Mitochondrial dysfunction following transthoracic countershocks in dogs

Trouton, Thomas G.; Allen, Jerilyn; Adgey, A.A.J.

doi:10.1016/0022-2828(89)91610-6

Cited by 5 publications

(6 citation statements)

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“…Most of the published data were obtained from open‐chest animals and shocks were delivered in sinus rhythm. It has been postulated that the mechanism of such damage is mediated through the generation of free radicals, which are toxic to the myocardium 25 . In our study there was evidence of less skeletal muscle damage in the 360 J group as evidenced by a lower rise in the comparative AST and CK levels in this group compared with the 200 J group.…”

Section: Discussionmentioning

confidence: 94%

Higher Energy Monophasic DC Cardioversion for Persistent Atrial Fibrillation: Is it Time to Start at 360 Joules?

Boos

Thomas

Jones

et al. 2003

Noninvasive Electrocardiol

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Section: Discussionmentioning

confidence: 94%

Higher Energy Monophasic DC Cardioversion for Persistent Atrial Fibrillation: Is it Time to Start at 360 Joules?

Boos

Thomas

Jones

et al. 2003

Noninvasive Electrocardiol

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“…4 However, in these studies, large strengths of current were used repeatedly. In humans, the strength of current delivered by the defibrillator has been standardised, and is considerably lower than the strengths used in animal experiments.…”

Section: Discussionmentioning

confidence: 99%

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

Rao

Naeem

et al. 1998

Heart

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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...

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“…However, that they came back to baseline very soon indicated that the electrical toxicity was limited and the myocardium recovered easily. Experimental studies have identified impaired mitochondrial function with transient suppression of oxidative metabolism and the generation of free intracellular radicals as possible mechanisms underlying transthoracic defibrillation injury (22)(23)(24). Although the ST-T segment elevation and dP/dt (40 mm Hg) between the two groups were no different, we could not exclude the difference in the metabolic levels.…”

Section: Discussionmentioning

confidence: 64%

Comparison of rectilinear biphasic waveform with biphasic truncated exponential waveform in a pediatric defibrillation model

Wang

Tang²,

Brewer³

et al. 2007

Critical Care Medicine

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Mitochondrial dysfunction following transthoracic countershocks in dogs

Cited by 5 publications

References 0 publications

Higher Energy Monophasic DC Cardioversion for Persistent Atrial Fibrillation: Is it Time to Start at 360 Joules?

Higher Energy Monophasic DC Cardioversion for Persistent Atrial Fibrillation: Is it Time to Start at 360 Joules?

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

Comparison of rectilinear biphasic waveform with biphasic truncated exponential waveform in a pediatric defibrillation model

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