Mitral Valve Closure Research Articles

Magnitude of mitral valve closure plays a pivotal role in enhancing the forward blood flow during cardiac massage in dogs with ventricular fibrillation.

Motion of mitral valve during cardiac massage was examined using beagle dogs with ventricular fibrillation (n=4). Active compression-decompression cardiac massage (ACD-CM) exhibited greater peak aortic pressure than standard cardiac massage (S-CM), reverse of which was true for peak pulmonary capillary wedge pressure in each animal. Accordingly, peak aortic pressure was greater than peak pulmonary capillary wedge pressure with ACD-CM, whereas its reverse was true with S-CM. Transesophageal echocardiography revealed that mitral valve was incompletely closed with S-CM with showing regurgitation. The valve was more effectively closed during ACD-CM. These results indicate that effective closure of mitral valve during cardiac massage may increase forward blood flow, supporting “cardiac pump theory” rather than “thoracic pump theory” as a principle in dogs.

Quantifying preload alterations using a sensitive chest-mounted accelerometer

Abstract Seismocardiography (SCG) is a technology where the chest wall vibrations from the beating heart are measured using a highly sensitive accelerometer. SCG offers continuous measurement of cardiac function and potential applications include remote monitoring, diagnostic assessments, prognostic health checks and biventricular pacemaker optimization. Aim In the current study we examined how changes in preload influence SCG time intervals, by acute saline infusion. Methods We included twenty-six subjects, sixteen subjects with cardiac disease such as hypertrophic cardiomyopathy, dilated cardiomyopathy, aortic valve disease or ischemic heart disease (age 45.8±17.7 years and 93% male) and ten subjects without known cardiac conditions (age 42.1±14.4 years and 70% male). SCG was recorded from the xiphoid process using a custom-made sensor before and after acute infusion saline (median 2.0 L). The SCG signals were sampled with 5000 samples per second in 60 seconds, the individual heartbeats were identified using a dedicated segmentation algorithm and an average SCG beat was computed and used for the data analysis. Using a recently proposed nomenclature the following SCG fiducial points was identified: Es which coinciding with mitral valve closure, Gs which to some degree coincides with aortic opening, Bd coinciding with aortic valve closure and Fd coinciding with mitral valve opening [1]. The Es-Gs time interval was used as a measure of isovolumetric contraction time (IVCT), the Gs-Bd time interval was used as an estimate of ejection time (ET) and the Bd-Fd time interval as an estimate of isovolumetric relaxation time (IVRT). Paired t-test was used to test for significant response after infusion, while a two sample t-test was used to test for a significant difference in the observed response in subjects with or with our cardiac disease. Results For two subjects SCG after infusion was not obtained thus, twenty-four subjects were included in the final data analysis. In the whole group, acute saline infusion shortened the IVRT (Bd-Fd) from 91.0±15.3 ms to 82.7±15.3 ms (p=0.004) and prolonged the ET (Gs-Bd) from 329.4±35 ms to 343.4±33 ms (p<0.001). There was no significant change in IVCT (Es-Gs) which was 39.5±15.1 ms at baseline and 38.1±14.9 ms post-infusion (p=0.88). There was no significant difference in response between subjects with or without cardiac disease. Conclusion Increase in preload shortened the SCG time intervals related to the isovolumetric relaxation period and prolonged the period related to ejection time. SCG time intervals capture changes in preload, which demonstrates that the SCG is a potential modality for quantification of cardiac dynamics. Funding Acknowledgement Type of funding sources: None.

Using Position‐Based Dynamics for Simulating Mitral Valve Closure and Repair Procedures

AbstractTo achieve the best treatment of mitral valve disease in a patient, surgeons aim to optimally combine complementary surgical techniques. Image‐based in silico simulation as well as visualization of the mitral valve dynamics can support the visual analysis of the patient‐specific valvular dynamics and enable an exploration of different therapy options. The usage in a time‐constrained clinical environment requires a mitral valve model that is cost‐effective, easy to set up, parameterize and evaluate. Working towards this goal, we develop a simplified model of the mitral valve and analyse its applicability for the sketched use‐case. We propose a novel approach to simulate the mitral valve with position‐based dynamics. The resulting mitral valve model can be deformed to simulate the closing and opening, and incorporate changes caused by virtual interventions in the simulation. Ten mitral valves were reconstructed from transesophageal echocardiogram sequences of patients with normal and abnormal physiology for evaluation. Simulation results showed good agreements with expert annotations of the original image data and reproduced valve closure in all cases. In four of five pathological cases, abnormal closing behaviour was correctly reproduced. In future research, we aim to improve the parameterization of the model in terms of biomechanical correctness and perform a more extensive validation.

