During cardiac fibrillation, the coherent mechanical contraction of the heart is disrupted by vortex-like rotating waves or scroll waves of electrical activity, which share topological analogies to point vortices and vortex filaments in hydrodynamic turbulence [1]. The dynamics of these filaments and their electro-mechanic instabilities due to the nonlinear interaction with the anisotropic, heterogeneous substrate and the complex boundaries of the heart result in self-organized disordered dynamics. Furthermore, it has been shown that tissue deformation itself may affect electrical wave propagation and its stability, where both pro-arrhythmic and anti-arrhythmic effects have been observed [2].
The measurement of electro-mechanical waves in cardiac tissue remains a major experimental challenge. Conventional fluorescence imaging of the heart (optical mapping) is significantly compromised by tissue deformation resulting in substantial motion artifacts in the optical signal. This limitation is usually addressed by preventing contractile motion using pharmacological motion uncouplers, which are known to alter the dynamical properties of the tissue. To overcome these limitations, we have developed an advanced optical mapping system that is capable of imaging contracting tissue.
In the heart, electrical excitation propagates through diffusively coupled cardiac cells and subsequently results in contraction and force generation (excitation-contraction or electromechanic coupling). Mechanical forces on cardiac cells may in turn change electrophysiological properties of the tissue, e.g. action potential duration, or induce after-depolarizations resulting in premature beats. This so-called mechanoelectric feedback is therefore considered an important mechanism facilitating cardiac arrhythmias, however many of its details remain elusive. The objective of this project is to develop and analyze a generic model of cardiac electro-mechanics and to study mechanisms underlying the onset and perpetuation of cardiac arrhythmias.
Two important questions in the investigation of cardiac arrhythmias are how these activation patterns develop and how their complexity can be characterized. What properties of the tissue determine its susceptibility to arrhythmias? Where and when are certain activation patterns most sensitive to perturbations? What makes irregular activity easy or difficult to terminate? We expect that the answers will yield valuable information for the prevention of arrhythmias and about strategies to terminate them.