Three representatives from the lab contributed a presentation to the Dynamics Days
There was a great representation of the major research areas of the biomedical physics group at the European stage. Three researchers presented their latest work at Dynamics Days Europe in Lisbon. Their talks were part of a mini-symposium co-organised by a former lab member (dr. T. Lilienkamp) on the complex dynamics of cardiac fibrillation, organised by a former member of the group. The session explored how the heart’s normally well-coordinated electrical and mechanical activity can turn into the rapid and disordered patterns seen in dangerous arrhythmias. Our contributions spanned 4D ultrasound imaging of cardiac mechanics, data assimilation and reconstruction of cardiac tissue properties, nonlinear modelling of cardiac excitation, and experimental studies of arrhythmia dynamics.
Benjamin Weiss gave us a look inside the fibrillating human heart using high-speed 4D ultrasound. By tracking the motion of the heart muscle in three dimensions, this technique can reveal rotating patterns deep inside the heart, also called mechanical rotors. The measurements also picked up short periods in which the otherwise chaotic motion became more synchronized, something that was not visible in the conventional ECG.
Peer Dresscher tackled a different challenge: can we learn about changes inside the heart without having to measure them directly? Changes in the structure of cardiac tissue can affect how electrical signals travel through the heart. By combining measurements of electrical activity with computer models, the presented approach works backwards to reconstruct these hidden tissue properties. In the future, methods like this could help us get a clearer picture of where abnormal electrical conduction comes from.
Tim De Coster looked at what makes cardiac tissue switch from normal electrical activity to abnormal rhythms and back again. Using both computer models and experiments with light-controlled cardiac cells (optogenetics), he explored how small changes in cell behaviour and the timing of incoming electrical waves can have surprisingly large effects. In some cases, simply changing the rhythm of stimulation could switch abnormal activity on or off. The results help us understand how complex arrhythmias can emerge from relatively simple interactions within cardiac tissue.
