Not just thick, but stiff? shear wave imaging unmasks differences in hypertrophic left ventricles

Abstract Background Increased left ventricular (LV) wall thickness is a common echocardiographic feature across diverse cardiac conditions, including hypertrophic cardiomyopathy (HCM), cardiac amyloidosis (CA), and hypertensive cardiomyopathy (HTN). Despite similar wall dimensions, these pathologies exhibit distinct myocardial tissue characteristics. Shear wave elastography (SWE), based on high frame rate echocardiography, provides a novel non-invasive method to quantify myocardial stiffness, potentially enabling differentiation between these pathologies. Purpose To determine whether shear wave velocity (SWV) varies depending on myocardial pathology independent of geometric factors such as wall thickness. Methods We enrolled 37 patients: 15 with HCM, 14 with CA, 8 with HTN. Based on late gadolinium enhancement on cardiac magnetic resonance, HCM patients were divided into 2 groups: with replacement fibrosis (HCM-RF) and without replacement fibrosis (HCM-NF). To control for geometric hypertrophy and isolate differences in myocardial stiffness, patients were matched 1:1 by interventricular septal wall thickness in 3 subgroup analyses: HCM-FB vs. CA (n=10), HCM-NF vs. HTN (n=3), CA vs. HTN (n=7). SWE was performed in parasternal long-axis view of the LV using an experimental scanner (HD-PULSE) equipped with a clinical phased array transducer at 1100±250 frames per second. Tissue acceleration maps were generated from an anatomical M-mode line along the septal midline. SWV at MVC was derived from the slope of wave propagation (Figure A). Results Mean SWV differed across groups: HCM-FB (8.8±1.3 m/s), CA (6.5±0.8 m/s), HCM-NF (6.2± 0.8m/s), and HTN (5.3±0.9 m/s) (p0.001). Despite matched wall thickness, SWV differed significantly between groups: HCM-FB vs. CA (8.8 ± 1.3 m/s vs. 6.4 ± 0.7 m/s; p0.001), CA vs. HTN with significantly higher SWV in CA (6.5 ± 0.9 m/s vs. 5.1 ± 0.8 m/s; p = 0.01), HCM-NF vs. HTN with a trend toward higher SWV in HCM-NF (5.7 ± 0.3 m/s vs. 5.0 ± 0.6 m/s; p = 0.2; Figure B). Conclusion Shear wave elastography identifies significant differences in myocardial stiffness among different myocardial pathologies even when wall thickness is matched. The observed differences reflect the underlying pathological substrates such as replacement fibrosis, protein deposition, interstitial remodelling and myocardial disarray. These findings support the integration of the new method of shear wave elastography into multimodality cardiac phenotyping. Larger studies are warranted to validate these preliminary findings and establish diagnostic thresholds.