Cardiovascular disease (CVD) is the biggest cause of deaths in the world. Our multi-disciplinary research programmes develop advanced knowledge on the causes, prevention and treatment of myocardial and vascular diseases for patient benefit.
Cardiovascular disease research undertaken by the Medical School is funded and supported by the British Heart Foundation Cymru making it the centre for this research in Wales.
We integrate leading-edge laboratory and clinical research, collaboration between the public, NHS, social care, innovation and industrial partners to improve the treatment and prevention of CVD.
Our research has clearly defined goals:
Recent research highlights include:
RyR2 channels are regulated by complex networks of interactions occurring within and between the component subunits of the channel. We used directed mutagenesis, biochemical approaches and cellular imaging to reveal a critical role for the amino-terminal b8-b9 loop in regulating RyR2 channel activation and suppression. The work helps explain the link between RyR2 channel hyperactivity and the onset of arrhythmias.
Atrial fibrillation (AF) is increasingly common in the aging population and implicated in many ischemic strokes. We showed that remote ECG acquisition and interpretation is at least 3 times more likely to identify incident AF than routine care. Our findings suggest that this approach could be considered for AF screening in routine practise, particularly in the highest-risk patients.
The signalling events that control the billions of cardiac cells that make up the heart are intricately controlled. Heart disease is associated with the loss of this control. Using experimental networks of human cardiac cells, new computational methods and the application of chaos theory, we have developed methods to map key events that drive the heart’s ‘health-to-disease’ transitions.
The development of drugs that bind to and modulate intracellular calcium release channels is an exciting approach for the treatment of heart rhythm disturbance. In experiments using human RyR2 channels incorporated into artificial lipid bilayers we showed that flecainide, a well-established anti-arrhythmic drug, does not block the physiologically-relevant movement of ions through the channel. Thus, the effectiveness of flecainide in the treatment of a type of stress-induced ventricular tachycardia called CPVT, cannot be due to a direct block of RyR2 channels. Other mechanisms must be involved in the clinical efficacy of flecainide. We are using mechanism-based drug design to tailor approaches to modulate RyR2 channels and prevent life-threatening arrhythmias.
