Ultrafast ultrasound shear wave elastography: a novel approach for assessing myocardial stiffening in congenital aortic stenosis

Abstract

Background

Congenital aortic stenosis (ConAoS) accounts for approximately 4%–8% of all congenital heart diseases. Chronic pressure overload may result in myocardial stiffening, leading to impaired cardiac filling, reduced contractility and ultimately contributing to the onset of symptomatic heart failure. Shear wave elastography (SWE), using high-frame-rate echocardiography, allows visualisation of myocardial shear waves. By measuring shear wave propagation velocity (SWV), this technique may enable non-invasive assessment of myocardial stiffness. This study aimed to explore the feasibility of SWE in adults with ConAoS and to compare SWV with healthy volunteers (HVs).

Methods

In 68 adult patients with ConAoS—including 17 patients after aortic valve replacement (AVR)—and 19 HVs, high-frame-rate recordings were acquired in the parasternal long-axis view. Custom software was used to measure SWV by manually placing M-mode lines through the interventricular septum after aortic valve closure.

Results

SWE feasibility was 73% in ConAoS patients with a native aortic valve (NV), 53% post-AVR and 100% in HVs. Median SWV was 4.7 m/s (3.2–5.5) in NV patients, 3.7 m/s (3.1–5.4) post-AVR and 3.4 m/s (3.0–4.4) in HVs (p=0.200). Patients with moderate-to-severe ConAoS demonstrated higher SWV compared with HVs (4.7 m/s (3.4–5.6) vs 3.4 m/s (3.0–4.4); p=0.035).

Conclusions

SWE is feasible in the majority of ConAoS patients. Higher SWV in moderate-to-severe ConAoS patients, despite preserved diastolic function in most cases, may reflect early myocardial mechanical alterations and provide a promising non-invasive marker for myocardial stiffening. Further technical optimisation and cross-platform validation are essential for clinical translation.

WHAT IS ALREADY KNOWN ON THIS TOPIC.

WHAT THIS STUDY ADDS

• Shear wave velocity (SWV) could be obtained in the majority of patients, including those after intervention. Higher SWV in patients with moderate-to-severe ConAoS, despite preserved diastolic function in most cases, may reflect early myocardial mechanical alterations and provide a promising non-invasive marker for myocardial stiffening. Following valve replacement, broad distribution of SWV values suggests heterogeneous myocardial mechanical properties following relief of pressure overload.

HOW THIS STUDY MIGHT AFFECT RESEARCH, PRACTICE OR POLICY

• SWV may serve as an early, non-invasive marker of myocardial mechanical alterations in ConAoS. Further technical optimisation and cross-platform validation are essential for clinical translation.

Introduction

Congenital aortic stenosis (ConAoS) accounts for approximately 4%–8% of all congenital heart disease.¹ It is often caused by a bicuspid aortic valve, with a prevalence of 0.5%–2% in the general population.²,⁵ While many patients remain asymptomatic for years, progressive worsening of the stenosis and subsequent pressure overload can result in left ventricular (LV) hypertrophy as a compensatory mechanism to normalise wall stress and maintain cardiac output.⁶ However, these initially adaptive changes may progress into myocardial fibrosis, leading to impaired cardiac filling, reduced contractility and ultimately contributing to the onset of symptomatic heart failure. Several studies suggest that myocardial stiffening is associated with increased mortality and adverse events, even after successful aortic valve replacement (AVR).⁷,¹⁵ Therefore, accurate assessment of myocardial stiffening is crucial for patients with ConAoS.

Invasive pressure-volume loop analysis remains the gold standard for assessment of LV chamber stiffness, but its clinical applicability is limited by its invasive nature and the associated risk of complications. Cardiovascular magnetic resonance (CMR) provides a non-invasive alternative for myocardial tissue characterisation, offering the possibility of late gadolinium enhancements, native T1 mapping and estimation of extracellular volume. Although these tools provide valuable insight into myocardial fibrosis, CMR is more costly, time-intensive and its use is often constrained by limited availability and patients’ contra-indications.

