Baldewsing Radj A, de Korte Chris L, Schaar Johannes A, Mastik Frits, van der Steen Antonius F W
Biomedical Engineering, Room Ee 23.02, Thoraxcenter, Erasmus Medical Center Rotterdam, P.O. Box 1738, Rotterdam 3000 DR, The Netherlands.
Ultrasonics. 2004 Apr;42(1-9):723-9. doi: 10.1016/j.ultras.2003.11.017.
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.
超过60%的心肌梗死由易损斑块破裂所致。易损斑块可描述为一个被薄纤维帽覆盖的大的、柔软的脂质池。斑块物质组成、几何形状以及巨噬细胞浸润引起的炎症被视为斑块破裂的主要决定因素。出于诊断目的，这些决定因素可从弹性图（即径向应变图像）中获取，弹性图由血管内超声（IVUS）测量得出。然而，IVUS弹性图不能直接解释为组织成分图像，因为径向应变取决于斑块几何形状、斑块物质特性以及所用导管位置。为了解并量化这些参数对测量的IVUS弹性图的影响，在一个模拟易损斑块IVUS弹性图的有限元模型（FEM）中对它们进行了变化。
在一个模拟血管的模型上进行IVUS弹性成像测量，该模型有一个嵌入硬壁的软斑块以及一条含有易损斑块的动脉粥样硬化人类冠状动脉。接下来，创建有限元模型以模拟相同物体的IVUS弹性图。在这些有限元模型中，对以下参数进行了变化：杨氏模量（E）、泊松比（nu）在0.49 - 0.4999范围内、导管位置（平移0.8毫米）以及帽厚度（t）在50 - 350微米范围内。据此确定并可视化得到的峰值径向应变（PRS）。
模型中斑块的测量静态E为4.2千帕，壁的为16.8千帕。在模型有限元模型中，将壁的E在8.4 - 33.2千帕范围内和/或斑块的E在2.1 - 8.4千帕范围内变化，导致PRS变化1.6%，即从1.7%到近3.3%；对于nu的变化，这仅为0.07%，即从2.37%到2.44%。在动脉有限元模型中，将脂质的E在6.25 - 400千帕范围内和帽的E在700 - 2300千帕范围内变化，导致PRS变化3.1%，即从0.6%到3.7%。较低的脂质E和帽E时PRS更高；它位于脂质池的肩部。nu的变化仅导致0.17%的变化。t和帽E的变化导致PRS变化1.4%，即从0.3%到1.7%；更薄且更弱的帽导致更高的PRS。导管位置变化改变径向应变值。
易损斑块的测量IVUS弹性图高度依赖于脂质和帽的杨氏模量，但不依赖于泊松比。不同的导管位置导致不同的IVUS弹性图，但脂质肩部具有诊断重要性的高应变区域通常仍可检测到。当帽变弱或帽厚度减小时，PRS增加。