Abstract 11585: Determination of Aortic and Mitral Valve Opening and Closing Times Using Only LV Pressure Data

Background: Identification of aortic and mitral valve opening and closure timing is crucial for assessment of left ventricle (LV) function, e.g. pressure-volume loops. This is particularly problematic when simultaneous imaging (e.g. echocardiography) is not available. We hypothesize that LV pressure and its time derivatives can detect valve opening and closure times. Our aim was to determine the aortic and mitral valve opening and closures using properties of the LV pressure waveform. Methods: For this pilot study, in 3 human participants in sinus rhythm, LV pressures were recorded with a high-fidelity catheter. Echocardiographic 2D-guided M-mode images were obtained across the aortic and mitral valves in the parasternal long axis view. The timing of aortic and mitral valve events was linked to the ECG tracing, using the peak of the ECG R wave as the reference point. For each participant, two consecutive heartbeats were selected and the first (dP/dt), second (d 2 P/dt 2 ), and third derivatives (d 3 P/dt 3 ) of LV pressure calculated. Local maxima and minima from these were compared with the valve timing from M-mode. Results: The maximum of dP/dt at the beginning of the systolic phase occurred consistently with the opening of the aortic valve. Local minimum and maximum d 2 P/dt 2 occurred at the closure of the aortic valve and pre-atrial contraction timing, respectively. The early diastolic minimum of d 3 P/dt 3 and early systolic maximum of d 3 P/dt 3 coincided with M-mode mitral valve opening and closure timing, respectively. There was a strong correlation between the valve events timing that was measured using these two methods (R 2 =0.98, p<0.001). Conclusion: Aortic and mitral valve timing defined using LV pressure waveform agrees with valve opening/closure timing determined using echo M-mode as the gold standard. Determination of these valve timings is helpful for advanced analysis of LV mechanics when simultaneous echocardiography is not available.

Myocardial stiffness assessed by natural shear wave elastography is related to pressure-volume loop derived parameters

Abstract Background Several cardiovascular disorders are accompanied by a stiffening of the myocardium and may result in diastolic heart failure. The non-invasive assessment of myocardial stiffness could therefore improve the understanding of the pathophysiology and guide treatment. Shear wave elastography (SWE) is a recent technique with tremendous potential for evaluating myocardial stiffness in a non-invasive way. Using high frame rate echocardiography, the propagation speed of shear waves is evaluated, which is directly related to the stiffness of the myocardium. These waves are induced by for instance mitral valve closure (MVC) and propagate throughout the cardiac muscle. However, validation of SWE against an invasive gold standard method is lacking. Purpose The aim of this study was to compare echocardiographic shear wave elastography against invasive pressure-volume loops, a gold standard reference method for assessing chamber stiffness. Methods In 15 pigs (31.2±4.1 kg) stiffness of the myocardium was acutely changed by inducing ischemia/reperfusion (I/R) injury. For this, the proximal LAD was balloon occluded for 90 minutes with subsequent reperfusion for 40 minutes. Conventional and high frame rate echocardiographic images were acquired simultaneously with pressure-volume loops during baseline conditions and after the induction of the I/R injury. Preload was reduced in order to acquire a set of pressure-volume loops to derive the end-diastolic pressure volume relation (EDPVR). From the EDPVR, the stiffness coefficient β and the operating chamber stiffness dP/dV were obtained. High frame rate echocardiographic datasets of the parasternal long axis view were acquired with an experimental ultrasound scanner (HD-PULSE) at an average frame rate of 1304±115 Hz. Tissue acceleration maps were obtained by drawing an M-mode line along the interventricular septum in order to visualize shear waves after MVC (at end-diastole). The propagation speed was assessed by semi-automatically measuring the slope (Figure A). Results I/R injury led to an elevated chamber stiffness constant β (0.09±0.03 1/ml vs. 0.05±0.01 1/ml; p<0.001) and operating chamber stiffness dP/dV (1.09±0.38 mmHg/ml vs. 0.50±0.18 mmHg/ml; p<0.01). Likewise, shear wave speed after MVC increased after the induction of the I/R injury in comparison to baseline (6.1±1.2 m/s vs. 3.2±0.8 m/s; p<0.001). Shear wave speed had a moderate positive correlation with β (r=0.63; p<0.001) (Figure B) and a strong positive correlation with dP/dV (r=0.81; p<0.001) (Figure C). Conclusion End-diastolic shear wave speed is strongly related to chamber stiffness, assessed invasively by pressure-volume loops. These results indicate that shear wave propagation speed could be used as a novel non-invasive measurement of the mechanical properties of the ventricle. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): FWO - Research Foundation Flanders

Cardiac shear wave elastography can distinguish healthy and scarred myocardium in patients with conduction delays

