A numerical study of blood flow patterns in cerebral aneurysms and the causal relationship with platelet aggregation

Past statistical studies demonstrating the likelihood of slow blood flow in most ruptured aneurysms have sug gested that thrombogenesis plays an important role in ruptures of cerebral artery aneurysms. In the authors’ previous study, it was reported that the degree of platelet aggregation in an aneurysm had a significant cor relation with the flow pattern in the aneurysmal dome. It is, therefore, crucial to investigate flow structures in various different aneurysms in order to understand better the relationship between thrombogenesis and ruptures. In this study, patterns of blood flow in three models of cerebral artery bifurcation aneurysms were numerically analysed and compared to discern the likelihood of platelet aggregation. The three model aneurysms had comparable aspect ratios (depth/neck width) but one model was larger in volume than the other two. Experimentally captured images of visualised flow in one of the three models were available and the calculated flow patterns in this model were seen to agree well with the images. Strong impingements of incoming main flows against aneu rysmal necks were observed in all models regardless of the bifurcation angle and direction of the aneurysmal protrusion. These impingements presumably caused haemolysis, with ADP originating from haemolysed red blood cells inducing platelet aggregation. Dispersion of flow paths was observed only in the largest model and, consequently, fluid motion was slower than in the other two models. Thus, platelet aggregation was considered to be more active in the largest model. Validity of this discussion was confirmed by application of a platelet aggregation model, which had been proposed in the authors’ previous study. It was concluded that the volume of the aneurysmal dome had a significant influence on formation of a low-speed region, which is held to be responsible for active platelet aggregation. Geometric features such as the bifurcation angle and direction of aneurysmal protrusion are considered to be secondary factors contributing to active platelet aggregation.