Arteriosclerosis

Background

Arteriosclerosis is characterized by the abnormal thickening and hardening of the arterial walls resulting in loss of elasticity. The primary form of arteriosclerosis, atherosclerosis, is a systemic disorder characterized by localized plaque deposits in and fibrosis of the inner layer of the arteries at selected sites on the arterial tree. Atherosclerosis is not essentially a continuous process leading inevitably to arterial blockage however it is the primary cause of coronary artery disease (heart attacks) and strokes. The disease is a disorder with multiple genetic and environmental contributions. It is both an acute and chronic disease resulting from hyperlipidemia (the presences of excess fats or lipids in the blood) and a complex interplay of many environmental, metabolic and genetic risk factors. As the intimal plaque enlarges it reduces the size of the artery’s lumen i.e. the area through which the blood flows is reduced. A blockage (stenosis) may not have any effect on a person at rest however during exercise the stenosis may go from being non-critical to critical.

Factors such as hypertension, smoking, high blood cholesterol and diabetes appear to increase the risk of atherosclerosis greatly. Often a change in diet and increasing exercise can greatly reduce the presence of disease however if the condition cannot be improved a bypass or stent is required. A bypass provides an alternative route for the blood to travel and a stent is a wire mesh which is inserted into the artery to hold it open thus allowing the blood to flow.

Challenge

The distal junction, shown in the picture below, of a femoral or femoropopliteal artery bypass graft has a predilection for failure due to reblockage (restenosis). However neither the initiation nor proliferation process of atherosclerotic plaque around the junction is completely understood. Presently it is hypothesized that the process of atherosclerosis initiates as a result of damage or ‘insult’ to the endothelium (inner most layer of the artery). The cause of this initial damage is unknown, although it is widely believed that wall shear stresses are a contributing factor.

A mechanical stress can control the growth of a living tissue and change not only its shape, but its chemical and cellular structures as well as changing its mechanical properties. The hypertrophy of the heart, caused by a rise in blood pressure, is the best known example of soft tissue remodeling due to a change of stress. The primary cause of plaque proliferation has not yet been identified, however it is our belief that intramural pressure plays a significant role.

Approach

Currently studies are underway within Stokes Institute, which involve numerical models of the proximal and distal junctions. This analysis was used to determine both the location and magnitude of the strains and stresses, existing around arterial junctions, caused by intramural pressure. The simulated artery bypass graft was examined under both static and dynamic conditions. Knowing the locations for the maximum stresses and strains from numerical analysis it has allowed us to assess the actual stresses and strains existing in the femoral artery following surgery. The measurements were taken during elective femoral and femoropopliteal surgery using a videoextensometer, which is a non invasive measurement technique. Attempts have also been made to monitor patients with a femoral artery bypass using duplex ultrasound to measure the outer diameter of the femoral artery with the aim of correlating strain to restenosis at 12 and 24 months post surgery.

Recent research centered on the cellular activities surrounding the formation and proliferation of atherosclerotic plaque, concludes that the interaction of the living cells can alter a cells function. Hence the study is advancing into the area of cell culture studies and assessment of cellular damage and dysfunction when they are subjected to intramural pressure.