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. Author manuscript; available in PMC: 2021 Sep 1.
Published in final edited form as: ASAIO J. 2020 Sep-Oct;66(9):1016–1024. doi: 10.1097/MAT.0000000000001145

Left Ventricular Thinning and Distension in Pig Hearts as a Reproducible Ex Vivo Model of Functional Mitral Regurgitation

Elorm J Agra 1, Kirthana Sreerangathama Suresh 1, Qi He 1, Daisuke Onohara 1,2, Robert A Guyton 1,2, Muralidhar Padala 1,2
PMCID: PMC7469430  NIHMSID: NIHMS1067880  PMID: 32870609

Abstract

Objective

Functional mitral regurgitation in the setting of an enlarged heart is challenging to repair surgically with an annular approach, and the need to develop sub-annular and ventricular approaches is recognized yet unrealized due to the lack of models for investigations. In this study, we report a novel model of functional mitral regurgitation induced by left ventricular thinning and distension in pig hearts.

Methods

Seven pig hearts were explanted at a local slaughterhouse, and left ventricular distension induced by thinning the ventricular myocardium by 60–65% of its original thickness. Distension of the thinned hearts with a 120mmHg column, confirmed significant left ventricular dilatation and mitral valve tethering. These hearts were then mounted into a pulsatile flow model, and animated at 120mm Hg left ventricular pressure, 5L/min cardiac output at 70 beats per minute. Echocardiography was used to assess valvular kinematics and hemodynamics.

Results

Left ventricular wall thickness reduced by 60.5±10.1% at the basal plane, 64.8±11.3% at the equatorial plane and 64.0±11.4% at the apical plane after thinning. Upon distension, ventricular volumes increased by 852.4±639.8% after LV thinning, with an 89.5±33.9% increase in sphericity index. Mitral valve systolic tenting height increased from 7.92±2.06 mm to 15.02±3.89 mm, systolic tethering area increased from 130.7±38.2 mm2 to 409.9±124.6 mm2 and an average mitral regurgitation fraction of 24.4±16.6% was measured. In a case study, use of multi-modality imaging to test the efficacy of transcatheter mitral devices was confirmed.

Conclusions

Ventricular wall thinning leading to passive left ventricular distension and dilatation is a reproducible ex vivo model of mitral valve tethering and functional mitral regurgitation, which in combination with multi-modality imaging provides a good simulation model.

INTRODUCTION

Functional mitral regurgitation (FMR), often diagnosed in patients with heart failure with ischemic or dilated cardiomyopathies is a challenging valve lesion to address using existing surgical or transcatheter mitral repair devices1, 2. In this lesion, the enlarged and distended myopathic left ventricle (LV) distorts the native geometry of the mitral valve (MV), restricts physiological LV-MV interactions, and restricts systolic MV closure and leads to FMR3, 4. Surgical repair of FMR continues to be a challenge to surgeons, as considering these varied geometric parameters on a patient-specific approach to develop a tailored surgical strategy is not trivial. Thus, valve replacement is increasingly chosen over repair, but several studies including the NIH-funded cardiothoracic surgical network trials demonstrate better outcomes and survival with a durable repair over a valve replacement5. The inadequacy of annular approaches to repair FMR is now recognized, and sub-valvular and ventricular approaches are necessary6. Several techniques such as papillary muscle approximation7–9, papillary muscle hoisting (Kron procedure)10–12, chordal cutting13, 14, ventricular restraint and reshaping15, 16 have been proposed, but none with systematic mechanistic datasets to enable wide clinical use.

Experimental simulation platforms that mimic FMR are needed to advance this field, which not only focus on the tethered mitral valve geometry, but replicate the complex geometric perturbations seen at the ventricular level. Our group has previously reported an isolated MV simulator with the ability to tether and distort the mitral valve, which enabled study of pathogenic mechanisms and annular therapies14, 17–19. However, lack of a left ventricle, and one that is dilated and distorts the ventricular component of the valve, did not enable our study of sub-valvular and ventricular approaches. Subsequently, we developed a swine model of FMR using a targeted percutaneous coronary embolization approach20, which faithfully created FMR and heart failure (HF), but is cost-prohibitive for technique development and training studies. This provided us the impetus to develop an ex vivo FMR model that can faithfully represent the clinical scenario of FMR in HF, providing an experimental platform for surgical and interventional investigations. The effectiveness of this model, with its simplicity and low-cost, and the ability to use it with any clinically used imaging modality, renders this model convenient for use in surgical training at any institution.

