Simulated acute mitral regurgitation increased left atrial energy dissipation and pressure while causing systolic reversal flow in pulmonary veins, whereas simulated atrial fibrillation caused slower left atrial appendage flow and loss of the late-diastole atrial reversal wave.
A novel fully coupled 3D computational model successfully captures complex hemodynamic interactions between the pulmonary circulation and left heart in pathophysiological states like atrial fibrillation and acute mitral regurgitation.
This paper aims to investigate detailed mechanical interactions between the pulmonary haemodynamics and left heart function in pathophysiological situations (e.g. atrial fibrillation and acute mitral regurgitation). This is achieved by developing a complex computational framework for a coupled pulmonary circulation, left atrium and mitral valve model. The left atrium and mitral valve are modelled with physiologically realistic three-dimensional geometries, fibre-reinforced hyperelastic materials and fluid-structure interaction, and the pulmonary vessels are modelled as one-dimensional network ended with structured trees, with specified vessel geometries and wall material properties. This new coupled model reveals some interesting results which could be of diagnostic values. For example, the wave propagation through the pulmonary vasculature can lead to different arrival times for the second systolic flow wave (S2 wave) among the pulmonary veins, forming vortex rings inside the left atrium. In the case of acute mitral regurgitation, the left atrium experiences an increased energy dissipation and pressure elevation. The pulmonary veins can experience increased wave intensities, reversal flow during systole and increased early-diastolic flow wave (D wave), which in turn causes an additional flow wave across the mitral valve (L wave), as well as a reversal flow at the left atrial appendage orifice. In the case of atrial fibrillation, we show that the loss of active contraction is associated with a slower flow inside the left atrial appendage and disappearances of the late-diastole atrial reversal wave (AR wave) and the first systolic wave (S1 wave) in pulmonary veins. The haemodynamic changes along the pulmonary vessel trees on different scales from microscopic vessels to the main pulmonary artery can all be captured in this model. The work promises a potential in quantifying disease progression and medical treatments of various pulmonary diseases such as the pulmonary hypertension due to a left heart dysfunction.
Feng et al. (Fri,) conducted a other in Atrial fibrillation and acute mitral regurgitation (computational model). Simulated acute mitral regurgitation and atrial fibrillation vs. Simulated normal left heart function was evaluated on Hemodynamic parameters (pressure, flow, wave intensity). Simulated acute mitral regurgitation increased left atrial energy dissipation and pressure while causing systolic reversal flow in pulmonary veins, whereas simulated atrial fibrillation caused slower left atrial appendage flow and loss of the late-diastole atrial reversal wave.