WO2020214463A1 - Fibrotic ventricular tissue disruption - Google Patents

Abstract

A process of disrupting fibrotic ventricular tissue involves advancing a compliant balloon device (50) to a ventricle (3) of a heart using a delivery catheter (60), expanding the compliant balloon device to contact target tissue associated with fibrotic tissue (25,26) of the ventricle, and further expanding the compliant balloon device to an expanded state to disrupt the target fibrotic tissue.

Description

FIBROTIC VENTRICULAR TISSUE DISRUPTION

RELATED APPLICATION

[0001] This application claims priority to U.S. Provisional Application No.

62/836,484, filed on April 19, 2019, entitled FIBROTIC VENTRICULAR TISSUE

DISRUPTION, the disclosure of which is hereby incorporated by reference in its entirety.

BACKGROUND

Field

[0002] The present disclosure generally relates to the field of medical devices and procedures.

Description of Related Art

[0003] Heart failure with preserved ejection fraction (HFpEF) is characterized by an increase in left ventricular wall thickness and reduced diastolic filling of the left ventricle. Such reduced diastolic filling can be caused in part by fibrous scar tissue present in the ventricular wall and the general thickening of the ventricle. Heart failure can result in serious complications.

SUMMARY

[0004] Described herein are methods and devices to facilitate ventricular dilation through disruption of fibrotic ventricular tissue. In some implementations, the present disclosure relates to a method of disrupting fibrotic ventricular tissue. The method comprises advancing a compliant balloon device to a ventricle of a heart using a delivery catheter, expanding the compliant balloon device to contact target tissue of the ventricle associated with fibrotic tissue, and further expanding the compliant balloon device to an expanded state to disrupt the fibrotic tissue.

[0005] In some embodiments, expanding the compliant balloon device to the expanded state to disrupt the fibrotic tissue increases end-diastolic volume of the ventricle or decreases end-systolic volume of the ventricle. Further expanding the compliant balloon device to the expanded state can involve expanding the compliant balloon device to a volume that is greater than a diastolic volume of the ventricle. In some embodiments, the method further comprises expanding the compliant balloon device to the expanded state in a pulsed manner. For example, expanding the compliant balloon device to the expanded state in a pulsed manner can be performed at a frequency and a phase associated with a heart rate of the heart. The method may further comprise determining the heart rate of the heart in real-time.

[0006] Expanding the compliant balloon device to the expanded state to disrupt the fibrotic tissue may be performed without damaging non-fibrotic tissue of the ventricle or with minimal or no disruption of non-fibrotic tissue of the ventricle. In some embodiments, the compliant balloon device has a volume that is more than 10% greater than a volume of the ventricle when the compliant balloon device is in the expanded state.

[0007] In some implementations, the present disclosure relates to a fibrotic tissue disruption device comprising a delivery catheter having a distal end, a compliant balloon attached to the distal end of the delivery catheter, and a fluid pump in fluid communication with the compliant balloon through the delivery catheter. The fluid pump is configured to, when the compliant balloon is disposed in a ventricle of a heart, expand the compliant balloon from a collapsed state to an expanded state in which the compliant balloon has a medial diameter that is greater than a medial diameter of the ventricle or has a volume that is greater than a volume of the ventricle.

[0008] In some embodiments, the fluid pump is further configured to pulse expansion of the compliant balloon to the expanded state based on a heart rate of the heart. For example, the fluid pump may be configured to contract the compliant balloon such that the compliant balloon is not in the expanded state during systolic periods. In some embodiments, the fibrotic tissue disruption device further comprises a pressure sensor configured to generate a signal indicative of a pressure of the ventricle.

[0009] In some implementations, the present disclosure relates to a method of disrupting fibrotic ventricular tissue. The method comprises identifying target fibrotic tissue in a ventricle of a heart, forming a non-compliant balloon device having form that is based at least in part on the identified target fibrotic tissue, advancing the non-compliant balloon device to the ventricle using a delivery catheter, orienting the non-compliant balloon device to align one or more tissue contact areas thereof with the target fibrotic tissue, and expanding the non-compliant balloon device to an expanded state to disrupt the target fibrotic tissue.

