Atrial fibrillation is the most common cardiac arrhythmia that is encountered clinically and it is associated with significant morbidity and mortality. A significant breakthrough in the understanding of atrial fibrallation occurred in the late 1990s when it was known that ectopic electrical activity that originates within the pulmonary veins is an important trigger for this type of arrhythmia. The pulmonary veins in most species are surrounded by an external sleeve of cardiomyocytes that extends from the left atrium towards the lungs. It is these cells that are considered to be responsible for generating the abnormal electrical activity that triggers atrial fibrillation, although the underlying mechanisms are unknown.

My current focus is on understanding the mechanisms whereby pulmonary vein cardiomyocytes generate spontaeneous electrical activity, and in particular the role that intracellular Ca²+ plays in this process. I am also interested in determining how electrical activity is propagated along the pulmonary vein to the atria, where it can then trigger atrial fibrillation. Since current drug treatments for atrial fibrallation are of limited efficacy, identification of potential novel therapeutic targets for future drug development is extremely important.