Influence of wall thickness and diameter on arterial shear wave elastography: a phantom and finite element study

Quantitative, non-invasive and local measurements of arterial mechanical properties could be highly beneficial for early diagnosis of cardiovascular disease and follow up of treatment. Arterial shear wave elastography (SWE) and wave velocity dispersion analysis have previously been applied to measure arterial stiffness. Arterial wall thickness (h) and inner diameter (D) vary with age and pathology and may influence the shear wave propagation. Nevertheless, the effect of arterial geometry in SWE has not yet been systematically investigated. In this study the influence of geometry on the estimated mechanical properties of plates (h = 0.5–3 mm) and hollow cylinders (h = 1, 2 and 3 mm, D = 6 mm) was assessed by experiments in phantoms and by finite element method simulations. In addition, simulations in hollow cylinders with wall thickness difficult to achieve in phantoms were performed (h = 0.5–1.3 mm, D = 5–8 mm). The phase velocity curves obtained from experiments and simulations were compared in the frequency range 200–1000 Hz and showed good agreement (R2 = 0.80 ± 0.07 for plates and R2 = 0.82 ± 0.04 for hollow cylinders). Wall thickness had a larger effect than diameter on the dispersion curves, which did not have major effects above 400 Hz. An underestimation of 0.1–0.2 mm in wall thickness introduces an error 4–9 kPa in hollow cylinders with shear modulus of 21–26 kPa. Therefore, wall thickness should correctly be measured in arterial SWE applications for accurate mechanical properties estimation

Imaging and modeling the cardiovascular system

Understanding cardiac pumping function is crucial to guiding diagnosis, predicting outcomes of interventions, and designing medical devices that interact with the cardiovascular system.  Computer simulations of hemodynamics can show how the complex cardiovascular system is influenced by changes in single or multiple parameters and can be used to test clinical hypotheses. In addition, methods for the quantification of important markers such as elevated arterial stiffness would help reduce the morbidity and mortality related to cardiovascular disease. The general aim of this thesis work was to improve understanding of cardiovascular physiology and develop new methods for assisting clinicians during diagnosis and follow-up of treatment in cardiovascular disease. Both computer simulations and medical imaging were used to reach this goal. In the first study, a cardiac model based on piston-like motions of the atrioventricular plane was developed. In the second study, the presence of the anatomical basis needed to generate hydraulic forces during diastole was assessed in heathy volunteers. In the third study, a previously validated lumped-parameter model was used to quantify the contribution of arterial and cardiac changes to blood pressure during aging. In the fourth study, in-house software that measures arterial stiffness by ultrasound shear wave elastography (SWE) was developed and validated against mechanical testing. The studies showed that longitudinal movements of the atrioventricular plane can well explain cardiac pumping and that the macroscopic geometry of the heart enables the generation of hydraulic forces that aid ventricular filling. Additionally, simulations showed that structural changes in both the heart and the arterial system contribute to the progression of blood pressure with age. Finally, the SWE technique was validated to accurately measure stiffness in arterial phantoms.QC 20161115</p

A Comparison of Shear Wave Elastography Pushing Sequences

QC 20141114</p

Contribution of the Arterial System and the Heart to Blood Pressure during Normal Aging - A Simulation Study

During aging, systolic blood pressure continuously increases over time, whereas diastolic pressure first increases and then slightly decreases after middle age. These pressure changes are usually explained by changes of the arterial system alone (increase in arterial stiffness and vascular resistance). However, we hypothesise that the heart contributes to the age-related blood pressure progression as well. In the present study we quantified the blood pressure changes in normal aging by using a Windkessel model for the arterial system and the time-varying elastance model for the heart, and compared the simulation results with data from the Framingham Heart Study. Parameters representing arterial changes (resistance and stiffness) during aging were based on literature values, whereas parameters representing cardiac changes were computed through physiological rules (compensated hypertrophy and preservation of end-diastolic volume). When taking into account arterial changes only, the systolic and diastolic pressure did not agree well with the population data. Between 20 and 80 years, systolic pressure increased from 100 to 122 mmHg, and diastolic pressure decreased from 76 to 55 mmHg. When taking cardiac adaptations into account as well, systolic and diastolic pressure increased from 100 to 151 mmHg and decreased from 76 to 69 mmHg, respectively. Our results show that not only the arterial system, but also the heart, contributes to the changes in blood pressure during aging. The changes in arterial properties initiate a systolic pressure increase, which in turn initiates a cardiac remodelling process that further augments systolic pressure and mitigates the decrease in diastolic pressure

A Comparison of Shear Wave Elastography Pushing Sequences

QC 20141114</p

Plaque characterization using shear wave elastography—evaluation of differentiability and accuracy using a combined ex vivo and in vitro setup

