In atrial fibrillation (AF), atrial biomechanics are altered, reducing atrial movement. It remains unclear whether these changes are due to altered anatomy, myocardial stiffness, or constraints from surrounding structures. Understanding the causes of changed atrial deformation in AF could enhance tissue characterization and inform AF diagnosis, stratification, and treatment. We created patient-specific anatomical models of the left atrium (LA) from CT images. Passive LA biomechanics were simulated using finite deformation continuum mechanics equations. LA stiffness was represented by the Guccione material law, where α scaled the anisotropic stiffness parameters. Regional passive stiffness parameters were calibrated to peak regional deformation during the reservoir phase and validated against deformation transients derived from retrospective gated CT images during the reservoir and conduit phase. Physiological LA deformation varies regionally, with the roof deforming significantly less than other regions during the reservoir phase. The fitted model matched peak patient deformations globally and regionally with an average error of [Formula: see text] mm over our cohort. We compared deformation transients through the reservoir and conduit phases and found that the simulated deformation transients were within an average of [Formula: see text] mm per unit time of the CT-derived deformation transients. Regional stiffness varied across the atria with average α values of 1.8, 1.6, 2.2, 1.6 and 2.1 across the cohort in the anterior, posterior, septum, lateral and roof regions respectively. Using mixed effect models, we found no correlation between regional patient LA deformation and regional estimates of wall thickness or regional volumes of epicardial adipose tissue. We found a significant correlation between regionally calibrated stiffness and CT-derived LA biomechanics (p = 0.023). We have shown that regional heterogeneity in stiffness contributes to regional LA biomechanics, while anatomical features appeared less important. These findings provide insight into the underlying causes of altered LA biomechanics in AF.

BACKGROUND: Cardiac Resynchronization Therapy (CRT) is one of the few effective treatments for heart failure patients with ventricular dyssynchrony. The pacing location of the left ventricle is indicated as a determinant of CRT outcome. OBJECTIVE: Patient specific computational models allow the activation pattern following CRT implant to be predicted and this may be used to optimize CRT lead placement. METHODS: In this study, the effects of heterogeneous cardiac substrate (scar, fast endocardial conduction, slow septal conduction, functional block) on accurately predicting the electrical activation of the LV epicardium were tested to determine the minimal detail required to create a rule based model of cardiac electrophysiology. Non-invasive clinical data (CT or CMR images and 12 lead ECG) from eighteen patients from two centers were used to investigate the models. RESULTS: Validation with invasive electro-anatomical mapping data identified that computer models with fast endocardial conduction were able to predict the electrical activation with a mean distance errors of 9.2 ± 0.5 mm (CMR data) or (CT data) 7.5 ± 0.7 mm. CONCLUSION: This study identified a simple rule-based fast endocardial conduction model, built using non-invasive clinical data that can be used to rapidly and robustly predict the electrical activation of the heart. Pre-procedural prediction of the latest electrically activating region to identify the optimal LV pacing site could potentially be a useful clinical planning tool for CRT procedures.

This paper studies the numerical computation of integrals, representing estimates or predictions, over the output $f(x)$ of a computational model with respect to a distribution $p(\mathrm{d}x)$ over uncertain inputs $x$ to the model. For the functional cardiac models that motivate this work, neither $f$ nor $p$ possess a closed-form expression and evaluation of either requires $\approx$ 100 CPU hours, precluding standard numerical integration methods. Our proposal is to treat integration as an estimation problem, with a joint model for both the a priori unknown function $f$ and the a priori unknown distribution $p$. The result is a posterior distribution over the integral that explicitly accounts for dual sources of numerical approximation error due to a severely limited computational budget. This construction is applied to account, in a statistically principled manner, for the impact of numerical errors that (at present) are confounding factors in functional cardiac model assessment.