Atherosclerotic plaque rupture

A problem presented at the UK MMSG Nottingham 2002.

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Presented by:
Prof Alan Moody (Academic Radiology, University of Nottingham)
Participants:
LJ Cummings, JEF Green, A Grief, A Moody, JH Siggers, JB van den Berg, SL Waters

Problem Description

Vascular disease causes significant morbidity and mortality in the western world. Vessel wall disease includes a spectrum of conditions from benign fatty streaks in early life to complicated atheromatous plaques resulting in vessel narrowing and distal thromboembolism. It has been recently realised that the vessel wall is not as passive conduit of blood but rather a highly complex organ that interacts with its environment. The major function of the vessel wall, and more specifically the endothelial lining, is to maintain adequate blood flow to the end organ it is supplying. This is achieved by regulatory mechanisms that control vascular tone, inflammation and anticoagulation.

The study group was asked to consider four questions:

  1. Does this change in morphology at a bifurcation cause any local reduction in vasa vasorum flow/pressure as one vessel divides into two?
  2. What nutrient/oxygen gradient exists across the vessel wall and what is the effect of disease (thickening) on this?
  3. At what degree of stenosis will there be a significant pressure gradient across the stenosis?
  4. What effect will the pressure gradient along the length of a stenosis have on the potential site of vasa vasorum rupture, haemorrhage and potential plaque rupture/activation?

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Study Group Report

We have developed and solved simple mathematical models in order to address the questions asked. The flow model postulates that plaque rupture may occur when the governing dimensionless parameters exceed critical values. The concentration model illustrates the effectiveness of the vasa vasorum network in supplying the outer portion of the artery wall with nutrients.

One interesting result of the flow model is that the larger the dimensionless viscosity, γ, the more susceptible the plaque is to rupture (according to our hypothesis). This result suggests that it might be profitable to study the effectiveness of blood-thinning drugs (e.g. aspirin) for patients with vascular disease (aspirin is currently used to prevent Deep Vein Thrombosis and heart attacks).

Possible refinements to improve the simple models used are also discussed.

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