We propose an integrated modelling and clinical protocol for characterising local tissue properties in the left atrium and validate the resulting personalised models in four patient cases. We generate a personalised model from a set of measured local activation times (LATs) obtained by pacing the left atrium in the proximity of the coronary sinus with a programmed pacing protocol. We validate the model by evaluating the correlation between a set of measured LATS, obtained by pacing on the high right atrium and a set numerically computed LATs. We then estimate if the tissue is capable of sustaining an atrial fibrillation or a tachycardia by triggering a spiral wave on the computational model and then analysing the activation frequencies and the time elapsed until the termination of the aberrant activation.
IntroductionAtrial fibrillation (AF) is an abnormal heart rhythm in which rapid and uncoordinated electrical activation of the atria resulting in deterioration of mechanical function. AF affects almost 2.5 million people in the US, [1] and is associated with an increased incidence of cardiovascular disease, stroke and premature death [2]. In drug refractory patients AF is treated through radio frequency catheter ablation, however, up to 40% of patients require multiple procedures. Computational models have been identified as a potential tool to help predict procedure outcomes and guide ablation targets, [3]; however, their inability to capture the significant variability in physiology typical of AF patients limits their potential to make quantitative predictions of patient response to treatment and thus to inform clinical procedures. In this work, we propose a novel method to generate and validate patient specific models of the left atria from readily available clinical measurements. In 4 patients pacing catheters were placed in the coronary sinus (CS) and the high right atrium (HRA). A 20 electrode PentaRay catheter was placed in the left atrium recording 10 bipolar electrograms (EGM). Recordings were made at up to 10 locations in each patient. At each location, an S1-S2 pacing protocol [4] was applied at both the CS and HRA catheters to generate two conduction velocity (CV) restitution curves and an estimate of the effective refractory period (ERP) for each pair of electrodes. We fitted a modified Mitchell-Schaeffer (mMS) cardiac cell model [5] that does not exhibit pacemaker behaviour to the restitution curves recorded during CS pacing with the algorithm developed in [6]. We then interpolated the fitted cell model parameters across the atrial anatomy derived from the anatomical mapping system. Finally, we validated the model by numerically evaluating the predicted LATs obtained during simulated HRA pacing against the clinical measurements. We then triggered a spiral wave (SW) activation pattern on each of the 4 cases with a cross-field stimulus and recorded the evolution of the transmembrane potential. We identified cases of atrial fibrillation (1/4), atrial tachycardia (1/4) and self-terminating abe...