cTnT) and high-sensitivity cardiac troponin I (hs-cTnI).
Methods:
This was a prospective study of patients undergoing elective external DC cardioversion for atrial fibrillation. hs-cTnT and hs-cTnI were measured precardioversion and at least 6 hours postcardioversion. Myocardial injury was present when there were significant changes in both hs-cTnT and hs-cTnI.
Results:
Ninety-eight subjects were analyzed. Median cumulative energy delivered was 121.9 (interquartile range [IQR] 102.2-302.7) J. Multiple cases 23 (23.5%) required 300 J or more. Maximum cumulative energy delivered was 2455.1 J. There were small significant changes in both hs-cTnT (median precardioversion 12 [IQR 7-19) ng/L], median postcardioversion 13 [IQR 8-21] ng/L; P < .001) and hs-cTnI (median precardioversion 5 [IQR 3-10) ng/L], median postcardioversion 7 [IQR 3.6-11) ng/L; P < .001). Results were similar in patients with high-energy shocks and did not vary based on precardioversion values. Only 2 (2%) cases met criteria for myocardial injury.
Conclusion:
DC cardioversion resulted in a small but statistically significant changes in hs-cTnT and hs-cTnI in 2% of patients studied irrespective of shock energy. Patients with marked troponin elevations after elective cardioversion should be assessed for other causes of myocardial injury. It should not be assumed the myocardial injury was from the cardioversion.
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