Experimental and computational investigation of the mechanisms behind deep vein thrombosis

Deep vein thrombosis (DVT) is a life threatening condition which is on the rise in the western world [1] yet the mechanisms behind DVT remain unknown. Using microfluidics and simulations it is possible to determine the physical mechanisms that could be the cause of DVT. By mimicking the murine model (stenosis model) it was possible to see if the amount of stenosis and presence of side branches influenced flow. I was determined that the influence of a restriction did not alter the flow enough to encourage thrombus formation, however the stenosis would increase the number of cell-cell collisions which could be the reason for a thrombus occurring in vivo. Finite element modelling was also used to surpass the limitations of the experiment, resulting in a the same conclusions. A major limitation of the murine model is that it ignores the possibility of a bypass of the stenosed region, leading to the second model.The bypass model was used to determine which set of parameters are important to encouraging a bypass: position of side branch, width of side branch channel and the size of stenosis. Finally, a third model was also developed, the valve model to explore how flow is influenced by flexible valves. The valves are fabricated with varying stiffness to better understand how the stiffness of valves can influence flow through a vein inducing pro-thrombotic conditions. This model is more relevant for larger mammals. Three models of biology have been implemented to demonstrate DVT can be instigated by physical parameters and these fundamental conditions are not to be dismissed