Introduction
It is widely accepted that the cardiac specific enzymes troponin T and I are highly specific markers of myocardial injury. These enzymes have been shown to be elevated during acute coronary syndromes such as myocardial infarction, acute heart failure, pulmonary embolism, infectious conditions of the heart including myocarditis and pericarditis, and sepsis (1-4). There is also evidence to suggest that atrial arrhythmias can cause myocardial injury as indicated by elevations in both C-reactive protein (CRP) and cardiac troponin T (5, 6).
Of the various types of atrial arrhythmias, atrial fibrillation is the most common and recent evidence suggests an increasing prevalence and incidence of atrial fibrillation worldwide (7, 8). Advances in electrophysiological procedures have resulted in external synchronised electrical direct current (DC) cardioversion becoming the gold-standard treatment for atrial arrhythmias (9). While other procedures that stimulate the myocardium, such as percutaneous coronary intervention, coronary artery bypass grafting, and pulmonary vein embolization have been shown to create an inflammatory response, as represented by an increase in circulatory inflammatory and serum cardiac markers (10, 11); there is limited data on the acute incidence of myocardial injury following the external DC cardioversion.
Previous studies in animals have suggested that electrical cardioversion can cause myocardial injury (12). However, these studies did not look directly at biochemical markers of myocardial injury. Additionally, it is unknown whether the energy levels used for cardioversion in animal models correspond to those used in humans. In humans, several clinical studies have attempted to characterize the changes in cardiac troponin I following cardioversion however the results are conflicting (13-16). Additionally, some of the data from these studies were collected following the use of a monophasic defibrillator, which has also been shown to cause greater myocardial injury when compared to the current gold-standard biphasic defibrillators (13, 17). A recent study investigating the effects of DC cardioversion on myocardial injury as measured by cardiac troponin T showed no significant changes following cardioversion (18); however these results have not been repeated using troponin I.
Therefore, the objectives of this study are to determine if synchronised DC cardioversion of atrial arrhythmias causes myocardial injury six hours post-cardioversion, by measuring the highly sensitive cardiac biomarker cardiac troponin I. Additionally, we aim to determine if there is a relationship between the change in cardiac troponin I and cumulative energy given during cardioversion or left ventricular mass (as measured by echocardiography).