Direct current cardioversion does not cause cardiac damage: evidence from cardiac troponin T estimation

Abstract

Aim-To determine whether elective direct current (dc) cardioversion of atrial fibrillation/flutter causes myocardial damage. Methods and results-Cardiac troponin T and creatine kinase were estimated 20-28 hours after dc cardioversion in 51 patients who received dc shocks for elective cardioversion of chronic atrial fibrillation/ flutter. Although creatine kinase was raised in 44 patients, cardiac troponin T was undetectable in all patients. Conclusion-Cardiac damage does not occur as a result of cardioversion. (Heart 1998;80:229-230) Keywords: cardioversion; troponin T; creatine kinase; atrial fibrillation Direct current (dc) cardioversion 1 revolutionised the management of cardiac arrhythmias. However, before the standardisation of outputs from external defibrillators there was controversy about the most appropriate strength of current to be used.2 Animal experiments have suggested that repeated high energy dc shocks result in myocardial damage.3 4 In humans, dc cardioversion causes a rise in the concentration of creatine kinase and its MB subfraction. [5][6][7] This observation, along with the electrocardiogram (ECG) changes (repolarisation abnormalities) sometimes seen after dc cardioversion, led to the suggestion that dc cardioversion causes myocardial damage. Most of the creatine kinase released after cardioversion comes from the chest wall skeletal muscles, 8 which also liberate the MB subfraction. Therefore, the extent that emergency dc cardioversion contributes to raised creatine kinase or its MB isoenzyme is unclear. The belief that myocardial damage might result from higher strengths of current may also have influenced recommendations about the choice of current strength. It remains uncertain whether dc cardioversion does actually cause myocardial damage.Cardiac troponin T is a cardiac specific protein component of the troponin/tropomyosin complex. 9 A rise in serum troponin T concentrations is specific for cardiac damage. It remains raised for up to 48 hours after myocardial injury, thus providing a wide time window. 9Currently available data suggest that the kinetics of cardiac troponin T release from acutely damaged myocardium are identical whatever the cause of damage. 10Our study was undertaken to determine whether there was any evidence of myocardial damage after elective dc cardioversion of atrial fibrillation/flutter by measuring concentrations of cardiac troponin T in patients undergoing dc cardioversion. MethodsFifty one consecutive patients undergoing elective dc cardioversion for atrial fibrillation/ flutter were entered into the study. None had chronic renal failure, acute myocardial infarction, or skeletal muscle disease. As described previously, 11 dc shocks were administered in increasing strengths of 100 J, 200 J, 300 J, and 360 J (only one shock of each strength), until either sinus rhythm was restored or 360 J was applied.A blood sample was taken 20-28 hours after dc cardioversion. Samples were centrifuged and analysed or frozen at −70°C until analysis (all analyses were p...

Serum troponin I level after external electrical direct current synchronized cardioversion in patients with normal or reduced ejection fraction: No evidence of myocytes injury

“…Previous studies were conducted in a small number of patients, and inclusion/exclusion criteria often were not strict; our results confirm those described in some previous studies. 1,[9][10][11][12][13][14] On the other hand, our findings are discordant with those of other studies involving smaller series of patients, demonstrating the presence of mild myocardial injury in some patients after elective EEC for AF. [4][5][6][7][8] Differences in inclusion criteria may account for the discrepancies in the observed conclusions.…”

“…Recently, several workers have reported the detection of a mildly elevated level of cTnI or transient ST-segment elevation in some patients after elective EEC for AF, implying myocardial injury could have been caused by this procedure. [4][5][6][7][8] Other studies showed no change in serum levels of either troponin I or T. 1,[9][10][11][12][13][14] To our knowledge there has not been any study of sufficiently large size addressing the effects of EEC and myocardial damage. Moreover, most of the troponin studies have included clinically unstable patients with raised levels of the biochemical markers, and only a small proportion of patients with reduced ejection fraction (EF) was studied.…”

Capability of ischemia-modified albumin to predict serious cardiac outcomes in the short term among patients with potential acute coronary syndrome

“…Although cTnT measurements have been used to indicate that direct-current cardioversion (DCCV) does not cause cardiac damage, 11 Roy and colleagues 12 reported that in patients with atrial fibrillation, IMA levels are significantly elevated at 1 and 6 hours after DCCV, especially in patients with electrocardiographic evidence of post-DCCV ischemia. Sinha and associates 13 evaluated ECG, cTnT and IMA levels individually and in combinations in patients diagnosed with non-ischemic chest pain, unstable angina and MI with ST-or non-ST-segment elevation.…”

Troponin: the biomarker of choice for the detection of cardiac injury

“…153,154 • Cardioversion, ablation and cardiac arrest: Elective electrical cardioversion in most patients does not result in troponin elevations. 155,156 When present, elevations are mild. 157,158 Elevations are more common in patients with cardiac arrest who have undergone direct-current shock (often multiple) or prolonged resuscitation, or both.…”