Closed-chest measurement of diastolic and systolic shear wave speed to assess myocardial stiffness

Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): Research Foundation Flanders (FWO): grant 1211620N TTW – Dutch Heart Foundation partnership program "Earlier recognition of cardiovascular diseases": project number 14740 Background Echocardiographic shear wave elastography (SWE) encompasses all ultrasound techniques tracking shear wave (SW) motion in the cardiac wall, of which the propagation speed is linked to the intrinsic mechanical properties. SWs can be induced naturally, for example by valve closure, or externally by using an acoustic radiation force (ARF). Although the latter is technically more demanding, it enables instantaneous stiffness assessment throughout the entire cardiac cycle (fig. a). However, it is unknown how factors such as cardiac loading and contractility, next to intrinsic mechanical properties, affect ARF-based SW speeds. Purpose We performed transthoracic SWE measurements in pigs to study the effects of hemodynamic alterations, inotropic state and myocardial infarction (MI) on diastolic and systolic SW speeds. Methods Different cardiac conditions were considered in three pigs: (i) baseline (BL), (ii) preload decrease (PD), (iii) afterload increase (AI), (iv) preload increase (PI), (v) administration of dobutamine (DOB), (vi) BL2, (vii) MI through 60-100 min. occlusion of the LAD and (viii) 40 min. reperfusion (REP). For each condition, transthoracic high frame rate ARF-based SWE acquisitions were taken in a parasternal long-axis view with a research ultrasound system. SWs were induced in the septum at 34 Hz during 1.5 s to track SW speeds throughout the cardiac cycle (fig. a&b). Systolic and diastolic SW speeds were determined from the 10% highest and lowest median values per condition, respectively. Left ventricular pressure-volume (PV) loops were recorded to estimate end-diastolic pressure (EDP), end-systolic pressure (ESP) and passive chamber stiffness (dPdV). dPdV was determined as the slope of the tangent to the fitted end-diastolic PV relationship at mean ED volume. Linear regressions and Pearson’s correlation coefficients were computed. Results Diastolic SW speed was correlated to EDP for conditions with changes in loading, and to dPdV for conditions with changes in chamber stiffness (fig. c). Both relationships were significant, with a moderate positive correlation for EDP (R = 0.48, p = 0.02) and a strong positive correlation for dPdV (R = 0.76, p < 0.01). Furthermore, the observed change in diastolic SW speed was smaller when altering EDP compared to dPdV (0.4 m/s vs. 1.0 m/s). For systolic SW speed, very strong positive correlations were found with ESP (R = 0.91, p < 0.01), and with dPdV (R = 0.81, p < 0.01) in fig. d. Conclusion This study shows that both diastolic and systolic SW speed are related to passive chamber stiffness. Moreover, loading also influenced systolic SW speed and, to a lesser extent, diastolic SW speed, presumably because of material nonlinearity. Systolic SW speed is linked to contractility as well. Thus, while SWs after valve closure occur at a certain moment in the cardiac cycle, the timing of ARF-based SWs can be chosen such to assess specific aspects of the cardiac (structural and functional) status