Characterization of troponin I levels post synchronized direct current cardioversion of atrial arrhythmias in patients with and without cardiomyopathy.

Abstract

Cardiac-specific markers of myocardial injury, such as troponin I (TnI), are often elevated following procedures that stimulate the myocardium. This study aimed to determine the effect of synchronized direct current (DC) cardioversion of atrial arrhythmias on myocardial injury 6-h post-procedure, as measured by cardiac TnI in patients with and without cardiomyopathy. Seventy-three individuals (59 M:14 F) participated in this study. Inclusion criteria were subjects 18 and older undergoing DC cardioversion for an atrial arrhythmia, including elective and non-elective admissions. Exclusion criteria included MI or CABG within the past month, cardioversion for a ventricular arrhythmia, or recent shock by implantable internal cardioverter defibrillator. Patients underwent standard DC cardioversion procedure with blood work (TnI and CRP) prior to and 6-h post-cardioversion. Primary outcome was change in TnI. Secondary outcomes included changes in CRP, correlation of TnI with cumulative energy and LVM, and a sub-group analysis in patients with cardiomyopathy. There was no significant change in TnI following cardioversion (20.4 ± 7.9 vs. 17.5 ± 6.5ng/L, F(1,72) = 2.651, p = 0.108). When stratified by cardiomyopathy status, there was a statistically significant reduction in TnI following cardioversion in the non-cardiomyopathy group (6.7 ± 3.7ng/L vs. 6.2 ± 3.2ng/L, F(1,58) = 6.481, p = 0.014) and a clinically significant reduction in the cardiomyopathy group (74.4 ± 136.7ng/L vs. 54.6 ± 104.3ng/L, F(1,13) = 3.676, p = 0.07). There was no significant relationship between change in TnI and cumulative energy or LVM (r = 0.137, p = 0.306 and r = 0.125, p = 0.412 respectively). Synchronized DC cardioversion of an atrial arrhythmia did not cause myocardial injury 6-h post-cardioversion. Sub-group analysis suggests that cardioversion of patients with cardiomyopathy may result in normalization of TnI levels.