Abstract Background Cardiac resynchronization therapy (CRT) is an established therapy for patients suffering from heart failure and left bundle branch block (LBBB) conduction delays. Despite its proven beneficial effects, CRT is associated with a high percentage of non-response. Since CRT has shown to be less effective in patients with ischemic cardiomyopathy, determining the presence of myocardial scar before implantation could help to improve the response-rate. However, the gold standard to assess myocardial scar, magnetic resonance imaging (MRI), cannot be used in every patient, due to already implanted devices and/or reduced renal function. Recently introduced shear wave elastography (SWE) allows the non-invasive assessment of myocardial stiffness. Natural shear waves are excited by mitral valve closure (MVC) and travel through the heart with a speed directly related to tissue stiffness. SWE has previously been proven to be able to detect myocardial scar, however this has never been shown in the presence LBBB. Purpose The aim of this study was to evaluate the capability of SWE as a novel method to determine myocardial scar in patients with conduction delays. Methods We included 24 heart failure patients (age: 68±10; 50% males) with ischemic (n=8) and non-ischemic (n=16) cardiomyopathy. The CRT device was set to AAI mode in order to obtain native ventricular conduction. For patients with ischemic cardiomyopathy, the presence and location of scar was determined by MRI or scintigraphy. All ischemic patients had septal scar only. For SWE, left ventricular parasternal long-axis views were acquired with an experimental high frame rate ultrasound scanner (average frame rate: ±1200 Hz). Shear waves were visualized in M-modes of the septum, colour coded for tissue acceleration. The slope of the shear waves in the M-mode represents their propagation speed (Figure A). Results There was no significant difference between the ischemic and non-ischemic patients in QRS width after CRT (149±31 ms vs 144±26 ms), systolic blood pressure blood pressure (135±11 mmHg vs 135±23 mmHg), diastolic blood pressure (74±9 mmHg vs 70±11 mmHg) and heart rate (58±4 bpm vs 63±9 bpm) (all p>0.05). Ejection fraction (33±8% vs 45±10%), end-diastolic volume (196±34 ml vs 129±64 ml) and global longitudinal strain (−9.8±3.1% vs −14.1±4.1%) differed significantly between the groups (all p<0.05). Shear wave speed after MVC was significantly higher in patients with septal scar compared to non-ischemic patients (8.2±1.9 m/s vs 5.5±1.2 m/s; p<0.01) (Figure B). Conclusion In the presence of scar, we found markedly elevated shear wave propagation speed compared to non-ischemic patients. These results indicate that SWE is able to identify scarred myocardium even in patients with LBBB. We therefore believe that SWE could be a novel easy and non-invasive method to evaluate septal myocardial scarring in patients before CRT implantation. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): FWO - Research Foundation Flanders

Quantifying preload alterations using a sensitive chest-mounted accelerometer

Abstract Seismocardiography (SCG) is a technology where the chest wall vibrations from the beating heart are measured using a highly sensitive accelerometer. SCG offers continuous measurement of cardiac function and potential applications include remote monitoring, diagnostic assessments, prognostic health checks and biventricular pacemaker optimization. Aim In the current study we examined how changes in preload influence SCG time intervals, by acute saline infusion. Methods We included twenty-six subjects, sixteen subjects with cardiac disease such as hypertrophic cardiomyopathy, dilated cardiomyopathy, aortic valve disease or ischemic heart disease (age 45.8±17.7 years and 93% male) and ten subjects without known cardiac conditions (age 42.1±14.4 years and 70% male). SCG was recorded from the xiphoid process using a custom-made sensor before and after acute infusion saline (median 2.0 L). The SCG signals were sampled with 5000 samples per second in 60 seconds, the individual heartbeats were identified using a dedicated segmentation algorithm and an average SCG beat was computed and used for the data analysis. Using a recently proposed nomenclature the following SCG fiducial points was identified: Es which coinciding with mitral valve closure, Gs which to some degree coincides with aortic opening, Bd coinciding with aortic valve closure and Fd coinciding with mitral valve opening [1]. The Es-Gs time interval was used as a measure of isovolumetric contraction time (IVCT), the Gs-Bd time interval was used as an estimate of ejection time (ET) and the Bd-Fd time interval as an estimate of isovolumetric relaxation time (IVRT). Paired t-test was used to test for significant response after infusion, while a two sample t-test was used to test for a significant difference in the observed response in subjects with or with our cardiac disease. Results For two subjects SCG after infusion was not obtained thus, twenty-four subjects were included in the final data analysis. In the whole group, acute saline infusion shortened the IVRT (Bd-Fd) from 91.0±15.3 ms to 82.7±15.3 ms (p=0.004) and prolonged the ET (Gs-Bd) from 329.4±35 ms to 343.4±33 ms (p<0.001). There was no significant change in IVCT (Es-Gs) which was 39.5±15.1 ms at baseline and 38.1±14.9 ms post-infusion (p=0.88). There was no significant difference in response between subjects with or without cardiac disease. Conclusion Increase in preload shortened the SCG time intervals related to the isovolumetric relaxation period and prolonged the period related to ejection time. SCG time intervals capture changes in preload, which demonstrates that the SCG is a potential modality for quantification of cardiac dynamics. Funding Acknowledgement Type of funding sources: None.

The comprehensive analysis of the determination of wavelet function-level pair for the decomposition and reconstruction of artificial S1 heart signals by using multi-resolution analysis

Two major sounds of the normal heart sound like “lub dub”. The “lub” is the first heart sound, commonly termed S1 results from mitral (M1) and tricuspid (T1) valve closure at the start of systole. In this work, the noisy-S1 heart signal was investigated to separate M1 and T1 components of it by making the comprehensive analysis of the determination of wavelet function-level pair for the decomposition and reconstruction of artificial S1 by using multiresolution analysis (MRA) and discrete wavelet transform (DWT). For this purpose, a synthetic S1 and its three different noisy-S1 signals were created by using the linear chirp transient model and then decomposed to their approximations and details at three different decomposition levels (3,4,5). 86 daughter wavelets of Biorthogonal, Coiflet, Daubechies, and Symlet were used to reconstruct noisy-S1 signals using comprehensive MRA&DWT. S1 and reconstructed noisy-S1 were compared qualitatively and quantitatively. For quantitative assessment, signal-to-noise-ratio (SNR), peak-SNR (PSNR), root-mean-square-error (RMSE), and structural-similarity (SSIM(%)) metrics were used for noisy-S1 signals at 3–4-5 decomposition levels. In the final evaluation of 86 daughter wavelets, db5, bior3.3, and bior3.9 performed superior results both qualitatively and quantitatively. The db5 was the superior one qualitatively at level 5, and quantitatively, the SNR values of the reconstructed signal by db5 were 8.620, 8.009, and 6.333 for %5-,%10-, and %20-noisy heart signals, respectively. The study proved that MRA&DWT provides a comprehensive analysis opportunity consisting of 86 daughter wavelets for perfect reconstruction of the S1 heart signals and detecting transients between M1 and T1 components.

