Our laboratory studies the electrophysiology of cardiac muscle and the generation of arrhythmias. Abnormalities in repolarisation, due to disease states or therapeutic drugs, can give rise to arrhythmias. By measuring electrical activity in isolated single cardiac myocytes and in excised perfused intact hearts, we aim to better understand the processes underlying cardiac repolarization and their modulation in disease states. Our projects are currently funded by the British Heart Foundation and Heart Research UK.
Repolarization of the ventricles is associated with the T wave of the electrocardiogram or ECG. The temporal association between repolarization and the T wave in an isolated perfused heart is illustrated below.
I work closely with Drs Jules Hancox and Harry Witchel in the Cardiovascular Research Laboratories. Currently, I am principal investigator on research projects investigating the electrical remodelling of the atrium in hypertension, sex differences in cardiac repolarization and G-protein-coupled receptors (GPCR).
Atrial fibrillation (AF) is the most common disturbance of cardiac rhythm and is associated with significantly increased mortality. Hypertension is the most prevalent independent risk factor for AF. This project using a common model of arterial hypertension is examining changes associated with hypertension in the electrophysiology of the atrium that might contribute to the incidence of AF.
Women are at significantly greater risk than men of the potentially fatal arrhythmia, torsades de pointes. This is associated with sex differences in the processes underlying ventricular repolarization and is likely to involve the sex hormones. This project is examining the roles of the gonadal steroids in sex differences in ventricular repolarization and drug-induced pro-arrhythmia.
Cardiac function is modulated by neurotransmitters and hormones that exert their effects via G-protein-coupled receptors on the membrane surface. In particular, hormones such as endothelin have been associated with pathological changes in cardiac function. A major interest of our group are the mechanisms by which GPCR hormones modulate cardiac cellular electrophysiology.
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