Discussion
The results of this study indicated that external DC cardioversion did not result in myocardial injury, as measured by cardiac troponin I, even at higher total cumulative energy. When stratifying by patients with cardiomyopathy, there was a statistically significant reduction in cardiac troponin I following cardioversion in the non-cardiomyopathy subgroup; however this was likely not clinically relevant change, as both before and after values were below the threshold of clinical significance. Additionally, when analyzing changes in CRP there was a statistically significant reduction in the whole group analysis and in the cardiomyopathy group following cardioversion.
When evaluating the changes in cardiac troponin I, we need to consider the clinical relevance of the changes following cardioversion in addition to the statistical significance of the changes. The assay used in this study to detect troponin I had an upper limit of normal of 34ng/L. As such, any measured value below this is not clinically significant. Although the non-cardiomyopathy group showed a statistically significant reduction in troponin I (Table 2) the difference of less than 1ng/L is of no clinical significance. Furthermore, the range of troponin I (5ng/L-26ng/L) revealed that none of the patients had clinically significant elevations in troponin. Alternatively, in the cardiomyopathy group the reduction in troponin I following cardioversion had greater clinical significance. The average troponin pre-cardioversion was above the upper limit of normal, suggesting possible myocardial injury at baseline. This is largely in agreement with the literature, which states that individuals with cardiomyopathy often have elevated troponin at baseline (23, 24). Additionally, given that troponin peaks approximately 12-hours following myocardial injury, the reduction provides evidence that delivery of the electrical current does not promote myocardial injury. Even though these values are not statistically significant, the clinical relevance is hypothesis generating for the role of cardioversions reversion to sinus rhythm in protection of the myocardium in patients suffering from atrial arrhythmias. To our knowledge there is no other evidence in the literature to suggest that cardioversion can result in an improvement in myocardial injury in patients with cardiomyopathy and an atrial arrhythmia.
Regarding the changes in CRP, the observed reductions, although statistically significant, do not likely carry clinical significance. Elevations in CRP have been shown to increase with myocardial injury and be a predictor of severity of myocardial injury (25). However, the specific test used in our study to assess CRP suggests that an elevation above 10mg/L is suggestive of mild inflammation. The average values of CRP detected in the whole population and cardiomyopathy group respectively (Table 2) are all below this value and therefore the detected differences are likely not of any clinical importance at the population level.
When comparing changes in cardiac troponin I to cumulative energy delivered during cardioversion, and left ventricular mass, no relationships were observed. This suggests that increased energy delivered during cardioversion does not injure the myocardium in a dose-dependent manner. Current guidelines for cardioversion recommend the initial shock to be delivered at 150J, only increasing the energy if the first shock failed to revert to sinus rhythm. This guideline is based on animal studies that create uncertainty over the relationship between higher energies and the potential for myocardial injury (26). Since we have shown that increased cumulative energy does not likely cause myocardial injury, the usage of higher energy shocks should be considered for emergent cardioversions in order to increase the likelihood of successful cardioversion (27).
This study has allowed for several hypotheses to be drawn when considering its clinical relevance. Firstly, it confirms the results from Lobo et. al (2018) who reported no evidence of myocardial injury following DC cardioversion by measuring changes in cardiac troponin T, hold true when assessing cardiac troponin I in an alternate cohort. Additionally, it reaffirms their conclusion that an elevated troponin following cardioversion should not be considered a typical or benign result of the procedure itself but may suggest a more serious myocardial pathology (e.g. myocardial infarction) (18) and thus an increased level of suspicion is required. Additionally, this study is hypothesis generating as it suggests that cardioversion in patients with cardiomyopathy who present to hospital with significant myocardial injury, as measured by severely elevated troponin I, may have a greater overall benefit from the return to sinus rhythm. It is possible that there is an additive effect of the cardiomyopathy and abnormal atrial arrhythmia that contributes towards myocardial injury.
This study has several notable strengths but is also not without limitations. Firstly, we observed clinically significant reductions in cardiac troponin I following cardioversion in the patients with cardiomyopathy however our sample size may be underpowered to detect statistically significant differences. Additionally, our study was only single centre and thus subject to possible population bias and limitations with generalizability of the results. Lastly, the Third Universal Definition guidelines on ‘Biomarker Detection of Myocardial Injury’ suggest that cardiac troponin peaks approximately 12 hours following an MI (21), which may limit the internal validity of this study as we used a time-point of six hours post-procedure to collect hematologic samples.
Further studies should focus on recruiting more individuals with cardiomyopathies and atrial arrhythmias to determine if cardioversion can result in an improvement in myocardial injury in as short as six hours post-procedure. Additionally, further time points post-cardioversion, up to 12 hours, should be assessed to determine if peak changes in troponin I occur after the six-hour time point.