In this report, the techniques to establish this FMR model in pig hearts obtained from healthy animals are described, the concept of ventricular thinning to induce distension is developed, and the hemodynamics of the mitral valve in this model are described.

METHODS

Porcine heart preparation steps

Acquisition

Porcine thoracic organs (plucks) were obtained from adult pigs from a local abattoir (Holifield farms, Covington, GA), with the anatomical attachments of the heart to the lungs and surrounding vessels being preserved (Figure 1A). The plucks were transported to the laboratory, cleaned and the lungs and esophagus were trimmed, while preserving the pulmonary veins, the ascending aorta, the pulmonary artery, and both inferior and superior venae cavae (Figure 1 – B1–B2).

Figure 1:

Figure 1:

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(A) Thoracic plucks from 350-lb pigs, with intact pericardium, lungs, trachea and the esophagus; (B1–2) The plucks are cleaned to extract the heart with an intact aorta and pulmonary artery; (C1–2) Photographs depicting the same heart after left ventricular thinning to induce enlargement when distended under pressure.

Baseline measurements

Prepared hearts were connected to a column of 0.9% saline via the aortic valve to generate a 120 mmHg left ventricular pressure, to close the mitral valve. An echocardiography probe (Z6MS, Siemens SC2000 PRIME, Seattle, WA) was placed on the left atrium to visualize the valve, and measure the mitral valve and left ventricular cavity dimensions. The left ventricular wall thickness was measured at multiple sites on the echocardiographic images, in the anterior, posterior, inferior and septal regions of the chamber. Hearts with a distance greater than 140 mm between the posterior mitral annulus and the left ventricular apex were selected, to provide an adequately large heart for these experiments. Seven such hearts were selected for this study, with the baseline measurements including mitral annular and leaflet dimensions as well.

Left ventricular thinning and distension

To displace the papillary muscles and create a severely dilated left ventricle at peak systolic pressure of 120 mm Hg, the left ventricular myocardium was resected to 60–65% of its baseline thickness (Figure 1C1–2). Though a thinner ventricle could result in better dilatation, when 60–65% of the muscle was resected, several holes formed in the tissue as the endocardial trabecular spaces opened from the thinning. At a thickness <60%, the ventricle remained stiff and prohibited dilatation when distended. Ventricular resection to the desired thickness was performed in steps: (Step 1) baseline thickness measured from the echo images was used to make a longitudinal incision to the desired depth; (Step 2) several such longitudinal slits were made around the left ventricle; (Step 3) the hearts were then thinned circumferentially, perpendicular to the longitudinal slits, to resect the tissue in the desired depth plane; (Step 4) echocardiography was repeated to confirm 60–65% reduction in thickness. The hearts were then pressurized to check for leaks and close them with pledgeted sutures, and the coronary arteries were ligated at their origin from the aorta to avoid any leaks through the myocardium. The hearts were weighed before and after thinning.

Pulsatile heart flow loop

A custom 3D printed connector was attached through the left ventricular apex, to attach a pipe that is connected to a programmable pulsatile pump (Super pump, Vivitro Systems, Victoria, Canada). The pump is programmed with a waveform generator (Agilent Inc, Santa Clara, CA) to generate close to physiologic left ventricular pressures and heart rate. The heart is then placed vertically in a stand, and a reservoir (pulmonary reservoir) is placed 13–15 cm above the left atrium and connected to it via a pair of pulmonary veins. A resistor is placed on the tubing between the reservoir and the left atrium to control the inflow into the left ventricle. Another clear tube is inserted into the aorta, and clamped at the sino-tubular junction (STJ), and connected to another reservoir (aortic reservoir) placed 160–170 cm above the aortic valve. A resistor is placed on the tubing between the STJ and the reservoir to control the afterload. The aortic reservoir was configured such that it overflowed into the left atrial reservoir, thus completing the closed loop circuit (Figure 2). A 0.9% saline solution was used as working fluid in this experiment, but the working fluid can be changed to a blood mimicking one with some modifications of this loop. Blood-mimicking fluid was not used in this specific study, as the pump head was not compatible with corrosive fluids that could lead to its damage. Separating the pump head and the flow loop with a silicone membrane can be used for blood mimicking fluids. The pump was programmed to generate 120 mm Hg peak left ventricular pressure, 5 lpm cardiac output at 70 beats/min throughout the study. Left ventricular, left atrial and aortic pressures were measured using individual pressure gauges and monitored throughout the experiment.