B-PO01-024 MECHANICAL AV SYNCHRONY PROVIDED BY A LEADLESS PACEMAKER SUCCESSFULLY TIMES VENTRICULAR ACTIVATION TO THE COMPLETION OF ATRIAL CONTRACTION

Current leadless ventricular pacemakers have the ability to provide AV synchronous (AVS) pacing by tracking late phase right ventricular filling from atrial mechanical contraction. How this accelerometer-based approach translates into appropriate left ventricular filling times is incompletely understood. To characterize left ventricular filling with accelerometer-based AVS pacing among patients with 3rd degree AVB in the MARVEL 2 study. Trans-mitral valve flow was collected on echo during AVS pacing for 6 beats. Each AVS beat was assessed for A-wave truncation. The time from end of A-wave to mitral valve closure was assessed (A-MV) as positive if the A-wave ended prior to MV closure and negative if A-wave truncation occurred. Echo data was available in 37 patients with 3rd degree AVB and AVS > 70%. The mean of each patient’s median peak p-wave to ventricular pace (P-V) time was 153±28 ms (range: 97 - 244 ms). The mean A-wave end to MV closure time was -7.6± 25.2 ms (min. = -46.5 and max. = 58.2), indicating minimal A-wave truncation that was not associated with P-V interval (R2<0.01, P=0.67, Figure). Among patients with a prolonged P-V time (n=6), the mean A-MV time was -9.0± 31.2 ms, suggesting that the accelerometer-based AV pacing may adapt to the patient’s electromechanical delay. Mechanical AV times by the leadless pacemaker are different from TV pacemakers. In patients with normal and prolonged P-V times, the mechanical AV timing algorithm facilitated normal mitral valve inflow patterns that might not be expected from empirically timed AV delays in traditional transvenous pacemakers.

Principal Morphomic and Functional Components of Secondary Mitral Regurgitation

ObjectivesThe aim of this work was to identify the key morphological and functional features in secondary mitral regurgitation (sMR) and their prognostic impact on outcome. BackgroundSecondary sMR in patients with heart failure and reduced ejection fraction typically results from distortion of the underlying cardiac architecture. The morphological components which may account for the clinical impact of sMR have not been systematically assessed or correlated with clinical outcomes. MethodsMorphomic and functional network profiling were performed on a cohort of patients with stable heart failure optimized on guideline-based medical therapy. Principal component (PC) analysis and subsequent cluster analysis were used to condense the morphomic and functional data first into PCs with varimax rotation (PCVmax) and second into homogeneous clusters. Clusters and PCs were tested for their correlations with clinical outcomes. ResultsMorphomic and functional data from 383 patients were profiled and subsequently condensed into PCs. PCVmax 1 describes high loadings of left atrial morphological information, and PCVmax 2 describes high loadings of left ventricular (LV) topology. Based on these components, 4 homogeneous clusters were derived. sMR was most prominent in clusters 3 and 4, with the morphological difference being left ventricular size (median end-diastolic volume 188 mL [interquartile range: 160 mL-224 mL] vs 315 mL [264 mL-408 mL]; P < 0.001). Clusters were associated with mortality (P < 0.001), but sMR remained independently associated with mortality after adjusting for the clusters (adjusted HR: 1.42; 95% CI: 1.14–1.77; P < 0.01). The detrimental association of sMR with mortality was mainly driven by cluster 3 (HR: 2.18; 95% CI: 1.32-3.60; P = 0.002), the “small LV cavity” phenotype. ConclusionsThese results challenge the current perceptions that sMR in heart failure with reduced ejection fraction results exclusively from global or local LV remodeling and are suggestive of a potential role of the left atrial component. The association of sMR with mortality cannot be purely attributed to cardiac morphology alone, supporting other complementary key aspects of mitral valve closure consistent with the force balance theory. Unsupervised clustering supports the association of sMR with mortality predominantly driven by the small LV cavity phenotype, as previously suggested by a conceptional framework and termed disproportionate sMR.

Physiological significance of pre- and post-ejection left ventricular tissue velocities and relations to mitral and aortic valve closures.

