Atrial fibrillation is a common cardiovascular disease, affecting the regular beating of the heart through chaotic contraction of the heart's upper chambers. On its own, the condition—increasingly prevalent among the elderly—is not life threatening, but it leads to an increased r
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Atrial fibrillation is a common cardiovascular disease, affecting the regular beating of the heart through chaotic contraction of the heart's upper chambers. On its own, the condition—increasingly prevalent among the elderly—is not life threatening, but it leads to an increased risk of stroke and heart failure. As of yet, there is no consensus on the physiological mechanisms responsible for initiating and sustaining atrial fibrillation. A more detailed view of cardiac activity would improve understanding of the disease, making earlier diagnosis possible and improving options for treatment.
The contraction of the cardiac muscles is governed by electrical signals propagating through the tissue. Cardiac activity can be monitored with a high spatial resolution by measuring the electrical potential directly on the epicardium of the heart during open-heart surgery, using an array of closely spaced electrodes. From these electrograms, estimating the time of local activation of the cardiac tissue underneath each electrode provides a quantitative way of mapping the mechanisms of atrial fibrillation. Various methods exist to estimate the activation times, but the complex signals that are typical of atrial fibrillation make it difficult to obtain accurate results. This thesis proposes combining two existing methods for estimating the local activation times. Based on a model of the electrogram as a spatial convolution of local transmembrane currents, an inverse problem is formulated and solved, resulting in a less opaque view of the cardiac activity at the electrode locations by attenuating distant disturbances and emphasizing local activity. The deconvolution output is fed to the second step, where cross-correlating certain pairs of signals gives an estimate for the mutual time delay in local activation. A graph representation of the electrode array is used to define neighbor order and decide which signal pairs are correlated. The set of pairwise time delays this produces is then converted to an estimate for the local activation times, using a least-squares estimator.
The proposed method is evaluated using different simulated cardiac settings. In a setting with one stimulation source, earlier results of the deconvolution and cross-correlation methods are confirmed, and the proposed method is seen to produce a slightly lower mean error than reference methods. In the higher-complexity triple-source setting, the latter effect is again visible. Reinforced by the performance of the different methods in increasingly noisy settings, the main merits of the proposed method for the estimation of local activation times can be said to be found in the form of increased consistency, not significantly improving on the accuracy of existing methods.