Figure 2:

Figure 2:

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The pulsatile programmable flow loop with the pig heart. (1) Pig heart cannulated at the left ventricular apex to connect to a pulsatile pump, the aorta connected to a tube as the outlet, and the left atrium connected to a pulmonary reservoir; (2) Systemic reservoir and compliance; (3) Pulmonary reservoir and compliance; (4) Programmable linear actuated pump; (5) Waveform generator and data acquisition system.

Echocardiographic imaging

A transesophageal ultrasound probe (Z6Ms, 3–6.3 MHz, Siemens SC2000 PRIME, Munich, Germany) was placed on the left atrial roof to obtain 2D, biplane 2D and 3D volume images of the mitral valve. This probe placement was well suited for accurate color and spectral Doppler imaging as well, without the need for angle correction and the corresponding errors it introduces. Two-chamber bi-plane long axis views were used to measure the left ventricular area, and calculate the left ventricular volume and sphericity index. Mitral annular septal-lateral diameter, tenting height, coaptation length (Figure 3A), anterior leaflet tenting area, posterior leaflet tenting area (Figure 3B), systolic anterior angle, systolic posterior angle (Figure 3C), anterior leaflet tethering angle (seagull angle) and posterior leaflet tethering angle were measured at peak systole before and after left ventricular thinning/distension and posterior papillary muscle tethering (Figure 3D). Mitral regurgitation (MR) was confirmed with color doppler and the regurgitant fraction was measured by tracing the MR jet area in the left atrium and normalized to the left atrial area, in the two-chamber long axis view.

Figure 3:

Figure 3:

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Echocardiographic views of the tethered mitral valve depicting a long axis, septal-lateral view, with the left atrium (LA), aorta (Ao) and left ventricle (LV). (A) Septal-lateral diameter (SL-D), tenting height (TH) and coaptation length (CL); (B) Tenting area of the anterior leaflet (TAant) and tenting area of the posterior leaflet (TApost); (C) Systolic anterior angle (∝) and systolic posterior angle (β); (D) Anterior tethering angle (ɣ) and posterior tethering angle (θ)

Feasibility case study for transcatheter mitral technology training and development

The distended LV model with FMR was prepared as a testing and training platform for trans-septal mitral repair devices. The right atrium was exposed, and a long vascular conduit was anastomosed into the foramen ovale, with its distal end externalized via the inferior vena cava and connected to a one-way valve - to mimic transfemoral access. The 3D TEE probe was placed on the roof of the left atrium, just adjacent to one of the pulmonary veins to mimic an in vivo high esophageal location. An endoscope was inserted via a small vascular conduit attached to the pulmonary vein to obtain direct mitral valve visualization. The entire setup was then moved under the field of view of a C-arm (OEC 9900, GE Medical) for fluoroscopic visualization. The setup in its final form is depicted in Figure 4 and Video 1. An 8Fr intracardiac echo probe (Biosense Webster, Irvine, CA) was inserted via the innominate artery into the aortic root to visualize the tip of any catheters inserted into the mitral annulus or between the two leaflets.

Figure 4:

Figure 4:

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Integration of the functional mitral regurgitation model with multimodality imaging for transcatheter device testing and training. (A) 3D echocardiography and endoscopy of the mitral valve via a trans-atrial approach; and (B) fluoroscopic imaging with a C-arm.

Power analysis and statistical methods

Sample size was estimated to test the null hypothesis that mitral valve coaptation length was atleast 25% lesser in the thinned hearts, with a power of 0.8, and an alpha of 0.5. Preliminary data was used to perform a power analysis, to detect different between the group means, which resulted in a minimum sample size of 6.5 per group. Normality of data was tested with Shapiro-Wilk test, and all the data is presented as mean ± standard deviation. Paired t-tests were used to compare parameters before and after thinning/distension. Statistical analysis was performed in GraphPad Prism 8 (La Jolla, CA).

