Bart W.L. De Boeck

Echocardiographic quantification of myocardial function using tissue deformation imaging, a guide to image acquisition and analysis using tissue Doppler and speckle tracking

Recent developments in the field of echocardiography have allowed the cardiologist to objectively quantify regional and global myocardial function. Regional deformation (strain) and deformation rate (strain-rate) can be calculated non-invasively in both the left and right ventricle, providing information on regional (dys-)function in a variety of clinical settings. Although this promising novel technique is increasingly applied in clinical and preclinical research, knowledge about the principles, limitations and technical issues of this technique is mandatory for reliable results and for implementation both in the clinical as well as the scientific field.In this article, we aim to explain the fundamental concepts and potential clinical applicability of strain and strain-rate for both tissue Doppler imaging (TDI) derived and speckle tracking (2D-strain) derived deformation imaging. In addition, a step-by-step approach to image acquisition and post processing is proposed. Finally, clinical examples of deformation imaging in hypertrophic cardiomyopathy (HCM), cardiac resynchronization therapy (CRT) and arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) are presented.

Septal rebound stretch reflects the functional substrate to cardiac resynchronization therapy and predicts volumetric and neurohormonal response

To develop a novel myocardial deformation index that is highly sensitive to the effect of cardiac resynchronization therapy (CRT) and that can be used to predict response to CRT.

Echocardiographic tissue deformation imaging of right ventricular systolic function in endurance athletes

AIMS To investigate the physiological adaptation of the right ventricle (RV) in response to endurance training and to define reference values for regional deformation in the RV in endurance athletes. METHODS AND RESULTS Healthy controls (n = 61), athletes (n = 58), and elite athletes (n = 63) were prospectively enrolled with a training intensity of 2.2 +/- 1.6, 12.5 +/- 2.3 and 24.2 +/- 5.7 h/week, respectively (P < 0.001). Conventional echocardiographic parameters, tissue Doppler imaging (TDI), and 2D strain echo (2DSE)-derived velocity, strain, and strain rate (SR) were calculated in three RV segments. Left ventricular and RV dimensions were significantly increased (P < 0.001) in both groups of athletes compared with controls. Right ventricular systolic velocities and displacement were not different between the groups. Right ventricular strain and SR values were reduced in the RV basal and mid-segment in athletes. Athletes with marked RV dilatation showed lower strain and SR values in the basal (-20.9 +/- 4.7 vs. -24.5 +/- 4.9%, P < 0.001 and -1.23 +/- 0.31 vs. -1.50 +/- 0.33 s(-1), P < 0.001) and mid (-29.3 +/- 5.4 vs. -32.1 +/- 5.3%, P = 0.017 and -1.58 +/- 0.41 vs. -1.82 +/- 0.42 s(-1), P = 0.009) segment, whereas athletes without RV dilatation showed no significant difference compared with the controls. CONCLUSION Regional deformation and deformation rates (TDI and 2DSE) are reduced in the basal RV segment in athletes. This phenomenon is most pronounced in athletes with RV dilatation and should be interpreted as normal when evaluating athletes suspected for RV pathology.

Echocardiographic Tissue Deformation Imaging Quantifies Abnormal Regional Right Ventricular Function in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy

BACKGROUND The aim of this study was to determine the accuracy of new quantitative echocardiographic strain and strain-rate imaging parameters to identify abnormal regional right ventricular (RV) deformation associated with arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). METHODS A total of 34 patients with ARVD/C (confirmed by Task Force criteria) and 34 healthy controls were prospectively enrolled. Conventional echocardiography, including Doppler tissue imaging (DTI), was performed. Doppler and two-dimensional strain-derived velocity, strain, and strain rate were calculated in the apical, mid, and basal segments of the RV free wall. RESULTS RV dimensions were significantly increased in patients with ARVD/C (RV outflow tract 19.3+/-5.2 mm/m2 vs 14.1+/-2.2 mm/m2, P<.001; RV inflow tract 23.4+/-4.8 mm/m2 vs 18.8+/-2.4 mm/m2, P<.001), whereas left ventricular dimensions were not significantly different compared with controls. Strain and strain rate values were significantly lower in patients with ARVD/C in all 3 segments. All deformation parameters showed a higher accuracy to detect functional abnormalities compared with conventional echocardiographic criteria of dimensions or global systolic function. The lowest DTI strain value in any of the 3 analyzed segments showed the best receiver operating characteristics (area under the curve 0.97) with an optimal cutoff value of -18.2%. CONCLUSIONS DTI and two-dimensional strain-derived parameters are superior to conventional echocardiographic parameters in identifying ARVD/C. This novel technique may have additional value in the diagnostic workup of patients with suspected ARVD/C.