Tissue Doppler shows short duration velocity spikes during pre- and post-ejection (protodiastole). They have been assumed to be isovolumic contraction and relaxation movements, but this is not in accordance with newer studies. We examined 22healthy volunteers. Valve closures and openings were determined from spectral Doppler from LVOT and mitral inflow and transferred to colour tissue Doppler recordings for comparison with tissue velocities, colour M-mode and strain rate (SR). Pre-ejection positive velocity spikes were simultaneous in both walls, starting ca. 24.8±10.1ms after start QRS, duration 51.5±10.8ms, ending 10.2±11.5ms after mitral valve closure (MVC) (p<0.001). There were corresponding colour tracings and negative strain rate. Protodiastolic lengthening was predominant in the septum. Negative velocity spikes had a duration of 35.5±10.7ms, ending 9.5±14.7ms after aortic valve closure (AVC, p<0.001) in septum. During isovolumic relaxation, strain rate showed apical lengthening (Peak SR-0.72±0.50s-1 ) and basal shortening (Peak SR 0.44±0.63s-1 ). Electromechanical activation of the LV is simultaneous in septum and lateral wall, occurs before MVC, is terminated by MVC itself and is thus not isovolumic. Protodiastole is a short event of lengthening, predominantly in the septum. It may be the mechanism for valve closure and ends by AVC itself. Isovolumic relaxation occurs after this velocity spike, and is characterized by elongation of the apex, shortening of the base, thus showing a volume shift from base towards apex.

Papillary muscle approximation reduces systolic tethering forces and improves mitral valve closure in the repair of functional mitral regurgitation

BackgroundUndersizing mitral annuloplasty (UMA) to repair functional mitral regurgitation (FMR) lacks durability, as it forces leaflet coaptation without relieving the subleaflet tethering forces. In this biomechanical study, we demonstrate that papillary muscle approximation (PMA) before UMA can drastically relieve tethering forces and improve valve function, without the need for significant annular downsizing. MethodsAn ex vivo model of FMR was used, in which pig mitral valves were geometrically perturbed to induce FMR, and the repairs were performed. Nine pig mitral valves were studied in the following sequence: normal (baseline), FMR, true-sized annuloplasty to 30 mm (true-sized ring [TSR]), and undersized annuloplasty to 26 mm (down-sized ring [DSR]), along with concomitant PMA at both ring sizes. Mitral regurgitation, valve kinematics, and chordal forces were measured and compared among the groups. ResultsFMR geometry induced a mean regurgitant fraction of 16.31 ± 7.33% compared with 0% at baseline. TSR reduced the regurgitant fraction to 6.05 ± 5.63%, whereas DSR reduced it to 5.06 ± 6.76%. The addition of PMA before the use of these rings reduced the mean regurgitant fraction to 3.87 ± 6.79% with the TSR (TSR + PMA) and 3.71 ± 6.25% with the DSR (DSR + PMA). Mean peak anterior and posterior marginal chordal forces were elevated to 0.09 ± 0.1 N and 0.12 ± 0.1 N, respectively, with FMR and were not reduced by annuloplasty of either sizes. The addition of PMA significantly reduced these forces to 0.23 ± 0.02 N and 0.51 ± 0.04 N. ConclusionsThis biomechanical study demonstrates that PMA relieves tethering forces, and concomitantly with annuloplasty it mobilizes the leaflets to achieve physiological valve closure. Such a result could be achieved without the need for extensive annular downsizing.

Noninvasive Patient-Specific Simulations of Mitral Valve Surgical Repair Using a High-Fidelity Functionally Equivalent Chordae Representation

Objective: Ischemic mitral regurgitation (IMR) is a highly prevalent heart valve disorder affecting over 1.6 million people in the United States. Its treatments often have high rates of failure which remain difficult to predict pre-surgically, and it is believed that therapeutic outcomes would be improved with more personalized treatments that account for patient-specific variations in mitral valve (MV) geometry and infarct kinematics. Methods: We have developed a substantially improved noninvasive computational modeling technique to model the dynamic response of the MV to repair surgery based on pre-surgical data alone. MV geometry for individual patients was first segmented from pre-surgical 3D echocardiographic images. We selected multiple representative papillary muscle (PM) origin points at each at the anterior and posterior locations to simulate the PM heads. Functionally equivalent chordae tendinae were built connecting these points to uniformly distributed leaflet insertions—either with or without a branched structure—and MV closure was simulated. The prestrain in each chord was calibrated through iterative correction proportional to the distance (L2 error) between the insertion point on the simulated MV and the segmented MV. The calibrated model was used to predict the state of the MV post-annuloplasty repair. Results: We have found that a more physiologically accurate PM model and iterative correction of chordal pre-strain improve the accuracy of both pre-surgical MV models and post-repair predictions. There is substantial reduction in the L2 norm error of the leaflets between the simulated and segmented MV geometry in both simulations, improving our estimates of strain and stress in the post-surgical MV and allowing us to better predict long-term changes in the tissue. Conclusions: Our image-based framework may be used as a valuable clinical tool to help surgeons pre-surgically assess annuloplasty repair performance for IMR and can be extended to optimizing other surgical repair methods including leaflet clipping or augmentation.

Clinical and echocardiographic predictors of decompensation in acute severe aortic regurgitation due to infective endocarditis.

