Insana Lab: Ultrasonic Imaging - The University of Illinois at Urbana-Champaign
Project 3: Vascular Wall Shear Rate (WSR) Measurements Using Ultrasound
5.5.05
![]() Fig 1. There is an extensive literature on the role of environmental factors and vascular endothelial cells (ECs) in the formation of arterial plaques and cardiovascular diseases (CVD) [2-7]. The following very brief (and simplistic) view of important CVD factors is meant to motivate the reader in the need for wall shear rate measurements. Our approach to this measurement is described below. As we age, the protective EC barrier is less effective and easily damaged, Fig 1 (above). Damage is accelerated in individuals that smoke, have poor diets, maintain stressful lifestyles (like professors) and are subjected to other adverse environmental factors. Under these conditions, the EC barrier breaks down and the endothelial cells change to an atherogenic phenotype: they release more vasoconstrictors than vasodilators, and vascular smooth muscle cells from the media proliferate to invade the intimal layer. Importantly, changes in the activity of adhesion molecules (e.g., ICAM-1 and VCAM-1) located on the EC surface is one inflammatory response to the damage [8]. These ligands capture monocytes circulating in the blood, pulling them into the intima where they differentiate into macrophages. Macrophages then combine with circulating low-density lipids (LDLs) that enter the wall through the leaky EC barrier to become foam cells that form the lipid pool of the arterial plaque. Adhesion molecules are expressed in regions of the vasculature where the wall shear stress (WSS) is low and oscillatory [9]. The role of adhesion molecules in plaque formation is usually studied in flow chambers using cell cultures rather than in animal models or patients, in vivo. Our goal is to adapt ultrasonic methods for accurate measurements of wall shear rate, in vivo, to describe how temporal and spatial variations influence atherosclerosis. |
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![]() Fig 4. Coded excitation, Fig 4, is used to increase the time average pulse energy without increasing the instantaneous spatial-peak intensity. We transmit in time an extended pulse sequence into the body and then filter the echoes to restore spatial resolution. We have been investigating coded pulse excitation for strain imaging applications [12], and are extending that study for WSR estimation. |
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![]() ![]() ![]() ![]() The chirp and optimal codes with matched-filter compression give the highest eSNR gain. However that is not the whole story. Range lobes degrade performance as well as low eSNR. |
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![]() Fig 12 shows that we need to answer another question before we can say whether our velocity estimator for WSR measurements is of any value for biological investigations. We are lowering measurement errors but are they low enough to make a difference? We need to know the relationship between errors in WSR estimates and differences in EC function. For example, if reduction in WSR errors from 20% to 10% allows us to see much greater differences in EC function, then our signal processing improvements are helpful. For these investigations, Jean Tsou is working with Scott Simon at UC Davis to develop a flow chamber in which EC are grown and where the WSR values are precisely known. Jean worked with Abdul Barakat at UC Davis to model the velocity in the PDMS chamber using computational fluid dynamics (CFD) software. They found that a linear WSR region with an adjustable slope is possible to develop (lower right). This unique phantom design, involving live EC, could help us answer the basic questions. |
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References:
[1] Weinbaum S, Zhang X, Han Y, Vink H, Cowin SC: Mechanotransduction
and flow across the endothelial glycocalyx, Proc Natl Acad Sci U S A. 100:7988-95, 2003 |