[0010] The non-compliant balloon device may have a width that is greater than an internal diameter of the ventricle in the expanded state. The method may further comprise pulsing expansion of the non-compliant balloon device to the expanded state at a frequency and phase associated with a diastolic phase of the heart. In some embodiments, expanding the non-compliant balloon device to the expanded state to disrupt the target fibrotic tissue involves applying strain to the target fibrotic tissue using the non-compliant balloon device that is greater than a strain tolerance of the target fibrotic tissue. For example, the strain may be less than a strain tolerance of non-fibrotic myocardial tissue connected to the target fibrotic tissue.

[0011] In some implementations, the present disclosure relates to a fibrotic tissue disruption device comprising a non-compliant balloon configured to be expanded to an expanded state, the non-compliant balloon comprising a first projection having a first tissue contact area, a second projection having a second tissue contact area, and a fluid coupling configured to receive fluid from a fluid source for expanding the first and second projections.

[0012] In some embodiments, the non-compliant balloon further comprises a third projection having a third tissue contact area. The non-compliant balloon may have a T-shaped form. In some embodiments, the non-compliant balloon has an at least partially round shape that is larger in volume than a determined volume of a target ventricle. The non-compliant balloon can comprise one or more radiopaque markers. In some embodiments, the non- compliant balloon is configured to transmit ultrasonic energy to disrupt fibrotic tissue.

BRIEF DESCRIPTION OF THE DRAWINGS

[0013] Various embodiments are depicted in the accompanying drawings for illustrative purposes and should in no way be interpreted as limiting the scope of the inventions. In addition, various features of different disclosed embodiments can be combined to form additional embodiments, which are part of this disclosure. Throughout the drawings, reference numbers may be reused to indicate correspondence between reference elements.

[0014] Figure 1 provides a cross-sectional view of a human heart.

[0015] Figure 2 provides a cross-sectional view of a heart experiencing heart failure with reduced ejection fraction.

[0016] Figure 3 provides a cross-sectional view of a heart experiencing heart failure with preserved ejection fraction.

[0017] Figure 4 provides a cross-sectional view of a heart experiencing heart failure with preserved ejection fraction.

[0018] Figure 5 shows a tissue disruption device in a non-expanded configuration in accordance with one or more embodiments.

[0019] Figure 6 shows a compliant tissue disruption device in accordance with one or more embodiments. [0020] Figure 7 is a flow diagram illustrating a process for disrupting fibrotic ventricular tissue using a compliant tissue disruption device in accordance with one or more embodiments.

[0021] Figure 8 shows a non-compliant tissue disruption device in accordance with one or more embodiments.

[0022] Figure 9 shows a non-compliant tissue disruption device in accordance with one or more embodiments.

[0023] Figure 10 is a flow diagram illustrating a process for disrupting fibrotic ventricular tissue using a compliant tissue disruption device in accordance with one or more embodiments

[0024] Figure 11 illustrates various access paths through which access to a target cardiac anatomy may be achieved in accordance with one or more embodiments.

DETAILED DESCRIPTION

[0025] The headings provided herein are for convenience only and do not necessarily affect the scope or meaning of the claimed invention. The present disclosure relates to systems, devices, and methods for breaking or otherwise disrupting fibrotic tissue. The terms“disrupt” and“disruption” are used herein according to their broad and ordinary meanings, and may refer to any breaking, tearing, cutting, rupturing, separating, or otherwise disturbing or destroying connective biological tissue, such as fibrotic tissue. The term “fibrotic tissue” is used herein according to its broad and ordinary meaning, and may refer to any fibrous connective tissue, such as excess fibrous tissue that may be associated with, or caused by, injury or other physiological event or process. Fibrotic tissue may be reactive, benign, or pathological. The term“fibrotic tissue” includes any type of scarring or scar tissue, as well as other types of fibrosis. Furthermore, where fibrotic tissue is disposed at least partially within, or intrinsic to, a tissue wall, references herein to fibrotic tissue or contacting fibrotic tissue may refer to the tissue wall in which the fibrotic tissue is disposed. That is, where fibrotic tissue is present within a ventricle wall, but not necessarily exposed on the interior surface of the ventricle wall, contact with the interior surface of the wall in an area behind or under which fibrotic tissue is present may be considered as contact with the fibrotic tissue even where such contact is not direct contact with the fibrotic tissue. In such cases, description of contact with tissue“associated with” fibrotic tissue refers to either the fibrotic tissue itself or to the tissue surface behind or under which the fibrotic tissue is disposed or present.