RESULTS

Extent of left ventricular thinning and chamber distension

At baseline, the myocardial wall thickness was 35.26 ± 5.34 mm in the basal short axis plane, 36.45 ± 4.57 mm in the equatorial short axis plane, and 31.92 ± 4.65 mm in the apical short axis plane. Upon thinning the heart, the average myocardial wall thickness reduced by 61.4% (p<0.0001) in the basal plane, by 65.8% in the equatorial plane (p<0.0001), and 11.21 ± 2.94 mm in the apical plane (64.9% reduction, p=0.0001). The average weights of the hearts reduced from 0.82±0.15 kg before thinning, to 0.45±0.08kg after thinning. Upon distension with a chamber pressure of 120 mmHg, the left ventricular internal diameters increased by 125.52% in the basal region (p<0.0001), by 192.4% in the equatorial region (p<0.0001), and 291.4% in the apical region (p=0.0004). Correspondingly, left ventricular area on long axis echo imaging increased by 252.24% (p=0.0004), and the left ventricular volume increased by 622.0% (p= 0.0004). Chamber sphericity index increased from 0.371 ± 0.079 before thinning to 0.681 ± 0.063 after thinning, an 83.6% increase (p<0.0001), mimicking a dilated and failing heart. The absolute values of each measurement before and after thinning are summarized in Table 1, and echocardiographic images of the pressurized hearts before ventricular wall thinning (Figure 5A) and after (Figure 5B). Pressure tracings in the left atrium and the left ventricle are shown in (Figure 5C–D).

Table 1 –

Left ventricular parameters before and after LV thinning

Before After p-value
Heart weight (kg) 0.82 ± 0.15 0.45 ± 0.08 <0.005
LV wall thickness (mm)
 Basal 35.26 ± 5.34 13.61 ± 2.45 <0.0001
 Equatorial 36.45 ± 4.57 12.48 ± 3.08 <0.0001
 Apical 31.92 ± 4.65 11.21 ± 2.94 0.0001
LVID (mm)
 Basal 30.40 ± 6.57 68.56 ± 9.02 <0.0001
 Equatorial 24.90 ± 3.93 72.80 ± 5.26 <0.0001
 Apical 15.53 ± 3.77 60.79 ± 7.20 <0.0001
LV sphericity
 Long axis (mm) 73.5 ± 9.2 114.5 ± 10.7 0.0012
 Short axis (mm) 26.9 ± 5.2 77.7 ± 6.5 <0.0001
 Sphericity index (%) 37.1 ± 7.9 68.1 ± 6.3 <0.0001
LV area (mm2) 1869.5 ± 761.9 6585.2 ± 1450.3 0.0004
LV volume (ml) 46.9 ± 29.8 338.6 ± 108.7 0.0004
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Figure 5:

Figure 5:

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2D biplane echocardiography images of thinned hearts before and after thinning. (A) Echo of hearts before thinning; (B) Echo of hearts after thinning. Pulsatile pump pressures shown after thinning for (C) aortic and left ventricular pressures and (D) atrial pressures.

Mitral valve geometry, kinematics and regurgitation severity

Changes in mitral valve geometric parameters from before and after LV thinning are shown in (Figure 6A–D). Mitral annular septal-lateral dimension increased by 48.2% after myocardial thinning, from 27.06 ± 4.22 mm to 40.11 ± 5.03 mm (p=0.019). The papillary muscle tips were displaced laterally away from each other, with a 658.6% increase in the interpapillary muscle distance, from 6.18 ± 2.39 mm to 46.85 ± 7.93 mm (p<0.0001). The combination of annular dilatation and papillary muscle displacement due to left ventricular distension caused a 89.6% increase in systolic tenting height (p<0.0024), a 50.2% decrease in coaptation length (p=0.0143) and a 213.6 % increase in tenting area (p=0.0007). Tenting area separated into anterior and posterior areas increased by 231.4% (p=0.0004) and 177.2% (p=0.0160) respectively. The anterior leaflet tethering angle increased by 48.9% (p =0.0033), whereas the posterior leaflet tethering angle was not altered (p=0.2394). The modified leaflet tethering angle that signified the angle between the smooth and rough zones of the leaflet in the “sea gull” shape that formed from tethering was decreased by 13.7% (p=0.0033) and remained unchanged in the posterior leaflet (p=0.1311). The absolute values of each measurement before and after myocardial thinning is reported in Table 2. Mitral regurgitation severity measured as regurgitant jet area over left atrial area increased from 0% at baseline to 24.41± 16.59 % after LV distension (p=0.008). Representative color doppler images of a non-regurgitant mitral valve before LV thinning and a regurgitant mitral valve after LV thinning are shown in Figure 7A–B.