Recently, shear wave elastography (SWE) has been proposed as a novel, non-invasive technique for assessing myocardial stiffness. By applying multiline acquisition and broad transmit beams, echocardiography can achieve a very high temporal resolution (>500–1000 frames/s), enabling the visualisation of rapidly propagating shear waves within the myocardium. Shear waves are mechanical waves that can be artificially induced by the radiation force of a focused ultrasound impulse or naturally generated by intrinsic cardiac events such as closure of the aortic or mitral valve or atrial contraction. Previous studies demonstrated that the velocity of shear wave propagation (SWV) through the myocardium is related to myocardial stiffness, offering a promising tool to assess the mechanical properties of the LV.¹⁶,²³

Despite growing evidence supporting the potential of SWE in various cardiac pathologies,²²²⁴,³¹ data on its clinical applicability in ConAoS patients and its use following intervention have not yet been presented. In this study, we apply in-house-developed software in combination with a clinical high-frame-rate scanner to (a) evaluate the feasibility of SWE in adult ConAoS patients and (b) assess differences in SWV compared with healthy volunteers (HVs).

Methods

Study population and design

Adult patients (≥18 years) with ConAoS were prospectively included between 2022 and 2023 at the outpatient clinic of our tertiary centre. Inclusion criteria were (1) aortic valve peak velocity ≥2.5 m/s or (2) prior AVR for aortic stenosis (AS). Exclusion criteria were known history of severe aortic regurgitation (AR), presence of significant aortic coarctation, genetic disorders, connective tissue disease or pacemaker/implantable cardioverter defibrillator (ICD). In all patients, clinical examination, ECG, transthoracic echocardiography (TTE) and high frame rate (HFR) echocardiography were performed at baseline. A group of HVs, who had also undergone HFR echocardiography for a previous study at our centre, was included for comparison.³² Patients or the public were not involved in the design, recruitment or conduct of this study.

Conventional TTE

Standard echocardiographic examination was performed by two experienced sonographers (BLB, DJB) using an EPIQ7 ultrasound system (Philips Medical Systems, Best, the Netherlands) equipped with a transthoracic broadband X5-1 matrix transducer. Baseline conventional echocardiographic measurements were obtained through offline analysis of acquired images using QLAB software (Philips Medical Systems) and Cardiac Performance Analysis software (TomTec Imaging Systems GmbH, Munich, Germany). Conventional measurements were assessed according to the recommendations of the European Association of Cardiovascular Imaging and the American Society of Echocardiography.^{33 34} Severity of AS was classified based on evaluation by Doppler echocardiography and graded as mild, moderate or severe.

HFR echocardiography

A clinical system programmed by the manufacturer to enable HFR imaging was used (Zonare, ZS3, P4-1C probe, Mindray Innovation Center, San Jose, California, USA). Images were acquired in the parasternal long-axis view using live B-mode imaging with low frame rate to ensure probe positioning in the correct echocardiographic view. Subsequently, multiple HFR (1000 Hz) recordings were captured (1.2 s) per patient and were saved offline as beamformed data for offline processing. Depending on the heart rate, one or two aortic valve closure (AVC) events were captured within each recording.