[0026] Although certain preferred embodiments and examples are disclosed below, inventive subject matter extends beyond the specifically disclosed embodiments to other alternative embodiments or uses and to modifications and equivalents thereof. Thus, the scope of the claims that may arise herefrom is not limited by any of the particular

embodiments described below. For example, in any method or process disclosed herein, the acts or operations of the method or process may be performed in any suitable sequence and are not necessarily limited to any particular disclosed sequence. Various operations may be described as multiple discrete operations in turn, in a manner that may be helpful in understanding certain embodiments; however, the order of description should not be construed to imply that these operations are order dependent. Additionally, the structures, systems, and devices described herein may be embodied as integrated components or as separate components. For purposes of comparing various embodiments, certain aspects and advantages of these embodiments are described. Not necessarily all such aspects or advantages are achieved by any particular embodiment. Thus, for example, various embodiments may be carried out in a manner that achieves or optimizes one advantage or group of advantages as taught herein without necessarily achieving other aspects or advantages as may also be taught or suggested herein.

[0027] Cardiac (ventricular) hypertrophy is the enlargement and thickening of the walls of the ventricle. This is often associated with heart failure with preserved ejection fraction (HFpEF). Hypertrophy can cause reduced diastolic filling of the left ventricle. Such reduced diastolic filling can be caused in part by fibrous scar tissue present in the ventricular wall and the general thickening of the ventricle. Reduced diastolic filling can impair perfusion and cardiac function.

[0028] The following includes a general description of human cardiac anatomy that is relevant to certain inventive features and embodiments disclosed herein and is included to provide context for certain aspects of the present disclosure. In humans and other vertebrate animals, the heart generally comprises a muscular organ having four pumping chambers, wherein the flow thereof is at least partially controlled by various heart valves, namely, the aortic, mitral (or bicuspid), tricuspid, and pulmonary valves. The valves may be configured to open and close in response to a pressure gradient present during various stages of the cardiac cycle (e.g., relaxation and contraction) to at least partially control the flow of blood to a respective region of the heart or to blood vessels (e.g., pulmonary, aorta, etc.). [0029] Figure 1 illustrates an example representation of a heart 1 having various features relevant to certain aspects of the present inventive disclosure. The heart 1 includes four chambers, namely the left ventricle 3, the left atrium 2, the right ventricle 4, and the right atrium 5. A wall of muscle 17, referred to as the septum, separates the left 2 and right 5 atria and the left 3 and right 4 ventricles. The inferior tip 19 of the heart 1 is referred to as the apex (or apex region) and is located on the midclavicular line, in the fifth intercostal space.

[0030] The left ventricle 3 is the primary pumping chamber of the heart 1. A healthy left ventricle is generally conical or apical in shape in that it is longer (along a longitudinal axis extending in a direction from the aortic valve 7 to the apex 19) than it is wide (along a transverse axis extending between opposing walls 25, 26 at the widest point of the left ventricle) and descends from a base 15 with a decreasing cross-sectional

circumference to the point or apex 19. The pumping of blood from the left ventricle is accomplished by a squeezing motion and a twisting or torsional motion. The squeezing motion occurs between the lateral wall 18 of the left ventricle and the septum 17. The twisting motion is a result of heart muscle fibers that extend in a circular or spiral direction around the heart. When these fibers contract, they produce a gradient of angular

displacements of the myocardium from the apex 19 to the base 15 about the longitudinal axis of the heart. The resultant force vectors extend at angles from about 30-60 degrees to the flow of blood through the aortic valve 7. The contraction of the heart is manifested as a

counterclockwise rotation of the apex 19 relative to the base 15, when viewed from the apex 19. A healthy heart can pump blood from the left ventricle in a very efficient manner due to the spiral contractility of the heart.

[0031] The heart 1 further includes four valves for aiding the circulation of blood therein, including the tricuspid valve 8, which separates the right atrium 5 from the right ventricle 4. The tricuspid valve 8 may generally have three cusps or leaflets and may generally close during ventricular contraction (i.e., systole) and open during ventricular expansion (i.e., diastole). The valves of the heart 1 further include the pulmonary valve 9, which separates the right ventricle 4 from the pulmonary artery 11, and may be configured to open during systole so that blood may be pumped toward the lungs, and close during diastole to prevent blood from leaking back into the heart from the pulmonary artery. The pulmonary valve 9 generally has three cusps/leaflets, wherein each one may have a crescent-type shape. The heart 1 further includes the mitral valve 6, which generally has two cusps/leaflets and separates the left atrium 2 from the left ventricle 3. The mitral valve 6 may generally be configured to open during diastole so that blood in the left atrium 2 can flow into the left ventricle 3, and advantageously close during diastole to prevent blood from leaking back into the left atrium 2. The aortic valve 7 separates the left ventricle 3 from the aorta 12. The aortic valve 7 is configured to open during systole to allow blood leaving the left ventricle 3 to enter the aorta 12, and close during diastole to prevent blood from leaking back into the left ventricle 3.