Patients with acute severe aortic regurgitation (AR) due to infective endocarditis can progress rapidly from the hemodynamically stable patient to pulmonary edema and cardiogenic shock. We sought to identify patients at risk of decompensation where emergent surgery should be undertaken. We identified 90 patients with acute severe AR from the echocardiography laboratory database. Baseline clinical, hemodynamic (heart rate (HR) and blood pressure (BP)), and echocardiographic data including mitral filling, premature mitral valve closure (PMVC), and diastolic mitral regurgitation (DMR) were identified. The primary endpoint was subsequent development of pulmonary edema or severe hemodynamic instability. Patients who met the primary endpoint had a higher HR (98.5bpm vs 80.5bpm), lower diastolic BP (54mmHg vs 61.5mmHg), higher mitral E-wave velocity (113cm/s vs 83cm/s), higher E/e' ratio (12.4 vs 8), higher proportion of DMR (27.8% vs 7.4%), and PMVC (25% vs 9.3%) than patients who did not meet the endpoint. The proportion of patients with the primary endpoint increased as HR increased ((≤81bpm) 3/30 (10%), (81-94bpm) 11/31 (35.5%), (≥94bpm) 22/29 (75.9%), P<.0001) and as the diastolic BP reduced ((≤54mmHg) 19/31 (61.3%), (54-63mmHg) 12/31 (38.7%), (≥63mmHg) 5/28 (17.9%), P=.003). Independent predictors were a higher HR (OR 1.08 (95% CI 1.04-1.13) P=.0003) and DMR (OR 4.71 (95% CI 1.23-18.09), P=.02). Decompensation in acute severe AR is common. Independent predictors of decompensation are increasing HR(≥94bpm) and the presence of DMR. Those with these adverse markers should be considered for emergent surgery.

Improvement in right ventricular function by mitral valve closure in hypoplastic left heart syndrome.

A male neonate presented with the aortic/mitral stenotic variant of hypoplastic left heart syndrome, wherein the suprasystemic left ventricular pressure and relatively large left ventricle had shifted the intraventricular septum. Despite bilateral pulmonary artery banding, the stroke volume was difficult to maintain owing to the compressed right ventricle, causing heart failure symptoms. Percutaneous balloon aortic valvuloplasty decreased the left ventricular pressure, restoring the right ventricular function. Norwood procedure with mitral valve closure after catheter intervention reduced the left ventricular size and improved the right ventricular function. This paper refers to the potential of mitral valve closure for hypoplastic left heart syndrome.

Natural shear wave propagation speed is influenced by both changes in myocardial structural properties as well as loading conditions

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Research Foundation - Flanders (FWO) Background Shear wave elastography (SWE) is a promising tool for the non-invasive assessment of myocardial stiffness. It is based on the evaluation of the propagation speed of shear waves by high frame rate echocardiography. These waves can be induced by for instance mitral valve closure (MVC) and the speed at which they travel is related to the instantaneous stiffness of the myocardium. Myocardial stiffness is defined by the local slope of the stress-strain relation and can therefore be altered by both changes in structural properties of the myocardium as well as loading conditions. Purpose The aim of this study was to investigate how changes in myocardial structural properties as well as loading conditions affect shear wave speed after MVC. Methods Until now, 8 pigs (weight: 33.6 ± 5.4 kg) were included. The following interventions were performed: 1) preload was reduced by balloon occlusion of the vena cava inferior, 2) afterload was increased by balloon occlusion of descending aorta, 3) preload was increased by intravenous administration of 500 ml of saline and 4) ischemia/reperfusion injury (I/R injury) was induced in the septal wall by balloon occlusion of the LAD for 90 min. with subsequent reperfusion for 40 min. Echocardiographic and left ventricular pressure recordings were simultaneously obtained during each intervention. Left ventricular parasternal long-axis views were acquired with an experimental high frame rate ultrasound scanner (average frame rate: 1279 ± 148 Hz). Shear waves were visualized on tissue acceleration maps by drawing an M-mode line along the interventricular septum. Shear wave propagation speed after MVC was calculated by assessing the slope of the wave pattern on the tissue acceleration map (Figure A). Results The change in left ventricular end-diastolic pressure (LVEDP) and shear wave speed after MVC between baseline and each intervention are shown in Figure B and C, respectively. Preload reduction resulted in significant lower LVEDP compared to baseline (p &amp;lt; 0.01), while the other loading changes did not have a significant effect. Shear wave speed after MVC significantly increased by afterload and preload increase (p &amp;lt; 0.01). I/R injury resulted in increased shear wave speed (p &amp;lt; 0.01) without significantly altering LVEDP. There was a good positive correlation between the change in LVEDP and the change in shear wave speed induced by loading changes (r = 0.76; p &amp;lt; 0.001) (Figure D). However, the correlation became less strong if data of I/R injury was taken into account as well (r = 0.63; p &amp;lt; 0.001). Conclusion Our results suggest that SWE is capable to characterize myocardial tissue properties and besides has the potential as a novel method for the estimation of left ventricular filling pressures. However, in the presence of structural changes of the myocardium, care should be taken when estimating filling pressures based on shear wave propagation speed. Abstract Figure.

Can shear wave imaging distinguish between diffuse interstitial and replacement myocardial fibrosis?