Figure 6:

Figure 6:

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Mitral valve systolic geometric measurements at a transvalvular pressure of 120 mmHg. (A) Septal-lateral annular diameter; (B) Tenting height; (C) Coaptation length; (D) Interpapillary muscle distance

Table 2 –

Mitral valve parameters before and after LV thinning

Before After p-value
MR jet area/ Left atrial area (%) 0.00 24.41 ± 16.59 0.0080
Anterior leaflet tenting area (mm2) 87.77 ± 15.44 290.9 ± 78.56 0.0004
Posterior leaflet tenting area (mm2) 42.93 ± 23.66 119.0 ± 61.24 0.0160
Systolic anterior angle (°) 32.6 ± 9.5 48.5 ± 13.0 0.0033
Systolic posterior angle (°) 43.4± 5.0 50.2± 12.6 0.2394
Anterior leaflet tethering angle (°) 159.0 ± 10.8 137.2 ± 10.5 0.0002
Posterior leaflet tethering angle (°) 122.0 ± 16.6 114.1 ± 13.7 0.1311
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Figure 7:

Figure 7:

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Representative biplane echocardiography images with color doppler of thinned hearts before and after LV thinning: (A) no mitral regurgitation in systole before ventricular thinning; (B) Severe mitral regurgitation in systole after ventricular thinning

Multi-modality imaging for transcatheter mitral technology development

2D and 3D echocardiographic views of the mitral valve are shown in Figure 8A–B, clearly depicting the anterior and posterior leaflets and the mitral annulus. The depth was sufficient to image the entire left atrium as well, providing a good view of a trans-septal catheter introduced via the foramen ovale as depicted in Figure 8C. Though these views were adequate to guide the catheter to the mitral valve, the reflections from the catheter confounded the precise positioning of the catheter tip onto the annulus. Thus, an additional intracardiac echocardiography probe was inserted into the aortic valve, to obtain a cross sectional view of the mitral valve and the annulus, as shown in Figure 8D. Additionally, endoscopes were inserted through the left atrium and the left ventricle, for direct optical access to the mitral valve, as shown in Figure 8E–F, which could be valuable in training physicians on new catheter techniques for mitral valve interventions.

Figure 8:

Figure 8:

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(A) 2D biplane echo of the left sided structures including the mitral valve via a probe placed on the left atrial roof; (B) 3D echo of mitral valve from the same view; (C) A trans-septal catheter inserted into the left atrium via image guidance; (D) Anterior and posterior leaflet views via an intracardiac echo probe placed in the aortic root, to help guide annular procedures;(E) Endoscopic view of the mitral valve from the left atrium; (F) Endoscopic view of the mitral valve from the left ventricle.

DISCUSSION

Based upon the data presented here, a robust ex vivo model of FMR is presented, that mimics the annular, sub-annular and ventricular geometric characteristics seen in some patients with heart failure and FMR21, 22. Thinning the left ventricular myocardium by removing 60–65% of its thickness was feasible and did not result in myocardial rupture during the experiments in any of the hearts. However, thinning the ventricle beyond 65% opened several trabecular spaces, resulting in significant leaks that precluded pressurization of the hearts. Ligation of the coronaries at their origin from the aorta reduced leakages through the thinned myocardium, but some bleeders were identified that were individually ligated with pledgeted sutures. Left ventricular thinning significantly decreased heart weight, increased ventricular cavity volume and sphericity index, mimicking the clinical situation of an enlarged heart with FMR. Specific changes such as increase in inter-papillary muscle separation4, distance from the papillary muscle tips to the mitral annulus23, and the sea gull shaped bending of the anterior leaflet24, are all hallmarks of an FMR valve in heart failure, which were mimicked in this model. The extent of left ventricular thinning governed the mitral valve geometric perturbations, though the effect of differential thinning was not studied. By thinning the myocardium between the basal and equatorial regions, but not in the equatorial to apical regions, isolated mitral annular dilatation can be mimicked without significant sub-annular deformations. Furthermore, concentric ventricular thinning resulted in a globular heart that mimics a dilated cardiomyopathic pathology. Uneven thinning of the myocardium, specifically of the inferior and lateral walls can mimic an ischemic cardiomyopathic pathology resulting in type IIIb-like mitral valve lesion. Thus, this ex vivo model presents several possibilities in mimicking left ventricular perturbations that alter mitral valve geometry and function, compared to a rigid acrylic or silicone left ventricular chamber. Mitral regurgitation of moderate severity was observed using this approach, with a valve tethering pattern that mimicked human patients. The sea gull shape of the anterior mitral leaflet is like the tethering pattern observed in humans, due to the papillary muscle tethering force that is transmitted to the leaflet via the strut chordal insertions into this mid-leaflet region. In this model, the posterior mitral leaflet was relatively more mobile than the anterior leaflet, which can be attributed to the longer posterior leaflet lengths observed in these pig hearts compared to humans. The significant increase in inter-papillary muscle distance in these hearts after thinning mimics one of the key geometric parameters that drives FMR severity, as previously reported by our group using cardiac imaging in humans4.

