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The characterization of troponin I levels post synchronised direct-current cardioversion in patients with atrial arrhythmias.
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  • Ryan Sless,
  • Gerry Allen,
  • Nathaniel Hayward,
  • Gerry Fahy
Ryan Sless
University College Cork College of Medicine and Health, PRN Lab

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Gerry Allen
Cork University Hospital Group
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Nathaniel Hayward
University College Cork College of Medicine and Health, PRN Lab
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Gerry Fahy
Cork University Hospital Group
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Abstract

Cardiac-specific markers of myocardial injury, such as troponin I, are often elevated following procedures that stimulate the myocardium. The aim of this study was to determine the effect of synchronised DC cardioversion of an atrial arrhythmia on myocardial injury 6-hours post procedure, as measured by cardiac troponin I A total of 73 individuals (59 men, 14 women) undergoing DC cardioversion of an atrial arrhythmia agreed to participate in this study. Inclusion criteria included subjects older 18 who were undergoing DC cardioversion for an atrial arrhythmia. This included elective and non-elective admissions. Exclusion criteria included an MI or CABG within the past month, cardioversion for a ventricular arrhythmia, or any recent shocks by an implantable internal cardioverter defibrillator. Patients underwent standard procedure for DC cardioversion with blood work (troponin I and CRP) performed prior to and six hours post cardioversion. Primary outcome was change in troponin I. Secondary outcomes included changes in CRP, relationships between troponin I and cumulative energy and LVM, and a sub-group analysis stratified by the presence of cardiomyopathy. There was no significant change in troponin I following cardioversion (F[1,72]=2.651, p=0.108). There was a significant reduction in troponin I following cardioversion in the non-cardiomyopathy group (F[1,58]=6.481, p=0.014). There was no significant relationship between change in troponin I and cumulative energy or LVM (r=0.137, p=0.306 and r=0.125, p=0.412 respectively). Synchronised DC cardioversion of an atrial arrhythmia did not cause myocardial injury 6-hours post-cardioversion. Sub-group analysis suggests that cardioversion of patients with cardiomyopathy may result in normalization of tropo