Shear wave elastography

Analysis of HFR data was performed using an in-house-developed analysis package written in MATLAB R2017a (The Mathworks, Natick, Massachusetts, USA) software, based on the data analysis of an earlier study.³⁵ A 250 Hz lowpass filter was applied to the in-phase/quadrature beamformed data in slow time (cut-off value of 5.2 cm/s, sixth-order Butterworth), to remove high-frequency tissue Doppler signal mainly arising from blood and noise. A one-lag autocorrelation technique was used to obtain axial tissue velocities. Before computing the phase, the effect of speckle and noise was reduced with a spatial smoothing filter of 4 mm by 6.7°. Timing of AVC was determined based on a tissue Doppler spectrogram of the aortic valve (figure 1). In the frame corresponding to AVC, an anatomical M-mode line (20 mm) was manually drawn on the interventricular septum. HFR tissue colour Doppler panels were generated showing the axial tissue velocity of the anatomical M-mode line over time and were then filtered with a band-pass filter between 15 and 100 Hz. Shear waves were then semi-automatically identified and their propagation velocity calculated. To account for measurement variability, 10 measurements were acquired per PLAX with slight variance in angulation. This process was applied across 2–6 acquisitions, and a median value was calculated for each patient.

Figure 1. Schematic overview of shear wave elastography analysis. (A) Timing of aortic valve closure (AVC) based on tissue Doppler spectrogram of the aortic valve, (B) manual placement of anatomical M-line in the interventricular septum and (C) high-frame-rate tissue Doppler of M-line with semi-automatic detection of shear wave and velocity calculation.

Measurement quality was visually checked by evaluating the HFR tissue colour Doppler signal and graded as good, moderate or poor imaging quality (figure 2). Images with poor quality were regarded as not feasible and excluded from analysis.

Figure 2. Quality assessment shear wave elastography. Quality of shear wave velocity measurements was assessed from the high-frame-rate tissue Doppler imaging (TDI) tracings and categorised as optimal (A), suboptimal (B) or poor (C). A clear, continuous and well-defined TDI wavefront (A) was considered indicative of optimal measurement quality. Examples of suboptimal quality (B) include a generally weak TDI signal (left) and signal drop-out toward the end of the tracing (right). (C) Poor-quality measurements, characterised by a fragmented or irregular TDI wavefront (left), a nearly horizontal wavefront indicating unphysiologically high SWV values (>10 m/s) (middle) or complete absence of a TDI wavefront (right).

Statistical analysis

ConAoS patients were categorised into two groups: patients with a native aortic valve (NV) and those who had previously undergone AVR (post-AVR). Comparisons were made between patient groups and with HVs. Additionally, NV patients were stratified by AS severity, and SWV was compared across groups.

Distribution of the data was examined through histograms and the Shapiro-Wilk test. When normally distributed, continuous data were expressed as mean±SD and compared using a Student’s t-test. Non-parametric data were presented as median and IQR and compared using a Mann-Whitney U test. Categorical data were presented as frequencies with percentages and compared using a χ² test. Comparison of continuous data between more than two groups was performed using a one-way analysis of variance test or Kruskal-Wallis test according to distribution of the data. To compare categorical data between more than two groups, a χ² test was applied. If significant, post-hoc pairwise comparisons with Bonferroni would identify which groups differed from each other. Pearson’s or Spearman’s correlation coefficient was calculated to measure correlation based on distribution.

A two-sided p value below 0.05 was considered statistically significant. Statistical analysis was performed using SPSS for Windows (V.28.0, SPSS, Chicago, Illinois, USA).

Results

Baseline characteristics

A total of 68 adult ConAoS patients (median age 42 years, 34% female) and 19 HVs (median age 22 years, 58% female) were included. Table 1 displays the baseline characteristics. 17 (25%) patients had previously undergone AVR, comprising 14 (21%) cases with a mechanical and 3 (4%) with a biological valve. All AVR patients with feasible SWE measurements were assessed at least 1 year after intervention.

Table 1. Baseline characteristics.

