Cerebral Arteriovenous Malformations: Computational Model: Evaluation of Results and Relevance to Clinical Application

There are many published reports of studies of blood flow in an Arterio-Venous Malformation. One such is the experiments by Casikar and Ramaswamy which has clearly demonstrated the unexpected relationship among vessel diameter, blood pressure and steal phenomenon. The present research was designed to create a computational model to critically analyse the experimental findings. In addition, due to the difficulty of measuring any values in vivo, a computational model is the most feasible response to enhance the current understanding of this vascular malformation in the medical and engineering communities. To initiate this examination of the factors leading to arteriovenous malfunction development and progression, a Buckingham Pi analysis was conducted in order to identify some dimensionless value connected with the specific blood flow found in the AVM network. Various assumptions were incorporated into the calculations. Critical variables (based on the assumptions made in this analysis) were identified. Overall the tests conducted pertained a high level of reliability, owing to the repeated testing procedures within this examination. Each CFD analysis was tested thrice over, to identify errors and ensure reliable testing procedure and results obtained. Each test yielded the same, or highly similar, data sets, identifying conclusively the overall reliability of the data obtained. These results can be reproduced. The paper explores additional mechanisms of vessel wall remodelling resulting from changes in wall shear stress experienced by the vessels. The article finds that increasing wall shear stress in the region results in an increase in wall thickness and vessel diameter in order to normalise the values. The model shows that when AVM fistula diameter increases, with all other variables constant, the pressure and velocity across the entire system shows significant changes. The computational evidence suggests that the critical change for both pressure and velocity are directly related steal phenomenon in the system. This further solidifies the various hypotheses relating to the critical nature of both diameter and the effect of the onset of steal phenomenon. The sudden alteration in pressure and velocity of blood in the AVM after during and after the onset of vascular steal may present further explanation for the dormant nature of the symptoms of the disorder where the symptoms are found to largely present only after steal occurs. The results obtained in this study highlight relationship between mass flow rate, fistula diameter, and amount of flow shunting upon the overall progression of an AVM. This study postulates that the combination of vessel dilation and diminished capacity of auto-regulation of the vessels may render the AVM incapable of approaching a point of equilibrium. This study has found evidence to explain the onset of symptomology of AVMs as a result of steal phenomenon and create highly volatile clinical conditions. All AVMs are due to a fistula between the artery and the vein. There is a specific connection between the arteries and veins as in other extra cranial situations. In this paper AVM refers collectively to all the fistulae. The word fistula is used when a single example is cited. The model does not explain “pial AVM”. The concept of pial AVM is influenced by early embryologists, before Padget. There is no evidence to support this based on principles embryology This study offers many potential avenues for future research. Much of the future work should focus on incorporating biological processes, such as auto regulation and cell renewal, into the computational model.