Spectral pulsed tissue doppler imaging in diastole: A tool to increase our insight in and assessment of diastolic relaxation of the left ventricle

BACKGROUND Conventional Doppler echocardiography offers an indirect assessment of left ventricular (LV) diastolic function, hampered by preload dependency. Tissue Doppler imaging (TDI) is a tool to study diastolic function in a more direct and less preload-dependent manner. METHODS The Medline database has been searched for literature on TDI for the analysis of diastolic function. A secondary search reviewed the relevant references related to TDI or diastolic function in general. RESULTS TDI measures myocardial velocities with a high temporal and velocity resolution but lacks spatial information. In particular, the velocity of early diastolic wall motion (E(m)) and its timing are promising indices of local myocardial relaxation. E(m) at the mitral annulus offers fair estimates of ventricular relaxation, relatively independent of preload and systolic function. Combined with early transmitral flow velocity (E), detection of pseudo-normalized filling patterns and estimation of filling pressures are enhanced by E/E(m). CONCLUSION TDI has an emerging role in the study and assessment of diastolic function. However, TDI-derived information needs to be integrated with other echocardiographic data because single diagnostic accuracy remains unsatisfactory.

Septal Deformation Patterns Delineate Mechanical Dyssynchrony and Regional Differences in Contractility: Analysis of Patient Data Using a Computer Model

Background— Response to cardiac resynchronization therapy depends both on dyssynchrony and (regional) contractility. We hypothesized that septal deformation can be used to infer integrated information on dyssynchrony and regional contractility, and thereby predict cardiac resynchronization therapy response. Methods and Results— In 132 cardiac resynchronization therapy candidates with left bundle branch block (LBBB)-like electrocardiogram morphology (left ventricular ejection fraction 19±6%; QRS width 170±23 ms), longitudinal septal strain was assessed by speckle tracking echocardiography. To investigate the effects of dyssynchronous activation and differences in septal and left ventricular free wall contractility on septal deformation pattern, we used the CircAdapt computer model of the human heart and circulation. In the patients, 3 characteristic septal deformation patterns were identified: LBBB-1=double-peaked systolic shortening (n=28); LBBB-2=early systolic shortening followed by prominent systolic stretching (n=34); and LBBB-3=pseudonormal shortening with less pronounced late systolic stretch (n=70). LBBB-3 revealed more scar (2 [2–5] segments) compared with LBBB-1 and LBBB-2 (both 0 [0–1], P<0.05). In the model, imposing a time difference of activation between septum and left ventricular free wall resulted in pattern LBBB-1. This transformed into pattern LBBB-2 by additionally simulating septal hypocontractility, and into pattern LBBB-3 by imposing additional left ventricular free wall or global left ventricular hypocontractility. Improvement of left ventricular ejection fraction and reduction of left ventricular volumes after cardiac resynchronization therapy were most pronounced in LBBB-1 and worst in LBBB-3 patients. Conclusions— A double-peaked systolic septal deformation pattern is characteristic for LBBB and results from intraventricular dyssynchrony. Abnormal contractility modifies this pattern. A computer model can be helpful in understanding septal deformation and predicting cardiac resynchronization therapy response.

Practical and conceptual limitations of tissue Doppler imaging to predict reverse remodelling in cardiac resynchronisation therapy

Recent, conflicting results about the use of tissue Doppler imaging derived (TDI‐) asynchrony indices to predict reverse remodelling after cardiac resynchronisation therapy (CRT) have raised questions about their physiological meaning and methodological limitations.

Septal Deformation Patterns Delineate Mechanical Dyssynchrony and Regional Differences in ContractilityClinical Perspective

Background— Response to cardiac resynchronization therapy depends both on dyssynchrony and (regional) contractility. We hypothesized that septal deformation can be used to infer integrated information on dyssynchrony and regional contractility, and thereby predict cardiac resynchronization therapy response. Methods and Results— In 132 cardiac resynchronization therapy candidates with left bundle branch block (LBBB)-like electrocardiogram morphology (left ventricular ejection fraction 19±6%; QRS width 170±23 ms), longitudinal septal strain was assessed by speckle tracking echocardiography. To investigate the effects of dyssynchronous activation and differences in septal and left ventricular free wall contractility on septal deformation pattern, we used the CircAdapt computer model of the human heart and circulation. In the patients, 3 characteristic septal deformation patterns were identified: LBBB-1=double-peaked systolic shortening (n=28); LBBB-2=early systolic shortening followed by prominent systolic stretching (n=34); and LBBB-3=pseudonormal shortening with less pronounced late systolic stretch (n=70). LBBB-3 revealed more scar (2 [2–5] segments) compared with LBBB-1 and LBBB-2 (both 0 [0–1], P<0.05). In the model, imposing a time difference of activation between septum and left ventricular free wall resulted in pattern LBBB-1. This transformed into pattern LBBB-2 by additionally simulating septal hypocontractility, and into pattern LBBB-3 by imposing additional left ventricular free wall or global left ventricular hypocontractility. Improvement of left ventricular ejection fraction and reduction of left ventricular volumes after cardiac resynchronization therapy were most pronounced in LBBB-1 and worst in LBBB-3 patients. Conclusions— A double-peaked systolic septal deformation pattern is characteristic for LBBB and results from intraventricular dyssynchrony. Abnormal contractility modifies this pattern. A computer model can be helpful in understanding septal deformation and predicting cardiac resynchronization therapy response.

