Local myocardial stiffness variations identified by high frame rate shear wave echocardiography

Figures

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  Fig. 1. Delayed enhancement MRI images in our patients. a, b: 4-chamber view and corresponding short-axis view respectively, in a patient in group 2 (HCM patients without septal reduction therapy). No scar is detected; c, d: similar views in a patient in group 3 (HCM patients having undergone septal reduction therapy), demonstrating a thin subendocardial layer of fibrosis (arrow) resulting from surgical myectomy; e, f: same views in another patient in group 3, showing transmural delayed enhancement (arrow) in the basal septum, corresponding to transmural scarring resulting from interventional septal ablation

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  Fig. 2. In vitro experiment: Dual-layer tissue phantom investigated using externally-induced shear waves. a: By using a clinical shear wave elastography system (scanner 2), color elastograms were generated (b); c: Regional stiffness quantification in the two layers, translated into shear wave velocity. The Q-boxes are manually placed in the middle of the layer-specific region; d: The same phantom imaged with a clinical high frame rate TDI system (scanner 1). Shear waves were induced by acoustic radiation force using a dedicated research system (V). e: a propagation difference is visible in the two layers. Because of the gain settings needed in the clinical system TDI, the interlayer separation is barely visible, and was marked with a dashed line; f: by computing the shear wave velocity along two M-mode lines, the values come very close to the expected shear wave velocities

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  Fig. 3. High frame rate color TDI shear wave tracking and analysis in the postprocessing software. a: classical parasternal long axis view and the focused TDI window over the interventricular septum. b: An M-Mode line is put in the septal wall, pointing towards the shear wave source. c: virtual M-mode map of a full heart cycle (reconstructed offline), at 510 Hz frame rate, demonstrating the shear waves after mitral and aortic valve closure (dotted slopes). The onset of the waves is marked with solid lines. The shear wave after aortic valve closure is pointed to by the dotted arrow; space and time directions are also indicated. d: mean tissue velocity curve as a function of time (averaged over the M-mode line, this velocity should not be mistaken with the shear wave propagation velocity), synchronous to the ECG (green) and PCG (yellow). The onset of both shear waves is synchronous to the onset of the respective heart sounds (S1, S2)

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  Fig. 4. Explanation of the multi-layer TDI method used in this study, in one HCM patient having an inner layer scar. a: parasternal long axis and the focused TDI window over the interventricular septum; two M-Mode lines are traced, one in the outer layer and one in the inner layer, pointing towards the shear wave source. c: The mid panel is extracted from the Qlab postprocessing output and depicts synchronous ECG signal (green) and phonocardiogram (white). The average velocity line (pink line) is automatically generated by the software and should not be mistaken with the shear wave propagation velocity. Heart sounds are marked with S1 and S2. The onset of the second heart sound (S2) is marked with a white line and acts as reference for the onset of the aortic closure shear wave. b, d: local tissue velocity along the virtual M-mode lines traced in the outer layer (b) and inner layer (d). The entry and exit points of the shear wave along the two M-mode lines are marked with empty circles, connected by a white dashed straight line as reference. The aortic shear wave front slope is traced with yellow dashed lines. In panel B the wave front line is superposed on the reference line, but in…

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  Fig. 5. Shear wave velocity variation in a M-mode panel, theoretical model (a,b) and patient demonstration (c, d). a: uniform propagation of a wave (theoretical model). By tracing the wave front from the upper (white arrow) and respectively lower (yellow arrow) point we obtain two parallel lines; b: velocity variation along the 3 cm M-mode line (theoretical model). The upper point wave front (white arrow line) forms an angle (α) with the lower point arrow line (yellow line). This angle is resolved if the opening on either side is at least 2 ms (one time-frame at 500 Hz). It demonstrates a change in propagation velocity; c: outer layer tracing in a HCM patient. The wave front of the aortic shear wave is linear, the upper (white) and lower (yellow) point arrow lines are parallel; d: inner layer tracing in the same patient. There is a visible shift in slope, and the two lines intersect and form an angle. The spatial position of this intersection coincided with the transition scar-myocardium visible on 2D images

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  Fig. 6. Strain results, represented as bull’s eye diagrams, by using a 16-segments model. a: normal volunteer. Local segmental strain (LSS) is homogeneous and normal in all the segments; b: HCM patient without septal reduction. LLS is globally lower than in the normal individual, with even lower values in the anteroseptal and inferior segments; c: HCM patient post septal reduction, having an inner layer scar visible on 2D and 3D echo. Anteroseptal segments have local strain values of > − 10%; d: HCM patient with transmural scar: anteroseptal segments have LSS values> − 5%