Abstract

Heart failure leads to gross cardiac structural changes. While cardiac resynchronization therapy (CRT) is a recognized treatment for restoring synchronous activation, it is not clear how changes in cardiac shape and size affect the electrical pacing therapy. This study used a human heart computer model which incorporated anatomical structures such as myofiber orientation and a Purkinje system (PS) to study how pacing affected failing hearts. The PS was modeled as a tree structure that reproduced its retrograde activation feature. In addition to a normal geometry, two cardiomyopathies were modeled: dilatation and hypertrophy. A biventricular pacing protocol was tested in the context of atrio-ventricular block. The contribution of the PS was examined by removing it, as well as by increasing endocardial conductivity. Results showed that retrograde conduction into the PS was a determining factor for achieving intraventricular synchrony. Omission of the PS led to an overestimate of the degree of electrical dyssynchrony while assessing CRT. The activation patterns for the three geometries showed local changes in the order of activation of the lateral wall in response to the same pacing strategy. These factors should be carefully considered when determining lead placement and optimizing device parameters in clinical practice.

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