Ultrasound elastography has shown potential for improved plaque risk stratification. However, no clear consensus exists on what output metric to use, or what imaging parameters would render optimal plaque differentiation. For this reason we developed a combined ex vivo and in vitro setup, in which the ability to differentiate phantom plaques of varying stiffness was evaluated as a function of plaque geometry, push location, imaging plane, and analysed wave speed metric. The results indicate that group velocity or phase velocity  ⩾1 kHz showed the highest ability to significantly differentiate plaques of different stiffness, successfully classifying a majority of the 24 analysed plaque geometries, respectively. The ability to differentiate plaques was also better in the longitudinal views than in the transverse view. Group velocity as well as phase velocities  &lt;1 kHz showed a systematic underestimation of plaque stiffness, stemming from the confined plaque geometries, however, despite this group velocity analysis showed lowest deviation in estimated plaque stiffness (0.1 m s−1 compared to 0.2 m s−1 for phase velocity analysis). SWE results were also invariant to SWE push location, albeit apparent differences in signal-to-noise ratio (SNR) and generated plaque particle velocity. With that, the study has reinforced the potential of SWE for successful plaque differentiation; however the results also highlight the importance of choosing optimal imaging settings and using an appropriate wave speed metric when attempting to differentiate different plaque groups

Shear wave elastography of the arterial wall : Where are we today

1. Introduction Shear Wave Elastography (SWE) is a recently developed noninvasive method for elastography assessment using ultrasound. The technique consists of sending an acoustic radiation force (pushing sequence) into the tissue that in turn generates an orthogonal low frequency propagating shear wave. The shear wave propagation is measured real time by high speed B-mode imaging. From the B-mode images, the shear wave is tracked via normalized cross-correlation and the speed is calculated, which is used to generate an elasticity map of the tissue’s shear modulus. To date, the technique has mostly been used in large homogeneous tissues such as breast and liver where it successfully detects lesions and tumors that are easily missed with normal B-mode ultrasound [1]. SWE could potentially be applied in vascular applications to assess elasticity of the arterial wall to characterize the stiffness as an early indicator of cardiac disease. Furthermore, SWE could aid in the characterization of plaques in the carotid artery, which is critical for the prevention of ischemic stroke 2. Methods and Results An initial study was performed using an Aixplorer SWE system (Supersonic Imagine, France) to measure the shear modulus in a polyvinyl alcohol phantom (PVA) vessel with a plaque inclusion (Figure 1). It was possible to distinguish the softer inclusion mean shear wave speed (2.1 m/s) from the arterial wall (3.5 m/s) on the SWE colour-map, but the Young’s Modulus calculation of the arterial wall (E=19.8 kPa) did not match the measured Young’s Modulus (E=53.1 kPa) from comparative mechanical testing.&lt;/p&gt;&lt;p&gt;We have begun implementing various pushing sequences (single unfocused push, single focused push, line push, comb push) on a programmable ultrasound machine (Verasonics, USA) using a linear transducer (Philips L7-4) in a homogeneous PVA phantom. An algorithm for one dimensional cross-correlation tracking and shear wave speed estimation has been developed and initially tested in an experimental setup 3. Discussion According to our initial results, it is possible that SWE could be applied in vascular applications. However, the initial mechanical testing vs. SWE comparison indicated that further development to the post processing is needed before applying it on the carotid artery, which is a heterogeneous tissue with other wave propagation properties than e.g. breast tissue. The carotid artery has a difficult geometry to study for several reasons. The intima-media complex is very thin (&amp;lt; 1mm), and the vessel wall is not stationary. Furthermore, the cylindrical shape of the artery produces complex wave reflections within the arterial wall, which result in a polychromatic propagation of the shear wave. A few studies have applied techniques based on SWE to the arterial wall with promising results and a pilot study demonstrating the feasibility of the technique in-vivo has been published [2]. Still, a considerable effort is needed to validate and optimize the technique for the clinical vascular setting

Hydraulic forces contribute to left ventricular diastolic filling

Myocardial active relaxation and restoring forces are known determinants of left ventricular (LV) diastolic function. We hypothesize the existence of an additional mechanism involved in LV filling, namely, a hydraulic force contributing to the longitudinal motion of the atrioventricular (AV) plane. A prerequisite for the presence of a net hydraulic force during diastole is that the atrial short-axis area (ASA) is smaller than the ventricular short-axis area (VSA). We aimed (a) to illustrate this mechanism in an analogous physical model, (b) to measure the ASA and VSA throughout the cardiac cycle in healthy volunteers using cardiovascular magnetic resonance imaging, and (c) to calculate the magnitude of the hydraulic force. The physical model illustrated that the anatomical difference between ASA and VSA provides the basis for generating a hydraulic force during diastole. In volunteers, VSA was greater than ASA during 75-100% of diastole. The hydraulic force was estimated to be 10-60% of the peak driving force of LV filling (1-3 N vs 5-10 N). Hydraulic forces are a consequence of left heart anatomy and aid LV diastolic filling. These findings suggest that the relationship between ASA and VSA, and the associated hydraulic force, should be considered when characterizing diastolic function and dysfunction