[0032] The atrioventricular (i.e., mitral and tricuspid) heart valves may comprise a collection of chordae tendineae (13, 16) and papillary muscles (10, 15) for securing the leaflets of the respective valves to facilitate proper coaptation of the valve leaflets and prevent prolapse thereof. The papillary muscles, for example, may generally comprise finger like projections from the ventricle wall. With respect to the tricuspid valve 8, the normal tricuspid valve may comprise three leaflets (two shown in Figure 1) and three corresponding papillary muscles 10 (two shown in Figure 1). The leaflets of the tricuspid valve may be referred to as the anterior, posterior and septal leaflets, respectively. The valve leaflets are connected to the papillary muscles 10 by the chordae tendineae 13, which are disposed in the right ventricle 4 along with the papillary muscles 10.

[0033] Surrounding the ventricles (3, 4) are a number of arteries (not shown) that supply oxygenated blood to the heart muscle and a number of veins that return the blood from the heart muscle. The coronary sinus (not shown) is a relatively large vein that extends generally around the upper portion of the left ventricle 3 and provides a return conduit for blood returning to the right atrium 5. The coronary sinus terminates at the coronary ostium (not shown) at which point the blood enters the right atrium.

[0034] With respect to the mitral valve 6, a normal mitral valve may comprise two leaflets (anterior and posterior) and two corresponding papillary muscles 15. The papillary muscles 15 originate in the left ventricle wall and project into the left ventricle 3. Generally, the anterior leaflet may cover approximately two-thirds of the valve annulus. Although the anterior leaflet covers a greater portion of the annulus, the posterior leaflet may comprise a larger surface area in certain anatomies.

Heart Failure

[0035] Heart failure generally occurs when the heart is unable to pump

sufficiently to maintain blood flow to meet the body's needs. Common causes of heart failure include coronary artery disease including a previous myocardial infarction (heart attack), high blood pressure, atrial fibrillation, valvular heart disease, infection, and various other types of cardiomyopathy. The various types of heart failure can generally be divided into two categories based on whether the ability of the left ventricle to contract during systole is affected, referred to as heart failure with reduced ejection fraction (HFrEF), or whether the heart’ s ability to relax during diastole is affected, referred to as heart failure with preserved ejection fraction (HFpEF). Some embodiments of the present disclosure relate primarily to HFpEF, although HFrEF is also described below to provide additional context that may be relevant to certain embodiments and inventive aspects disclosed herein.

[0036] Figure 2 provides a cross-sectional view of a heart 1 experiencing heart failure with reduced ejection fraction (HFrEF), also known as systolic dysfunction. As shown in Figure 2, HFrEF may be characterized by a dilated left ventricle 3 or right ventricle 4, which may result in impaired ejection of blood from the ventricles. The ventricle walls, including the septum 17 and posterior wall 18, may be thinned or weakened as a result of the dilation of the left ventricle 3 or right ventricle 4. The term“ejection fraction,” in the context of cardiac anatomy, generally refers to the volumetric fraction (i.e., portion of the total) of fluid (e.g., blood) ejected from a chamber (e.g., left ventricle) with each contraction or heartbeat. Normal ejection fraction of a human heart is typically defined as 55-70 percent of the heart’s volume of blood with each beat. Although ejection fraction can also be used to refer to ejection of blood from the atria, embodiments disclosed herein are generally described with reference to ejection from the left (or right) ventricle. Ejection fraction, as a physiological parameter, can be used as a measure of the pumping efficiency of the heart and to classify heart failure types with respect to HFrEF and HFpEF, as described above. Left ventricular ejection fraction can be calculated by dividing the volume of blood pumped from the left ventricle per beat (i.e.,“stroke volume”) by the volume of blood collected in the left ventricle at the end of diastolic filling (i.e.,“end-diastolic volume”). Left ventricular ejection fraction can provide an indicator of the effectiveness of pumping into the systemic circulation. With respect to the right ventricle, right ventricular ejection fraction can provide a measure of the efficiency of pumping into the pulmonary circulation. Although certain inventive embodiments are disclosed herein in the context of improvement of left ventricular function and left ventricular fibrotic tissue disruption, it should be understood that the principles disclosed herein are applicable to the right ventricle and disruption of right ventricular fibrotic tissue.