Abstract Funding Acknowledgements Type of funding sources: None. Background Diffuse interstitial or myocardial replacement fibrosis are common features of a large variety of cardiomyopathies. These alterations contribute to functional changes, particularly to an increased myocardial stiffness (MS). Histological examination is the gold standard for myocardial fibrosis quantification, however, it requires endomyocardial biopsy which is invasive and not without risks. Cardiac magnetic resonance (CMR) can characterize the extent of both diffuse and replacement fibrosis and may have prognostic value in various cardiomyopathies. Echocardiographic shear wave (SW) elastography is an emerging approach for measuring MS in vivo. SWs occur after mechanical excitation of the myocardium, e.g. after mitral valve closure (MVC), and their propagation velocity is directly related to MS, thus providing an opportunity to assess stiffness at end-diastole. Purpose The aim was to investigate if velocities of natural SW can distinguish between interstitial and replacement fibrosis. Methods We prospectively enrolled 47 patients (22 patients after heart transplant [54.2 ± 15.8 years, 82.6% male] and 25 patients with established hypertrophic cardiomyopathy [54.0 ± 13.5 years, 80.0% male]) undergoing CMR during their check-up. We performed SW elastography in parasternal long axis views of the LV using a fully programmable experimental scanner (HD-PULSE) equipped with a clinical phased array transducer (Samsung Medison P2-5AC) at 1100 ± 250 frames per second. Tissue acceleration maps were extracted from an anatomical M-mode line along the midline of the LV septum. The SW propagation velocity at MVC was measured as the slope in the M-mode image. All patients underwent T1 mapping as well as late gadolinium enhancement (LGE) cardiac magnetic resonance at 1.5 T to assess the presence of diffuse or replacement fibrosis (Figure A). Therefore, patients were divided in three groups: no fibrosis, diffuse fibrosis and replacement fibrosis. Results Mechanical SW’s were observed in 46 subjects starting immediately after MVC and propagating from the LV base to the apex. SW propagation velocity at MVC correlated well with native myocardial T1 values (r = 0.65, p &amp;lt; 0.0001) and differed significantly among groups (p &amp;lt; 0.0001), with a significant post-test between any pair of groups (Figure B). SW velocities below a cut-off of 6.01 m/s showed the highest accuracy to identify patients without any type of fibrosis (sensitivity 88 %, specificity 89%, area under the curve = 0.93) (Figure C). A cut-off of 8.11 m/s could distinguish replacement fibrosis from diffuse fibrosis with a sensitivity and specificity of 59% and 92 %, respectively (area under the curve = 0.80) (Figure D). Conclusions Shear wave velocities after mitral valve closure can distinguish between normal and pathological myocardium and can detect differences between diffuse and replacement fibrosis. Abstract Figure.

Shear wave elastography: can we discover elevated diastolic filling pressures?

Abstract Funding Acknowledgements Type of funding sources: Public hospital(s). Main funding source(s): University Hospitals (Uz) Leuven Background The assessment of the left ventricular diastolic function is complex, as there is no single invasive parameter that provides a direct measurement of myocardial relaxation, myocardial compliance, or – as a surrogate - LV filling pressure. Estimation of diastolic function is therefore based on the combination of several parameters. Shear wave (SW) elastography is a novel method based on high frame rate echocardiography. SWs occur after mechanical excitation of the myocardium, e.g. after mitral valve closure (MVC), and their propagation velocity is directly related to myocardial stiffness (MS). Purpose The aim of this study was to investigate if velocities of natural shear waves are related to MS at end-diastole (ED) and, thus, could be used to estimate left ventricular end-diastolic pressures (LVEDP) as marker of diastolic function. Methods So far, we have prospectively enrolled 42 patients with a wide range of diastolic function, scheduled for heart catheterization so that LV filling pressures could be invasively measured. Patients with severe aortic stenosis, mitral stenosis of any degree and a more than moderate mitral regurgitation, as well as regional myocardial abnormalities or dysfunction in the anteroseptal wall were excluded. Echocardiography was performed immediately after catheterization. SW elastography in parasternal long axis views of the left ventricle (LV) was performed using an experimental scanner (HD-PULSE) at 1100 ± 250 frames per second. Tissue acceleration maps were extracted from an anatomical M-mode line along the midline of the LV septum. The SW propagation velocity at MVC was measured as the slope on the M-mode acceleration map (Figure A). Standard echocardiographic parameters of diastolic function were obtained with a high end ultrasound machine. Results SW velocities at ED correlated well with the invasively measured LVEDP (r = 0.74, p &amp;lt; 0.001, Figure B). In comparison, classical echocardiographic parameters correlated only weakly with LVEDP (E/A: r = 0.398, p = 0.02, Figure C; E/E’: r = 0.204, p = 0.247, Figure D). For the detection of an elevated LVEDP above 15 mmHg, a cut off value for the SW velocity at MVC of 4.395 m/s (Figure A) was associated with a sensitivity of 91.3% and a specificity of 90.9%. Conclusions End-diastolic shear wave velocities, measured by high frame rate shear wave elastography, showed a significant correlation with the end-diastolic filling pressure of the LV and allowed to differentiate normal from elevated filling pressure which indicates a potential clinical value of the new method for a non-invasive and direct assessment of LV diastolic function. More patients will be included to confirm these findings. Abstract Figure.

