Morphing the left atrium geometry: A deeper insight into blood stasis within the left atrial appendage

Abstract

Background: The left atrium appendage (LAA) is a protruding cavity located in the left atrium (LA), which is known to be associated with flow stagnation. This phenomenon, which occurs primarily during atrial fibrillation (AF) episodes, is highly suspected to cause thrombosis in the LAA and has been clinically associated with the incidence of systemic embolism and ischemic stroke. Although clinical studies have suggested a relationship between with the risk of stroke in AF patients due to blood stasis and atrial geometric parameters, such as the LAA volume, LAA ostium area or pulmonary vein (PV) orientations, the underlying mechanism is not yet fully understood. Reaching a consensus would be essential for updating clinical protocols and assessing risk quantification of AF patients. Aim: A novel method to physiologically parameterise the LA starting from a patient-specific atrial geometry, instead of working with a synthetic and idealized geometry. This method would make it possible to perform a parametric and extensive analysis of the different parameters that are known to affect left atrium appendage (LAA) stasis in the absence of atrial contraction, and to evaluate and compare their influence on the formation of a dead volume within the LAA. A new method to clearly quantify this dead volume and, thus, the blood stasis in the LAA is proposed, based on the fourth moment of the blood age probability distribution (M4). Methods: The atrial geometry of a cardiac patient has been segmented. The resulting geometry has been rigged and parameterised, providing it with an armature, which had been employed to apply plausible variations of geometrical and flow parameters, such as pulmonary vein (PV) orientation, LAA ostium area, LAA volume and cardiac output. Results: The findings of this study illustrate and quantify the influence of different geometric and flow parameters on the LAA stasis in the absence of atrial contraction due to fibrillation and thus could have future clinical implications for improving thrombosis risk medium and long-term prediction. Moreover, the herein proposed method to quantify the LAA dead volume employing the M4 index has proven to be an effective way of marking the volume in which stagnation occurs and detecting a fluid dynamic behaviour independent from the rest of the LAA.