[0037] Heart failure with preserved ejection fraction (HFpEF), also known as diastolic dysfunction, is characterized by an increase in left ventricular wall thickness and reduced diastolic filling of the left ventricle. HFpEF can further be characterized by ventricular stiffness and reduced diastolic filling caused at least in part by fibrous scar tissue present in the ventricular wall and general thickening of the ventricle walls. Figures 3 and 4 are cross-sectional views of a heart 1 suffering from HFpEF. As shown, the walls or muscle affected by thickening or stiffness may include the septum 17 and posterior walls 18. While the left ventricle 3 and right ventricle 4 may have typical size when HFpEF is present, the ventricles may lose the ability to fill before contraction due to the thickness or stiffness of the heart muscle, which may cause reduced output of the ventricles. A heart experiencing HFpEF may provide an ejection fraction of over 50 percent; however, the volume of ejected blood may be significantly reduced in comparison to a heart that is not experiencing HFpEF.

Improvement in Ventricular Function Through Disruption of Fibrotic Tissue

[0038] Some embodiments disclosed herein provide solutions for treating HFpEF using minimally-invasive or surgical means through disruption of fibrotic ventricular tissue. Fibrosis in the ventricle may be embodied in a three-dimensional matrix of muscle and connective fibrotic tissue. Fibrotic tissue may form in the ventricle (e.g., left ventricle) due at least in part to ischemia, or lack of perfusion, in one or more areas of the ventricle, which may be caused by various pathologies, including artery blockages, rupture, mechanical compression, vasoconstriction, or other conditions. Fibrotic tissue may form as a result of such tissue death/ischemia and may generally exist regionally, rather than uniformly around a circumference of the ventricle. Furthermore, because the blood vessels that provide perfusion to the ventricle walls may generally be larger toward the outside of the ventricle, whereas relatively smaller vessels may be situated or disposed towards the inside of the ventricle, fibrosis from lack of perfusion may form predominantly from the inside of the ventricle, and farther toward the outside of the ventricle as blood loss time increases.

[0039] For patients with heart failure with preserved ejection fraction (HFpEF), achieving an increase in end-diastolic volume without damage or detriment to the patient’ s healthy, non-fibrotic, ventricular tissue can greatly improve the patient’s physiological well being. According to certain solutions for reducing the effect of ventricular fibrotic tissue on the ability of the ventricle to adequately expand and contract can involve cutting the ventricle wall or fibrotic tissue associated therewith using a blade or other instrument. For example, an inner layer of the ventricle may be at least partially removed or cut-off in order to prevent such tissue from restricting expansion and contraction of the ventricle. However, such solutions may introduce undesirable risks of damage to the cardiac anatomy within the ventricle. Furthermore, targeting of the fibrotic tissue may be difficult in some

implementations . [0040] Embodiments of the present disclosure provide systems, devices, and methods for mechanically disrupting the fibrous tissue component(s) of the ventricular walls, such as the left ventricular walls. Such disruption of the fibrotic tissue may serve to at least partially increase end-diastolic volumes of the ventricle by allowing the ventricle walls to expand in connection with the diastolic phase of the cardiac cycle. For example, the strain tolerance of certain fibrotic tissue associated with the interventricular walls may generally be lower than that of viable myocardial tissue, which may exist behind or adjacent to the fibrotic tissue. Therefore, by inducing a strain on the interventricular wall (e.g., during relaxation), or portions thereof, that is greater than what the ventricle typically experiences in connection with the preload phase of a cardiac cycle, it is possible to disrupt or break one or more portions of the fibrotic tissue of the ventricular wall, thereby allowing for increased end- diastolic volume without a substantial increase in end-systolic volume. For example, such artificially induced strain in the ventricular wall may advantageously be greater than a strain tolerance of the fibrotic tissue, but not greater than the strain tolerance of the relatively healthy myocardial tissue. Therefore, disruption of the fibrotic tissue of the ventricle may be achieved substantially without damaging healthy myocardial tissue.