	ConAoS (n=68)	HV (n=19)	P value
Age, years	42 (29–52)	22 (21–25)	<0.001
Female, n (%)	23 (34)	11 (58)	0.057
BMI, kg/m2	25±4	22±3	0.001
Heart rate, bpm	69 (60–76)	60 (56–66)	0.007
Systolic blood pressure, mm Hg	127±17	119±12	0.069
Diastolic blood pressure, mm Hg	77±8	69±10	0.002
ECG
Sinus rhythm, n (%)	68 (100)	19 (100)
QRS duration, ms	100 (94–108)	94 (89–102)	0.013
Intervention aortic valve
Prior AVR, n (%)	17 (25)
Mechanical valve, n (%)	14 (21)
Biological valve/homograft, n (%)	3 (4)

AVR, aortic valve replacement; BMI, body mass index; ConAoS, Congenital aortic stenosis; HVs, healthy volunteers.

Table 2 provides an overview of the conventional and HFR echocardiographic data in cases with feasible SWE measurements. Although only statistically significant in NV patients, greater LV dimensions were observed in both patient groups compared with HVs (184 mL (152–210) vs 176 mL (131–186) vs 119 mL (104–160); p<0.001). LV systolic function was preserved in all subjects (60% (58–64) vs 58% (57–64) vs 59% (56–63); p=0.545). Despite elevated E/e′ ratios in both NV and post-AVR patients compared with HVs (9±2 vs 10±2 vs 6±2; p<0.001), diastolic dysfunction was identified in only four patients, comprising three cases of grade I and one case of grade II. In NV patients, the median AV peak velocity was 3.7 m/s (3.2–4.2), and moderate or greater AR was observed in 20 cases (54%).

Table 2. Conventional and HFR echocardiography.

	ConAoS
	NV (n=37)	Post-AVR (n=9)	HV (n=19)	P value
LV dimensions
LVEDD, mm	55±6*	52±5	50±4	0.028
LVESD, mm	34±6	33±3	33±4	0.815
LVEDV, mL	184 (152–210)*	176 (131–186)	119 (104–160)	<0.001
LVESV, mL	76 (56–91)*	74 (50–79)	48 (38–64)	0.002
LVPW, mm	8 (8–9)*	8 (7–8)	7 (6–8)	0.001
IVS, mm	11 (9–12)	10 (8–14)*	8 (7–8)	<0.001
LV mass index, g/m2	95 (82–124)*	79 (78–99)	66 (55–77)	<0.001
LV function
LVEF, %	60 (58–64)	58 (57–64)	59 (56–63)	0.545
GLS, %	−20±2	−20±2	−20±2	0.834
Average e′, cm/s	11±2	10±2	12±2	0.069
E/A ratio	1.3 (1.1–1.6)*	1.3 (0.9–1.4)*	2.2 (1.3–2.3)	0.001
E/e′ ratio	9±2*	10±2*	6±2	<0.001
LAVI, mL/m2	31 (28–39)	32 (25–38)	31 (24–38)	0.892
Diastolic dysfunction
Grade I, n (%)	2 (5)	1 (11)	0 (0)	0.400
Grade II, n (%)	1 (3)	0 (0)	0 (0)	0.681
Aortic valve
AVPV, m/s	3.7 (3.2–4.2)	2.4 (2.2–2.9)		<0.001
Mild stenosis, n (%)	6 (16)	7 (78)		<0.001
Moderate stenosis, n (%)	19 (51)	2 (22)		0.116
Severe stenosis, n (%)	12 (32)	0 (0)		0.047
Moderate regurgitation, n (%)	19 (51)	0 (0)		0.005
Severe regurgitation, n (%)	1 (3)	0 (0)		0.618
Mitral valve
Moderate regurgitation, n (%)	1 (3)	0 (0)		0.618
Shear wave elastography
Feasibility rate, (%)	73*	53*	100	0.004
SWV, m/s	4.7 (3.2–5.5)	3.7 (3.1–5.4)	3.4 (3.0–4.4)	0.200

^*P<0.05 versus controls.

^†P<0.05 between native valve and mechanical valve.

^‡For comparisons involving more than two groups, p values were reported based on a one-way analysis of variance test. Post-hoc analyses with Bonferroni correction for multiple comparisons were conducted to assess pairwise differences.

