Simulation of particle-hemodynamics in a partially occluded artery segment with implications to the initiation of microemboli and secondary stenoses

J Biomech Eng. 1998 Aug;120(4):446-54. doi: 10.1115/1.2798013.

Abstract

Computational results of laminar incompressible blood-particle flow analyses in an axisymmetric artery segment with a smooth local area constriction of 75 percent have been presented. The flow input waveform was sinusoidal with a nonzero average. The non-Newtonian behavior of blood was simulated with a modified Quemada model, platelet concentrations were calculated with a drift-flux model, and monocyte trajectories were described and compared for both Newtonian and Quemada rheologies. Indicators of "disturbed flow" included the time-averaged wall shear stress (WSS), the oscillatory shear index (OSI), and the wall shear stress gradient (WSSG). Implications of the vortical flow patterns behind the primary stenosis to the formation of microemboli and downstream stenoses are as follows. Elevated platelet concentrations due to accumulation in recirculation zones mixed with thrombin and ADP complexes assumed to be released upstream in high wall shear stress regions, could form microemboli, which are convected downstream. Distinct near-wall vortices causing a local increase in the WSSG and OSI as well as blood-particle entrainment with possible wall deposition, indicate sites susceptible to the onset of an additional stenosis proximal to the initial geometric disturbance.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Algorithms
  • Arterial Occlusive Diseases / blood
  • Arterial Occlusive Diseases / complications*
  • Arterial Occlusive Diseases / physiopathology*
  • Humans
  • Models, Cardiovascular*
  • Monocytes / physiology
  • Numerical Analysis, Computer-Assisted*
  • Oscillometry
  • Platelet Count
  • Reproducibility of Results
  • Rheology*
  • Stress, Mechanical
  • Thrombin / physiology
  • Thromboembolism / blood
  • Thromboembolism / etiology*
  • Thromboembolism / physiopathology*

Substances

  • Thrombin