[0041] By implementing disruption of fibrotic ventricular tissue in accordance with embodiments of the present disclosure, end-diastolic volume and ejection fraction may be improved for patients suffering from heart failure with preserved ejection fraction, or ventricles associated with hypertrophy, thickened walls or fibrosis. Furthermore, when ventricular fibrotic tissue is disrupted in accordance with embodiments of the present disclosure, end-systolic volume may also be reduced or improved. For example, fibrotic tissue may be considered to exhibit tensional, rather than compressional, resistance.

Therefore, disruption of such tensional resistance in the fibrotic tissue can allow for healthy myocardial muscle to contract more efficiently and effectively, thereby ejecting a greater volume of blood with each cardiac cycle. However, it should be understood that

embodiments of the present disclosure can provide benefits to patients suffering from certain heart failure conditions by improving end-diastolic volume, or filling volume, regardless of whether muscle contractibility is also improved. Furthermore, various embodiments disclosed herein advantageously provide for the treatment of HFpEF that can be executed on a beating heart, thereby allowing for the ability to assess the efficacy of the treatment and potentially implement modification thereto without the need for bypass support. Beating-heart implementations of devices/processes disclosed herein may be improved by delivering the strain on fibrotic tissue in phasic synchronization with cardiac rhythm, whereas such synchronization may not be necessary in implementations performed during cardiac surgery utilizing cardiopulmonary bypass. Heartbeat synchronization can serve to cause the application of peak strains to occur only or primarily during diastole.

Fibrotic Tissue Disruption Balloon Devices and Processes

[0042] In some implementations, disruption of fibrotic ventricular tissue may be achieved at least in part through the application of strain onto the fibrotic tissue using ventricular balloon devices and techniques, as described herein. Embodiments of the present disclosure can involve utilization of one or more compliant or non-compliant balloon devices, which may be expanded or inflated within at least a portion of a diseased ventricle to present strain on the internal ventricular walls associated therewith. In some embodiments, non- compliant balloons may be shaped or configured to apply pressure onto the ventricular wall in a targeted or selective/strategic manner, thereby providing for more localized tissue strain/disruption. Additionally or alternatively, one or more compliant balloons may be inflated or expanded to provide a more general application of pressure to the ventricular walls, or one or more portions thereof.

[0043] In some embodiments, historical ventricular pressure data associated with a patient may be referenced to determine or calculate an appropriate increase in the pressure applied to the ventricular walls in order to determine and execute the desired fibrotic tissue disruption. Such processes may allow for optimization of the strain or disruption of the fibrotic tissue, while resulting in reduced or minimal damage to the local viable muscle tissue of the ventricle. In some implementations, it may be advantageous to apply ventricular tissue strain/disruption in accordance with the present disclosure selectively during diastole in order to preserve myocardial tissue that may be in an at least partially contracted or collapsed configuration during systole, and therefore application of strain to the ventricular wall at such times may result in damage to the functioning muscle/tissue. That is, by concentrating the application of strain/stress on the ventricle wall during diastole, such strain/stress may be directed or induced mainly on the fibrotic tissue of the ventricle.

[0044] In some implementations, disruption of ventricular fibrotic tissue in accordance with embodiments of the present disclosure may be applied to the ventricle wall(s) in connection with or during a surgical operation in which the heart is in a relatively relaxed state. For example, in cardiopulmonary bypass surgeries, the heart muscle may be substantially relaxed, such that the risk of damage to healthy myocardial tissue may be reduced or negligible with respect to the desired amount of strain necessary to disrupt the target fibrotic tissue. The coronary vessels providing blood to the ventricle wall tissue generally decrease in size as they penetrate deeper into the ventricular tissue to feed the heart wall. Therefore, a substantial portion of fibrosis/scar tissue may form at or near the inside wall of the ventricle, depending on when the patient receives intervention for an ischemic condition.

[0045] Figure 5 illustrates a cross-sectional portion of a heart ventricle 3 having a balloon tissue disruption device 50 disposed at least partially therein. For example, the ventricle 3 may represent a left ventricle of an example diseased heart having relatively thick left ventricle walls 18, 17 (interventricular septum). The ventricle walls 17, 18 may represent walls of a ventricle having one or more regions thereof that are associated with or covered by fibrotic tissue at or near internal wall surfaces 25, 26 thereof.

