Finite element modeling and intravascular ultrasound elastography of vulnerable plaques: parameter variation

More than 60% of all myocardial infarction is caused by rupture of a vulnerable plaque. A vulnerable plaque can be described as a large, soft lipid pool covered by a thin fibrous cap. Plaque material composition, geometry, and inflammation caused by infiltration of macrophages are considered as major determinants for plaque rupture. For diagnostic purposes, these determinants may be obtained from elastograms (i.e. radial strain images), which are derived from intravascular ultrasound (IVUS) measurements. IVUS elastograms, however, cannot be interpreted directly as tissue component images, because radial strain depends upon plaque geometry, plaque material properties, and used catheter position. To understand and quantify the influence of these parameters upon measured IVUS elastograms, they were varied in a finite element model (FEM) that simulates IVUS elastograms of vulnerable plaques.

IVUS elastography measurements were performed on a vessel mimicking phantom, with a soft plaque embedded in a hard wall, and an atherosclerotic human coronary artery containing a vulnerable plaque. Next, FEMs were created to simulate IVUS elastograms of the same objects. In these FEMs the following parameters were varied: Young's modulus (E), Poisson's ratio (nu) in range 0.49-0.4999, catheter position (translation of 0.8 mm), and cap thickness (t) in range 50-350 microm. Hereby the resulting peak radial strain (PRS) was determined and visualized.

Measured static E for phantom was 4.2 kPa for plaque and 16.8 kPa for wall. Variation of E-wall in range 8.4-33.2 kPa and/or E-plaque in range 2.1-8.4 kPa using the phantom FEM, gave a PRS variation of 1.6%, i.e. from 1.7% up to almost 3.3%; for variation in nu this was only 0.07%, i.e. from 2.37% up to 2.44%. Variation of E-lipid in range 6.25-400 kPa and E-cap in range 700-2300 kPa using the artery FEM, gave a PRS variation of 3.1%, i.e. from 0.6% up to 3.7%. The PRS was higher for lower E-lipid and E-cap; it was located at a shoulder of the lipid pool. Variation of nu gave only a variation of 0.17%. Variation of t and E-cap resulted in a PRS variation of 1.4%, i.e. from 0.3% up to 1.7%; thinner and weaker caps gave higher PRS. Catheter position variation changed radial strain value.

Measured IVUS elastograms of vulnerable plaques depend highly upon the Young's modulus of lipid and cap, but not upon the Poisson's ratio. Different catheter positions result in different IVUS elastograms, but the diagnostically important high strain regions at the lipid shoulders are often still detectable. PRS increases when cap weakens or cap thickness decreases.