| description abstract | A serious complication in aortic dissection is dynamic obstruction of the true lumen (TL). Dynamic obstruction results in malperfusion, a blockage of blood flow to a vital organ. Clinical data reveal that increases in central blood pressure promote dynamic obstruction. However, the mechanisms by which high pressures result in TL collapse are underexplored and poorly understood. Here, we developed a computational model to investigate biomechanical and hemodynamical factors involved in Dynamic obstruction. We hypothesize that relatively small pressure gradient between TL and false lumen (FL) are sufficient to displace the flap and induce obstruction. An idealized fluid–structure interaction model of type B aortic dissection was created. Simulations were performed under mean cardiac output while inducing dynamic changes in blood pressure by altering FL outflow resistance. As FL resistance increased, central aortic pressure increased from 95.7 to 115.3 mmHg. Concurrent with blood pressure increase, flap motion was observed, resulting in TL collapse, consistent with clinical findings. The maximum pressure gradient between TL and FL over the course of the dynamic obstruction was 4.5 mmHg, consistent with our hypothesis. Furthermore, the final stage of dynamic obstruction was very sudden in nature, occurring over a short time (<1 s) in our simulation, consistent with the clinical understanding of this dramatic event. Simulations also revealed sudden drops in flow and pressure in the TL in response to the flap motion, consistent with first stages of malperfusion. To our knowledge, this study represents the first computational analysis of potential mechanisms driving dynamic obstruction in aortic dissection. | |
