The change in propagation speed of natural shear waves by altering preload might differentiate patients with increased myocardial stiffness

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Research Foundation Flanders - FWO. Background Shear wave (SW) elastography (SWE) is a novel ultrasound-based technique for the assessment of myocardial stiffness. SWE tracks the propagation of SWs travelling through the myocardium, induced by e.g. mitral valve closure (MVC). The speed of SWs is related to myocardial stiffness. As myocardial stiffness is defined by a non-linear stress-strain relation, it is dependent on the operating stress levels and thus left ventricular (LV) loading. As a result, elevated SW speed values could be caused by both increased LV preload or structural remodelling of the myocardium. In this way, performing SWE measurements at different loading states could potentially provide additional information aiding with the interpretation of these measurements. Purpose to investigate if performing SWE before and after a loading change could provide more information on tissue properties of the myocardium. Methods Twelve patients [age: 76(41–82)] receiving intermittent hemodialysis (HD) and 12 age-matched healthy volunteers [age: 67(47–71); p = 0.19] were included. Patients were scanned before and 1 hour after the start of HD. Parasternal long-axis views were acquired using an experimental ultrasound scanner with an average frame rate of 1086±185 Hz. Patients were divided into 2 equal groups based on the grade of diastolic dysfunction (DD), determined using conventional echo parameters (group 1: DD grade 0–1 and group 2: DD grade 2−3). SWs after MVC were visualized on M-mode maps along the septum which were colour coded for tissue acceleration (Figure A). The speed was semi-automatically calculated by measuring the slope of the SW. Results The average ultra-filtrated volume after 1h of HD was 0.64±.27 L, which did not significantly differ between patient groups (p = 0.44). Patients in group 2 had significantly higher indexed LV wall mass compared to group 1 (128±39 g/m² vs. 72±24 g/m²; p = 0.02), indicative of LV structural remodelling. SW speed after MVC was significantly different between healthy volunteers and the patient groups at baseline (p<0.01) (Figure B). After 1h of HD, SW speed decreased in both groups, with the largest decrease in group 2 (Figure B). Furthermore, SW speed values of patient group 1 decreased to values similar to healthy volunteers, while patient group 2 still had significantly increased SW propagation speed. Conclusions Overall, myocardial stiffness, assessed using SW propagation speed, of patients with end-stage kidney disease was increased compared to healthy volunteers. This could result from increased LV preload or structural remodelling. Our data indicate that in addition to single measurements, assessing the change in SW speed by altering the loading state might aid in differentiating these causal mechanisms underlying increased myocardial stiffness. Therefore, adding a loading challenge, e.g. leg lifting, when doing SWE could provide additional information. Further research needs to confirm these initial findings.