To our knowledge, this ex vivo model is the first of its kind that mimics the ventricular and valvular pathologies seen in heart failure patients. Preserving the ventricular and valvular native anatomies enables the testing of not only isolated mitral valve repair and replacement techniques and technologies, but also left ventricular remodeling and reshaping devices to correct FMR. We have reported an earlier model using isolated pig mitral valves in an acrylic ventricular chamber, with papillary muscle rods that enable their spatial manipulation25. Robust control over the papillary muscle locations was possible, albeit it was quite challenging to implement any papillary muscle or ventricular approaches due to the constraints imposed by the rods and the acrylic chamber. He & colleagues used a silicone left ventricular model with wall motion, but the feasibility of using ventricular bags of different stiffnesses and shapes was not studied26. Such attempts would be labor intensive and would still require suspension of the papillary muscles into the silicone bags using rods or actuators, which prohibits implementation of any papillary muscle or ventricular repair techniques.

Native pig heart tissues are easier to visualize on echocardiography, as they induce minimal attenuation to the ultrasound signal and thus do not generate artifacts or signal drop off. The 2D and 3D images obtained in our simulator have a quality that is equivalent to images obtained in vivo and are adequate for transcatheter device testing and training. The transfemoral approach using a conduit sutured to the foramen ovale provides a test bed for new catheter delivery systems and robots. This approach can be further modified to include the right atrium as well, and thus provide a true simulation environment for trans-septal mitral procedures. Use of intracardiac echo in the aortic root presents a novel approach to closely image the mitral annulus, and drive anchor deployment into these tissues that is often challenging to perform with transesophageal echo imaging alone. A high esophageal view of the mitral valve often includes the catheters inserted into the left atrium and requires trimming of the 3D volume until the mitral annulus is visible. Despite such trimming, reflections from the catheters in the path of the ultrasound signal generates artifacts that often confound accurate positioning and imaging of the anchors. The aortic intracardiac echo imaging resolves these issues and can be used reproducibly for driving annular and leaflet anchoring devices. Finally, the use of native tissue and silicone tubing makes this ex vivo model compatible for fluoroscopic, computed tomographic and magnetic resonance imaging. Though we only tested the compatibility of this system with fluoroscopy, we expect that translation of this setup to other modalities is possible.

As with any experimental model, some limitations should be considered when comparing this model to patients with FMR. This ex vivo model uses explanted hearts that do not have active contractility, which limits the use of this model to mimicking dilated ventricles with tethered mitral valve geometries, but not in understanding the valvular-ventricular interaction. Despite this limitation, mimicking the tethered mitral valve geometry in a dilated native left ventricle, interaction between devices and the native valvular and ventricular structures can be studied. These possibilities provide new opportunities in understanding device-valve interactions in this disease state, especially for biomechanical and imaging studies. There is a certain learning curve in ensuring that the hearts are not too thin or too thick prior to experimentation. The procedures we have outlined in measuring baseline myocardial thickness and using that as a guide to perform longitudinal slits of required depth, helped provide landmarks to guide the thinning process.

CONCLUSION

Left ventricular thinning and distension presents a faithful representation of a heart failure patient with functional mitral regurgitation. Preserving the native valvular and ventricular structures enables the testing of new valvular and ventricular approaches for this disease state.

Supplementary Material

Video 1
Download video file (24.9MB, mp4)

Acknowledgments

Funding

This work was funded by the following grants to M.P: 14SDG20380081 from the American Heart Association; R01HL135145, R01HL133667, and R01HL140325 from the National Institutes of Health; and seed funding from the Carlyle Fraser Heart Center at Emory University Hospital Midtown

Conflict of interest

R.G is a scientific advisor for Edwards Lifesciences and receives a consulting fee. M.P. is an advisor for Edwards Lifesciences & Heart Repair Technologies and receives a consulting fee. None of these entities funded or were involved in any manner in this work.

ABBREVIATION

FMR

Functional mitral regurgitation

MV

Mitral valve

LV

Left ventricle

PM

Papillary muscle

LA

Left atrium

Ao

Aorta

SL-D

Septal lateral diameter

TH

Tenting height

CL

Coaptation length

TA

Tenting area

IPMD

Inter-papillary muscle distance

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