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Assessing aortic strain and stiffness: don't forget the physics and engineering
  1. Bart Bijnens1,
  2. Paula Rudenick1,
  3. Arturo Evangelista2
  1. 1ICREA-Universitat Pompeu Fabra, Barcelona, Spain
  2. 2Hospital Vall d'Hebron, Barcelona, Spain
  1. Correspondence to Bart Bijnens, ICREA-Universitat Pompeu Fabra, Barcelona, Spain; bart.bijnens{at}

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To the Editor There is increasing evidence that the mechanical properties of the aorta, and arterioventricular coupling, are of great clinical importance in cardiovascular diseases. Therefore, we read the paper by Vitarelli et al with great interest.1

Given the recent evolution of ultrasound equipment and processing tools, the suggestion of assessing the aorta using velocity and deformation information is interesting, but the way it is used by the authors is confusing.

They measure the velocity of one point on the aortic wall and suggest that this is related to stiffness of the wall. However, the velocity describes the motion of the wall within the thorax rather than the extension of the wall due to the internal pressure (the intrinsic deformation, determined by the pressure within and the stiffness of the vessel). As opposed to the carotid artery, which is not showing substantial overall motion, to measure aortic distension, the difference in motion of the proximal and distal walls has to be assessed, as described, for example, by Long A, et al.2 This can easily be seen in the m-mode (figure 1A),1 where the whole aorta is moving substantially during the cardiac cycle and the velocity thus mainly describes this motion.

Figure 1

(A) Range of radial strain values as a function of end-diastolic (ED) radius and wall thickness for a large distensibility (D) range in normal (2nd and 4th layers) and hypertensive subjects (top and third layers). (B) Radial strain as a function of ED radius for a wall thickness of 2.5 mm. (C) Radial strain as a function of wall thickness for an ED radius of 12 mm.

Additionally, from aortic pressure curves, there is no evidence of biphasic diastolic decrease of the aortic diameter, with a large atrial phase, as shown in figure 1B. Although measurement of this motion might be interesting for assessments in pathological cases in clinical practice, it does not directly describe the properties of the aorta. It is more related to the motion of the aorta by the left ventricle and therefore represents left ventricular systolic and diastolic function.

Distensibility was calculated as D=2(As-Ad)/(Ad(Ps-Pd)). Most authors would not use multiplication by 2. There also seems a problem with the units since they report a normal average of D=79 Pa−1 whereas published values are of the order of 37×10−3 kPa−1.3

A more important problem is the assessment of radial strain (aortic wall thinning), which is calculated from the temporal integration of strain rate, and strain rate is assessed based on spatial differences in velocities. To calculate this, a region of interest and a calculation length has to be chosen. The authors used a 3 mm strain length and a region of interest of 2–4 mm. Looking at the implementation of the strain analysis in the system, experience suggests that this corresponds to a range of >5 mm used for the quantification.4 Considering that the wall of the aorta is not 5 mm and a scan plane close to the valve is used, it is clear that velocities of the blood in the right ventricle outflow and aortic lumen are included. Therefore, the calculated strain is not the radial deformation (or thinning) of the aortic wall. This is clearly seen from the strain curve in figure 1C, where it is difficult to explain why the aortic wall would thin substantially during atrial contraction and not start thinning quickly and gradually from aortic valve closure as would be expected when analysing pressure traces in the aorta (keeping in mind that aortic strain is directly related to pressure so it should have a profile similar to local aortic pressure).

Additionally, the measured strain values are not realistic. To show this, we simulated the radial strain (wall thinning) in a tube resembling the aorta and assumed that the wall is incompressible (conservation of volume). We used a wide range of realistic parameters: end-diastolic diameter ranging from 20 to 40 mm; wall thickness of 2–4 mm; distensibility between 4×10−3 and 9×10−3 mm Hg−1 for normal individuals and between 1×10−3 and 3×10−3 mm Hg−1 for hypertensive subjects3; and a pressure gradient of 45 mm Hg (normal subjects) and 70 mm Hg (hypertensive subjects) (the extreme values in the paper of Vitarelli et al).1 Additionally, a longitudinal strain of 1% was assumed to account for the lengthening of the aorta during systole. Figure 1 shows the resulting ranges for the radial strain. In extreme conditions (certainly not the average patient), the strain can range from 6% to15% in normal subjects and from 3% to 9% in hypertensive subjects. This is clearly substantially less than Vitarelli's reported average values of 23.1% and 8.8%.1

A thorough analysis of what is measured using these techniques would be appropriate before reporting clinical results.

As reported by the authors, the measured values might correlate with changes induced by hypertension, but they surely do not specifically describe changes in the aortic wall. Analysis of aortic properties should be carried out with measurements that directly reflect aortic wall mechanics or blood hydrodynamics rather than by statistical analysis of a set of observations.


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  • Competing interests None.

  • Provenance and peer review Not commissioned; not externally peer reviewed.

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