Mechanistic Evaluation of Echocardiographic Dyssynchrony Indices Patient Data Combined With Multiscale Computer Simulations

Background— The power of echocardiographic dyssynchrony indices to predict response to cardiac resynchronization therapy (CRT) appears to vary between indices and between studies. We investigated whether the variability of predictive power between the dyssynchrony indices can be explained by differences in their operational definitions. Methods and Results— In 132 CRT-candidates (left ventricular [LV] ejection fraction, 19 ± 6%; QRS width, 170 ± 22 ms), 4 mechanical dyssynchrony indices (septal systolic rebound stretch [SRSsept], interventricular mechanical dyssynchrony [IVMD], septal-to-lateral peak shortening delay [Strain-SL], and septal-to-posterior wall motion delay [SPWMD]) were quantified at baseline. CRT response was quantified as 6-month percent change of LV end-systolic volume. Multiscale computer simulations of cardiac mechanics and hemodynamics were used to assess the relationships between dyssynchrony indices and CRT response within wide ranges of dyssynchrony of LV activation and reduced contractility. In patients, SRSsept showed best correlation with CRT response followed by IVMD, Strain-SL, and SPWMD (R=−0.56, −0.50, −0.48, and −0.39, respectively; all P<0.01). In patients and simulations, SRSsept and IVMD showed a continuous linear relationship with CRT response, whereas Strain-SL and SPWMD showed discontinuous relationships characterized by data clusters. Model simulations revealed that this data clustering originated from the complex multipeak pattern of septal strain and motion. In patients and simulations with (simulated) LV scar, SRSsept and IVMD retained their linear relationship with CRT response, whereas Strain-SL and SPWMD did not. Conclusions— The power to predict CRT response differs between indices of mechanical dyssynchrony. SRSsept and IVMD better represent LV dyssynchrony amenable to CRT and better predict CRT response than the indices assessing time-to-peak deformation or motion.Background— The power of echocardiographic dyssynchrony indices to predict response to cardiac resynchronization therapy (CRT) appears to vary between indices and between studies. We investigated whether the variability of predictive power between the dyssynchrony indices can be explained by differences in their operational definitions. Methods and Results— In 132 CRT-candidates (left ventricular [LV] ejection fraction, 19 ± 6%; QRS width, 170 ± 22 ms), 4 mechanical dyssynchrony indices (septal systolic rebound stretch [SRSsept], interventricular mechanical dyssynchrony [IVMD], septal-to-lateral peak shortening delay [Strain-SL], and septal-to-posterior wall motion delay [SPWMD]) were quantified at baseline. CRT response was quantified as 6-month percent change of LV end-systolic volume. Multiscale computer simulations of cardiac mechanics and hemodynamics were used to assess the relationships between dyssynchrony indices and CRT response within wide ranges of dyssynchrony of LV activation and reduced contractility. In patients, SRSsept showed best correlation with CRT response followed by IVMD, Strain-SL, and SPWMD ( R =−0.56, −0.50, −0.48, and −0.39, respectively; all P <0.01). In patients and simulations, SRSsept and IVMD showed a continuous linear relationship with CRT response, whereas Strain-SL and SPWMD showed discontinuous relationships characterized by data clusters. Model simulations revealed that this data clustering originated from the complex multipeak pattern of septal strain and motion. In patients and simulations with (simulated) LV scar, SRSsept and IVMD retained their linear relationship with CRT response, whereas Strain-SL and SPWMD did not. Conclusions— The power to predict CRT response differs between indices of mechanical dyssynchrony. SRSsept and IVMD better represent LV dyssynchrony amenable to CRT and better predict CRT response than the indices assessing time-to-peak deformation or motion.

Colour M-mode velocity propagation: a glance at intra-ventricular pressure gradients and early diastolic ventricular performance.

The physiology of early‐diastolic filling comprises ventricular performance and fluid dynamical principles. Elastic recoil and myocardial relaxation rate determine left ventricular early diastolic performance. The integrity of left ventricular synchrony and geometry is essential to maintain the effect of their timely action on early diastolic left ventricular filling. These factors not only are prime determinants of left ventricular pressure decay during isovolumic relaxation and immediately after mitral valve opening; they also instigate the generation of a sufficient intra‐ventricular pressure gradient, which enhances efficient early diastolic left ventricular filling. Accurate assessment of diastolic (dys)function by non‐invasive techniques has important therapeutic and prognostic implications but remains a challenge to the cardiologist. The evaluation of left ventricular relaxation by the standard Doppler echocardiographic parameters is hindered by their preload dependency. The colour M‐mode velocity propagation of early diastolic inflow (Vp) correlates with intra‐ventricular pressure gradients and is a largely preload independent index of ventricular diastolic performance. In this article, the physiologic background, utility and limitations of this promising new tool for the study of early diastolic filling are reviewed.