AVPV, aortic valve peak velocity; AVR, aortic valve replacement; ConAoS, congenital aortic stenosis; GLS, global longitudinal strain; HV, healthy volunteer; IVS, interventricular septum; LAVI, left atrial volume index; LV, left ventricle; LVEDD, LV end-diastolic diameter; LVEDV, LV end-diastolic volume; LVEF, left ventricular ejection fraction; LVESD, LV end-systolic diameter; LVESV, LV end-systolic volume; LVPW, LV posterior wall thickness; NV, native aortic valve; SWE, shear wave elastography; SWV, shear wave velocity.

Shear wave elastography

SWV could be successfully measured in 37 of the 51 NV patients, demonstrating a feasibility of 73%. In patients post-AVR, a feasibility of 53% was observed with feasible measurements in nine patients, all of whom had a mechanical aortic valve. In the three patients with a biological valve or homograft, no SWV could be measured. SWE was feasible in all 19 (100%) HVs.

Lower feasibility was observed in older patients (p<0.001) and with higher body mass index (p=0.015). Although sample size was small, the presence of prior AVR was not significantly different between groups (p=0.134). A complete comparison of baseline characteristics between feasible and non-feasible cases is presented in online supplemental table 1.

Figure 3 provides an overview of the observed SWVs across the different patient groups and HVs. Although not statistically significant, SWV was higher in NV patients compared with HVs, while lower SWV values were found in both post-AVR patients and HVs (4.7 m/s (3.2–5.5) vs 3.7 m/s (3.1–5.4) vs 3.4 m/s (3.0–4.4); p=0.200).

Figure 3. Overview of shear wave velocity (SWV). Comparison of SWV between healthy volunteers (blue), patients with a native aortic valve (red) and patients who had previously undergone aortic valve replacement (AVR) (green).

When stratifying for AS severity, a significantly higher SWV with a value of 4.7 m/s (3.4–5.6) was observed in patients with moderate-to-severe AS compared with HVs with a value of 3.4 m/s (3.0–4.4) (p=0.035) (figure 4).

Figure 4. Shear wave velocity (SWV) in patients with moderate-to-severe aortic stenosis. Comparison of SWV between patients with a native aortic valve and moderate-to-severe aortic stenosis (red), compared with healthy volunteers (blue). The data point marked with an asterisk (*) represents an outlier; analyses were performed including this observation.

In NV patients, SWV was moderately correlated with body mass index (BMI) (r=0.37; p=0.024) and interventricular septal thickness (r=0.38; p=0.019) (figure 5, online supplemental table 3).

Figure 5. Correlation between shear wave velocity (SWV) and baseline characteristics. Scatterplots of the relation between SWV and baseline characteristics. Correlation between SWV and body mass index (A) and interventricular septal thickness (B).

Discussion

The aim of this study was to evaluate the feasibility of SWE in a clinical population of patients with ConAoS and to explore its potential as a marker of myocardial stiffening. SWV could be obtained in the majority of patients, indicating that SWV allows for the practical assessment of myocardial mechanical properties in a heterogeneous population, including those after intervention. Moreover, SWV was significantly higher in patients with more advanced stages of aortic valve disease compared with healthy individuals, despite preserved diastolic function in most cases. These findings may reflect early myocardial mechanical alterations in ConAoS.

Feasibility of SWE in the clinical patient population

SWV could be successfully measured in 73% of patients with an NV and in all HVs, indicating good overall feasibility in a real-world setting. This rate exceeds that reported by Espeland et al,³⁰ who obtained valid SWV data in 62% of AS patients and 45%–66% of HVs. The relatively young age and favourable imaging conditions in our cohort likely contributed to improved visualisation of the interventricular septum, although no patients were excluded based on image quality to ensure representative results.