The influence of hemodialysis-induced preload changes on the propagation speed of natural shear waves

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Research Foundation - Flanders (FWO) Background Shear wave elastography (SWE) is a novel ultrasound technique based on the detection of transverse waves travelling through the myocardium using high frame rate echocardiography. The propagation speed of these shear waves is dependent on the stiffness of the myocardium. Previous studies have shown the potential of SWE for the non-invasive assessment of myocardial stiffness. It is unclear, however, if preload changes lead to measurable changes in the shear wave propagation speed in the left ventricle. In patients undergoing hemodialysis, the volume status is acutely changed. In this way, the effect of preload changes on shear wave speed can be assessed. Purpose The aim of this study was to explore the influence of preload changes on end-diastolic shear wave propagation speed. Methods Until now, 6 patients (age: 80[53-85] years; female: n = 2) receiving hemodialysis treatment were included. Echocardiographic images were taken before and every hour during a 4 hour hemodialysis session. Left ventricular parasternal long-axis views were acquired with an experimental high frame rate ultrasound scanner (average frame rate: 1016[941-1310] Hz). Standard echocardiography was performed with a conventional ultrasound machine. Shear waves were visualized on tissue acceleration maps by drawing an M-mode line along the interventricular septum. Shear wave propagation speed after mitral valve closure (MVC) was calculated by measuring the slope of the wave pattern on the acceleration maps (Figure A). Results Over the course of hemodialysis, the systolic (141[135-156] mmHg vs. 165[105-176] mmHg; p = 0.35 among groups) and diastolic blood pressure (70[66-75] mmHg vs. 82[63-84] mmHg; p = 0.21 among groups), heart rate (56[54-73] bmp vs. 57[50-67] bpm; p = 0.76 among groups), E/A ratio (1.6[0.7-1.8] vs. 1.2[0.6-1.4]; p = 0.43 among groups) and E/e’ (14[9-15] vs. 9[8-13]; p = 0.24 among groups ) remained the same. The ultra-filtrated volumes are shown in Figure B. The shear wave propagation speed after MVC gradually decreased during hemodialysis (6.7[5.4-9.7] m/s vs. 4.4[3.6-9.0] m/s; p = 0.04 among groups) (Figure C). There was a moderate negative correlation between shear wave speed and the ultra-filtrated volume (r=-0.63; p &amp;lt; 0.01) (Figure D). Conclusion The shear wave propagation speed at MVC significantly decreased over the course of hemodialysis and correlated to the ultra-filtrated volume. These results indicate that alterations in left ventricular preload affect the speed of shear waves at end-diastole. End-diastolic shear wave speed might therefore be a potential novel parameter for the evaluation of the left ventricular filling state. More patients will be included in the future to further explore these findings. Abstract Figure.

Relationship between myocardial properties and myocardial stiffness in hearts with thick walls: a shear wave imaging study using ultra-high frame rate echocardiography

Abstract Funding Acknowledgements Type of funding sources: None. Background Shear wave (SW) imaging, based on high frame rate (HFR) echocardiography, is a new non-invasive approach for assessing myocardial stiffness. Operating myocardial stiffness increases with increasing wall stress, therefore measured myocardial stiffness does not necessarily reflect intrinsic myocardial properties only, but can be influenced by cavity pressure and chamber geometry. Purpose To explore the relationship between local myocardial geometry, cavity pressure and pathological substrate with SW velocity and to determine to which extent the above mentioned factors influence SW velocity. Methods We included 26 healthy controls (55 ± 14 years, 77 % male) and 61 patients with thick heart (24 patients with cardiac amyloidosis (AML) [70 ± 9 years, 52 % male], 37 patients with hypertrophic cardiomyopathy (HCM) [54 ± 14 years, 78 % male]). Left ventricular (LV) parasternal long axis views were acquired with an experimental HFR scanner at 1142 ± 282 frames per seconds. Propagation velocity of the SW occurring after mitral valve closure in the interventricular septum (IVS) served as measure of myocardial stiffness (Figure A). While conventional echocardiographic measurements were used to evaluate local myocardial geometry (LV end-diastolic diameter [EDD], IVS thickness) and LV cavity pressure (LV diastolic pressure-estimated by E/e` and LV systolic pressure-estimated by systolic blood pressure and potential LV outflow gradient in HCM). Results LV cavity pressure and local geometry differed significantly between controls and patients (p &amp;lt; 0.05, for all, Figure B). SW velocity correlated with cavity pressure (E/e`: r = 0.375, p &amp;lt; 0.001, LV systolic pressure: r = 0.264, p = 0.020) and local geometry (IVS thickness: r = 0.700, p &amp;lt; 0.001; EDD: r=-0.307, p = 0.007) and differed significantly among groups (Figure C). Multivariate analysis revealed that SW velocity was independently related only with the pathological substrate and IVS thickness (p = 0.006 and p &amp;lt; 0.001, respectively). In a regression model, the pathological substrate, cavity pressure and local geometry accounted for 56% of variation in SW velocity (p &amp;lt; 0.001), while the pathological substrate alone accounted for nearly half of the variance (R2 = 0.44, p &amp;lt; 0.001) (Figure D). Conclusions Our study demonstrated that SW velocity is related to both pathological substrate and local geometry and LV pressures. Additionally, our results suggest that variations in myocardial tissue properties had the most influence on SW velocity, while LV pressure and local geometry played a minor role. Therefore, the changes in SW velocity reflect predominantly tissue properties that are altered by underlining disease rather than cavity pressure and morphological abnormalities. Thus, SW elastography could provide useful novel diagnostic information in the evaluation of cardiomyopathies. Abstract Figure A, B, C, D