For the quantification of myocardial function, myocardial stiffness can potentially be measured non-invasively using shear wave elastography. Clinical diagnosis requires high precision. In 10 healthy volunteers, we studied the reproducibility of the measurement of propagation speeds of shear waves induced by aortic and mitral valve closure (AVC, MVC). Inter-scan was slightly higher but in similar ranges as intra-scan variability (AVC: 0.67 m/s (interquartile range [IQR]: 0.40–0.86 m/s) versus 0.38 m/s (IQR: 0.26–0.68 m/s), MVC: 0.61 m/s (IQR: 0.26–0.94 m/s) versus 0.26 m/s (IQR: 0.15–0.46 m/s)). For AVC, the propagation speeds obtained on different day were not statistically different (p = 0.13). We observed different propagation speeds between 2 systems (AVC: 3.23–4.25 m/s [Zonare ZS3] versus 1.82–4.76 m/s [Philips iE33]), p = 0.04). No statistical difference was observed between observers (AVC: p = 0.35). Our results suggest that measurement inaccuracies dominate the variabilities measured among healthy volunteers. Therefore, measurement precision can be improved by averaging over multiple heartbeats.

In cardiac high-frame-rate color tissue Doppler imaging (TDI), a wave-like pattern travels over the interventricular septum (IVS) after atrial contraction. The propagation velocity of this myocardial stretch post-atrial contraction (MSPa) was proposed as a measure of left ventricular stiffness. The aim of our study was to investigate the MSPa in patients with hypertrophic cardiomyopathy (HCM) compared with healthy volunteers. Forty-two healthy volunteers and 33 HCM patients underwent high-frame-rate (>500 Hz) TDI apical echocardiography. MSPa was visible in TDI, M-mode and speckle tracking. When assuming a wave propagating with constant velocity, MSPa in healthy volunteers (1.6 ± 0.3 m/s) did not differ from that in HCM patients (1.8 ± 0.8 m/s, p = 0.14). Yet, in 42% of patients with HCM, the MSPa had a non-constant velocity over the wall: in the basal IVS, the velocity was lower (1.4 ± 0.5 m/s), and in the mid-IVS, much higher (6.1 ± 3.4 m/s, p < 0.0001), and this effect was related to the septal thickness. The reason is hypothesized to be the reaching of maximal longitudinal myocardial distension in HCM patients.

We apply a high frame rate (over 500 Hz) tissue Doppler method to measure the propagation velocity of naturally occurring shear waves (SW) generated by aortic and mitral valves closure. The aim of this work is to demonstrate clinical relevance. We included 45 healthy volunteers and 43 patients with hypertrophic cardiomyopathy (HCM). The mitral SW (4.68 ± 0.66 m/s) was consistently faster than the aortic (3.51 ± 0.38 m/s) in all volunteers (p < 0.0001). In HCM patients, SW velocity correlated with E/e’ ratio (r = 0.346, p = 0.04 for aortic SW and r = 0.667, p = 0.04 for mitral SW). A subgroup of 20 volunteers were matched for age and gender to 20 HCM patients. In HCM, the mean velocity of 5.1 ± 0.7 m/s for the aortic SW (3.61 ± 0.46 m/s in matched volunteers, p < 0.0001) and 6.88 ± 1.12 m/s for the mitral SW(4.65 ± 0.77 m/s in matched volunteers, p < 0.0001). A threshold of 4 m/s for the aortic SW correctly classified pathologic myocardium with a sensitivity of 95% and specificity of 90%. Naturally occurring SW can be used to assess differences between normal and pathologic myocardium.

The propagation velocity of shear waves relates to tissue stiffness. We prove that a regular clinical cardiac ultrasound system can determine shear wave velocity with a conventional unmodified tissue Doppler imaging (TDI) application. The investigation was performed on five tissue phantoms with different stiffness using a research platform capable of inducing and tracking shear waves and a clinical cardiac system (Philips iE33, achieving frame rates of 400–700 Hz in TDI by tuning the normal system settings). We also tested the technique in vivo on a normal individual and on typical pathologies modifying the consistency of the left ventricular wall. The research platform scanner was used as reference. Shear wave velocities measured with TDI on the clinical cardiac system were very close to those measured by the research platform scanner. The mean difference between the clinical and research systems was 0.18 ± 0.22 m/s, and the limits of agreement, from −0.27 to +0.63 m/s. In vivo, the velocity of the wave induced by aortic valve closure in the interventricular septum increased in patients with expected increased wall stiffness.