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.

Cardiac muscle stiffness can potentially be estimated non-invasively with shear wave elastography. Shear waves are present on the septal wall after mitral and aortic valve closure, thus providing an opportunity to assess stiffness in early systole and early diastole. We report on the shear wave recordings of 22 minipigs with high-frame-rate echocardiography. The waves were captured with 4000 frames/s using a programmable commercial ultrasound machine. The wave pattern was extracted from the data through a local tissue velocity estimator based on one-lag autocorrelation. The wave propagation velocity was determined with a normalized Radon transform, resulting in median wave propagation velocities of 2.2 m/s after mitral valve closure and 4.2 m/s after aortic valve closure. Overall the velocities ranged between 0.8 and 6.3 m/s in a 95% confidence interval. By dispersion analysis we found that the propagation velocity only mildly increased with shear wave frequency.

This paper describes an in-vivo pilot study in which the systolic myocardial stiffness of four pigs was measured with various acoustic techniques. We compare the propagation velocity of shear waves in open chest and closed chest experiments, in which the open-chest shear wave was either physiologically induced by aortic valve closure (N=3), or externally induced by acoustic-radiation force (N=1). The results of closed-chest versus open-chest recordings are consistent within 1 unit of standard error, whereas the acoustic-radiation force measurement showed lowest standard deviation (7% versus 13%).