Background: Arteriosclerotic plaque disruption accounts for about 20% of global mortality. Mechanical forces acting on the plaque include the torsional component of shear stress, radial stress, and elastic mismatch between the plaque and the surrounding structures. This study used an in-vitro experimental model employing an artificial plaque and porcine arteries to look at the possible contribution of fluid viscosity to plaque disruption in a pulsatile-flow perfusion model.

Objectives: To examine the possible contribution of viscosity to plaque/wall stress in an artificial perfusion model, and the possible interaction between pulse pressure and fluid viscosity.

Key results/findings: Above a threshold of about 1.34 mPa-s fluid viscosity augmented the radial force acting on the “plaque”. Pulse pressure significantly affected plaque disruption force in an additive fashion.

Conclusion: The viscosity threshold observed corresponds with the plasma viscosity noted to significantly increase the incidence of adverse cardiovascular events in clinical studies. It is hypothesised that plasma viscosity may exert its effect both directly on the forces acting to disrupt the plaque, and indirectly to increase plaque vulnerability via an inflammatory mechanism induced by mechanical strain.

Thomas Day got interested in the biomechanical aspects of atherosclerosis during his Part 2 project at Cambridge. Work as a vascular surgeon persuaded him that this aspect of the disease merited further research. Retirement gave him the possibility to pursue this inquiry further. He is the author of numerous largely clinical research publications conducted during the course of a long career in surgery in the UK National health Service and abroad.