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).