In contrast, studies in patients with cardiac amyloidosis and hypertrophic cardiomyopathy reported higher feasibility rates (88%–100%).^{24 25} This difference may stem from disease-specific factors, as aortic valve pathology might hinder the generation or propagation of shear waves through altered wave mechanics.³⁶ Notably, technical differences, such as ultrasound settings, tissue Doppler filtering and post-processing methods, may also contribute to different SWE feasibility.

In our study, older age and higher BMI were both associated with reduced feasibility, in line with the known negative effect of body habitus on ultrasound penetration and signal-to-noise ratio. The most common technical limitation hindering reliable SWV measurement was the absence of a distinct Doppler waveform, likely due to limited spatial resolution and septal misalignment, both of which were frequently encountered in these patients.

Despite growing interest in SWE across various cardiac diseases, data on its applicability postintervention remain scarce. To explore its applicability across the entire disease course, this study also included patients following AVR. Successful measurements were obtained in 53% of post-AVR patients, all with mechanical valves. These findings suggest that mechanical prostheses, composed of rigid materials such as carbon and titanium, can generate sufficient mechanical energy to initiate shear waves that propagate into the adjacent myocardium. In contrast, no measurable SWV was obtained in patients with biological valves or homografts, possibly due to their reduced rigidity or damping of vibrational energy.

However, abnormal tissue Doppler patterns were common in patients with prosthetic valves. While poor image quality and valve-related artefacts likely contributed, the possibility of absent SW generation cannot be excluded as movements of the myocardium or blood flow may also be misinterpreted as shear waves.

SWV as a marker of myocardial stiffening in ConAoS

After stratification for AS severity, significantly higher SWV values were observed in patients with moderate-to-severe AS compared with HVs. This may support the hypothesis that SWV reflects myocardial stiffness, which increases in response to chronic pressure overload. Importantly, these patients exhibited preserved LV systolic function, with diastolic dysfunction observed in only two cases (one grade I, one grade II), suggesting subclinical myocardial remodelling prior to overt functional impairment. However, given that the HVs were significantly younger, age-related myocardial alterations may also have contributed to our findings.^{24 37 38}

Our findings align with the results of Espeland et al,³⁰ who reported SWVs of 3.4 m/s and 4.2 m/s in patients with severe AS (mean Vmax 5.3 m/s), showing a comparable relative increase of approximately 1.3–1.6 m/s compared with controls. The observation of similar SWV elevations in our patients with less advanced disease supports the notion that SWV may detect early myocardial stiffening. Notably, Wouters et al³⁶ reported substantially higher values, with a mean SWV of 5.9 m/s±1.6 in 17 patients with severe AS (mean peak gradient (PG) 56.7 mm Hg±14.6). Although mild phenotype and younger age may underlie these differences, interindividual variability and methodological differences between studies, including acquisition techniques, frame rate and post-processing algorithms, must also be considered. Standardisation of methodology and calibration across systems is crucial for inter-study comparability.

Our observed SWVs are also consistent with those in other cardiac disease populations, where even greater myocardial stiffening would be expected. In patients with cardiac amyloidosis—where myocardial stiffness is markedly increased due to amyloid fibril deposition in the myocardial interstitium—Petrescu et al²⁴ and Jin et al²⁹ reported elevated SWVs with values of 5.63±1.13 m/s and 5.58±1.10 m/s, respectively. Validating SWV against histopathological findings in explanted hearts, Dukefoss et al²² also reported similar elevations in SWV in end-stage heart failure patients. Interestingly, despite finding moderate to strong correlations between septal collagen volume fraction and SWV after both AVC and MVC, no correlation was observed when AVC waves were measured in the PLAX view. Together, these findings not only reinforce the concept that elevated SWV reflects mechanical changes in diseased myocardium but also highlight the need for further research to identify the optimal imaging approach and elucidate the exact mechanisms driving increased SWV.

