Shear wave elastography in cardiac imaging: promise and questions ahead

This editorial refers to ‘Ultrasound shear wave elastography for detection of myocardial fibrosis’, by A. Petrescu et al., https://doi.org/10.1093/ehjci/jeaf200. Echocardiography remains a cornerstone in cardiac diagnostics, offering real-time, non-invasive assessment across a broad range of cardiac diseases. However, one of its key limitations lies in tissue characterization—particularly in the detection of myocardial fibrosis,1 a pathological substrate central to the progression of many heart conditions.2,3 In other medical specialties, ultrasound elastography has become an established technique for assessing tissue stiffness, notably in liver disease and breast lesion evaluation. These applications use shear wave elastography (SWE), which quantifies the velocity of shear waves propagating through tissue as a surrogate for stiffness. In relatively static organs, shear waves can be induced by an external stimulus. However, the heart’s anatomical position and continuous dynamic motion present unique challenges for the application of this method in cardiology. Interestingly, prior studies have demonstrated that cardiac shear waves can be generated intrinsically by specific mechanical events during the cardiac cycle.4–6 The current study by Petrescu et al. builds on this principle, focusing on shear waves generated after mitral valve closure. The closure of the mitral valve is a mechanical event that occurs during the isovolumetric contraction phase of the cardiac cycle. It is important to note that this phase is influenced by both myocardial contractility and afterload,7 which raises an important question: to what extent does shear wave velocity specifically indicate myocardial fibrosis,8 rather than more general changes in myocardial mechanics? This concern is important to consider. In the study population, systolic blood pressure and heart rate show some variation between groups, but other haemodynamic and structural variables—including age, height, body surface area, and ejection fraction—remain statistically similar. On the other hand, there are statistically significant differences in other parameters that could potentially influence the shear wave propagation. These include diastolic blood pressure, and, interventricular septal thickness (IVSd). The study’s core finding—an association between shear wave velocity and fibrosis on cardiac magnetic resonance (CMR)—is encouraging. The CMR technique has its obvious limitations and the T1 mapping technique is either not optimal to discover interstitial fibrosis. However, if further validated, SWE could offer a more accessible, ultrasound-based method for fibrosis detection, especially in settings without routine access to CMR. The study’s methodological strengths, including blinding to clinical information and acceptable inter-observer variability, further support the potential clinical feasibility of this technique (Figure 1). Illustration of shear wave measurements obtained using the Shear Q software. Left panel shows a shear wave corresponding to the mitral valve closure (3.9 m/s), while the right panel shows a shear wave associated with aortic valve closure (4.1 m/s) in the interventricular septum. Both measurements are from a healthy volunteer. While the findings in their study support the potential of shear wave velocity as a surrogate for myocardial fibrosis, it also underscores important confounding factors—such as hypertrophy and altered loading conditions—that may independently influence wave propagation. As such, the paper highlights both the promise and the complexity of using SWE as a fibrosis-specific diagnostic tool. Nonetheless, an important limitation to consider is the focus on a single myocardial segment, which raises questions about the generalizability of the results. Given that fibrosis is often patchy and can involve various myocardial regions.9,10 Particularly in patients with fibrosis related to ischaemia or myocarditis,9,11 future studies should investigate wave propagation in other areas of the heart to better assess the diagnostic capabilities of this technique. Finally, while the authors chose to analyse shear waves in response to mitral valve closure, one might ask whether aortic valve closure or the atrial kick could serve as complementary or alternative triggers. Aortic valve closure has in previous studies shown promise for evaluation in patients with aortic stenosis,12 but the isovolumic relaxation period is also influenced by rapid and abrupt pressure changes as the myocardial shear waves after mitral valve closure measures. Myocardial shear waves acquired from the atrial kick are, however, in a more stable pressure phase and may represent another opportunity for assessment of myocardial fibrosis by the echocardiographic shear waves technique. The optimal timing and cardiac phase for SWE measurements remain areas for ongoing exploration. In conclusion, Petrescu et al. present compelling early data supporting the feasibility of cardiac shear wave elastography as a non-invasive tool for detecting myocardial fibrosis. While additional validation and methodological refinement are necessary, the technique holds promise for enhancing tissue characterization in echocardiography—an advancement that would be both timely and clinically impactful. No new data were generated or analysed in support of this research.