We then demonstrate a ‘patient-specific’ simulation of deformation in a patient with a conduction disorder called left bundle-branch block. We quantitatively compare model simulations to deformation patterns recorded during an experimental study of pacing-induced electrical asynchrony. We present the MultiPatch module for simulating the effects of asynchronous electrical activation on cardiac contraction in the relatively simple CircAdapt model of the heart and circulation. There is considerable interest in using computer simulations to understand how asynchronous electrical activation affects cardiac deformation, and how pathologies of the cardiac conduction system can be treated by pacing the heart. The result is discoordinated contraction and a reduction in the ability to pump blood. Due to either pathology or electrical pacing, the heart can be activated asynchronously. Under normal conditions, the electrical activation of the heart is almost synchronous, leading to uniform contraction. The CircAdapt model is therefore capable of fast and realistic simulations of dyssynchronous myocardial deformation embedded within the closed-loop cardiovascular system. We conclude that the MultiPatch module produces realistic regional deformation patterns in the asynchronous heart and that activation time is more important than tissue location within a wall for determining myocardial deformation. Local myofibre strain in the patient simulation shows qualitative agreement with circumferential strain patterns observed in the patient using tagged MRI. Direct comparison between simulated and experimental strain patterns shows both qualitative and quantitative agreement between model fibre strain and experimental circumferential strain in terms of shortening and rebound stretch during ejection. We perform simulations representing an experimental study of myocardial deformation induced by ventricular pacing, and a patient with LBBB and heart failure using endocardial recordings of electrical activation, wall volumes, and end-diastolic volumes. We test the hypothesis that activation time is more important than tissue location for determining mechanical deformation in asynchronous hearts. Consequently, spatial location within the wall is not required to calculate deformation in a patch. All patches within a wall share a common wall tension and curvature. ![]() ![]() Tissue properties and activation time can differ between patches. Cardiac walls are subdivided into an arbitrary number of patches of homogeneous tissue. We present an alternative based on the CircAdapt lumped-parameter model of the heart and circulatory system, called the MultiPatch module. Simulations of mechanical dyssynchrony within the heart are typically performed using the finite element method, whose computational intensity may present an obstacle to clinical deployment of patient-specific models. Computational models provide a tool for understanding pathological consequences of dyssynchronous contraction. Electrically asynchronous activation causes myocardial contraction heterogeneity that can be detrimental for cardiac function. Cardiac electrical asynchrony occurs as a result of cardiac pacing or conduction disorders such as left bundle-branch block (LBBB).
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