SWV after AVR

In post-AVR patients, each assessed at least 1 year after intervention, broad distribution of SWV values was observed. These variations may reflect heterogeneous myocardial mechanical properties and potentially different stages of reverse remodelling following relief of pressure overload. These observations align with previous imaging studies showing that LV mass regression and normalisation of strain parameters after AVR may take months to years, and that residual fibrosis may persist despite haemodynamic improvement.^{39 40}

However, caution is warranted when interpreting these findings, as differences in excitation source introduced by the prosthetic valve may alter wave mechanics and potentially influence measured SWV. Although SWV itself did not significantly change in a small longitudinal study by Wouters et al³⁶ of nine AS patients undergoing AVR, wave amplitude and width differed from matched controls.

Together, these findings suggest that SWV may have potential for longitudinal assessment following intervention, although larger longitudinal studies combining SWV with advanced tissue characterisation techniques such as CMR are needed to further validate this hypothesis.

Correlation of SWV with conventional echocardiography

In our cohort of patients with an NV, SWV did not significantly correlate with conventional echocardiographic markers of diastolic function, such as E/e′, E/A, e′ and LAVI. As these parameters can exhibit discrepancies in detecting diastolic dysfunction and must therefore be used in combination, our findings support the potential of SWV as an independent biomarker.

A moderate association was observed between SWV and both LV interventricular septal and posterior wall thickness, measures of LV hypertrophy linked to myocardial stiffening. Compared with previous studies, the association observed in our cohort was weaker, which may reflect the relatively mild phenotype of our population.^{26 37 38} Alternatively, this finding could support the notion that SWV captures direct mechanical properties of the myocardium, providing incremental diagnostic value beyond conventional measures.

Limitations

This study has several limitations. First, measurement variability remains a concern, partly due to suboptimal image quality, potentially resulting from limited spatial resolution, especially at the periphery of the acoustic window. Optimising echocardiographic setup may improve spatial resolution and consistency.

Although post-processing is semi-automated, key steps still require manual input, such as identifying the time instance of AVC and placing M-mode lines. Further automation could reduce user dependence, shorten analysis time, and enable multi-beat assessment, as previously suggested by Vos et al.⁴¹

A recent proof-of-concept study by Papadacci et al⁴² explored three-dimensional SWE by measuring SWV along multiple propagation directions from time-of-flight maps. While confirming a base-to-apex propagation pattern, the study also highlighted the complexity of 3D shear wave propagation. Notably, misalignment through 2D measurement may contribute to the measurement inaccuracy observed in our study.

Besides technical limitations, SWE is also constrained by physiological factors. SWV is shown to be impacted by cardiac morphology, with differences in wall thickness and fibre architecture influencing measured SWV.^{26 29 37 42 43} Additionally, it is important to recognise that only regional measurements are obtained that may not reflect global LV stiffness in the presence of regional disease. Furthermore, SWV is shown to be impacted by loading conditions, with altered loading states leading to shifts along the stress-strain relation, affecting operational stiffness and measured SWV.²⁴,2729 37 43 44 Finally, SWV measured at AVC captures myocardial properties during early relaxation and should therefore be interpreted within the context of the cardiac cycle.

Conclusions

SWV measurement using ultrafast ultrasound is feasible in the majority of adult patients with ConAoS and may provide a quantitative, non-invasive parameter reflecting myocardial stiffness. Increased SWV in patients with moderate-to-severe AS, despite preserved diastolic function in most cases, may reflect early myocardial mechanical alterations prior to overt functional decline. Following valve replacement, broad distribution of SWV values suggests heterogeneous myocardial mechanical properties and potentially different stages of reverse remodelling following relief of pressure overload. Although image quality, measurement variability and lack of standardisation currently limit widespread application, SWV has considerable promise as a biomarker for early detection, disease monitoring and therapy evaluation in pressure-overload cardiomyopathies. Further technical optimisation and cross-platform validation are essential to establish reproducibility and facilitate clinical translation.

Data availability statement

Data are available upon reasonable request.