[0046] As referenced above, fibrosis or hypertrophy in a ventricle can be caused at least in part by damage or excess pressures experienced thereby, resulting in an increased load on the ventricles. In such a condition, the heart muscle may compensate through the thickening of the walls of the heart to push against the relatively high load. Over time, the thickened heart muscle may not receive enough blood supply, thereby resulting in portions or areas thereof becoming ischemic. Ischemic heart tissue may form scar/fibrotic tissue, thereby resulting in a matrix of fibrosis and scar tissue in the heart. However, generally such hearts retain some amount of viable myocardial muscle in spite of the presence/formation of ischemia and fibrosis, although the fibrotic tissue may at least partially impede the natural or healthy movement/contraction of the viable heart muscle and keep the ventricle from dilating/stretching-out sufficiently to receive the desired amount of blood therein.

Furthermore, the contracting/squeezing of the relatively healthy muscle of the heart may likewise be impeded, thereby reducing the amount of ejection from the ventricle.

[0047] The contracted/collapsed tissue disruption device 50 may be advanced to the target ventricle 3 using any suitable or desirable procedure. For example, although access to the ventricle 3 is illustrated as via the left atrium 2, such as through a transfemoral or other transcatheter procedure, other access methods may be implemented in accordance with embodiments of the present disclosure, as described in further detail in connection with Figure 11 below. Prior to inflation or expansion of the tissue disruption device 50, the device 50 may be in an at least partially collapsed state or configuration, as shown. The tissue disruption device 50 may be coupled to a delivery catheter 60 at least for a period prior to expansion and utilization thereof in the ventricle 3. In an expanded state, the balloon device 50 may be a compliant balloon, a non-compliant balloon, or a partially-compliant balloon. Fibrotic Tissue Disruption Using Compliant Balloons

[0048] As described herein, application of stress/strain to ventricle walls for the purpose of disrupting fibrotic ventricular wall tissue may be achieved in accordance with embodiments of the present disclosure using either non-compliant balloon devices or compliant balloon devices. When it is desired to apply pressure relatively evenly to the internal ventricular walls, one or more compliant balloon devices may be utilized to achieve the desired tissue stress/strain. Such compliant balloon devices may comprise any suitable or desirable compliant material(s). For example, in some embodiments, a compliant balloon device comprises latex, silicone, or the like. The term“compliance” is used here and according to its broad and ordinary meaning and may refer to any material having tension or shape memory characteristics designed to store energy when the material is stretched or expanded. That is, a compliant balloon device may be configured to at least partially change shape and volume in response to internal or environmental pressure changes. Conversely, non-compliant balloon devices may not substantially expand or stretch under changing pressure conditions.

[0049] Generally, micro-characteristics of fibrotic/scar tissue relative to healthy myocardial tissue are such that healthy myocardial tissue may be more elastic than fibrotic scar tissue. Therefore, under increasing stress and pressure, fibrotic tissue may generally be disrupted or damaged before healthy myocardial muscle tissue becomes damaged. That is, healthy myocardial muscle tissue may be able to sustain a higher level of strain substantially without damage. Therefore, embodiments of the present disclosure advantageously provide for the inducement of strain/stress on the internal walls of a ventricle that is greater than the strain tolerance of the targeted fibrotic tissue, while being less than the strain tolerance of healthy tissue that is intended to remain undamaged. In some implementations, the amount of stress that is sufficient to disrupt the targeted fibrotic tissue, but not enough as to cause undesired damage to the healthy myocardial tissue, may be determined through testing. As healthy myocardial tissue is beneficial for cardiac function, reducing the risk of damage thereto can be desirable.

[0050] Figure 6 illustrates a cross-sectional portion of a heart ventricle 3 having a compliant balloon tissue disruption device 52 at least partially expanded therein in order to produce dilation of the internal walls 17, 18 of the ventricle 3, which may be the left ventricle of the heart. The compliant balloon device 52 may advantageously have the ability to expand/distend and increase volume with increasing internal pressure. [0051] In some embodiments, the device 52 may be configured to expand to a volume or medial diameter that is more than 5% greater than the natural internal volume or medial diameter of the ventricle 3, between 5-10% greater than the natural internal volume or medial diameter of the ventricle 3, between 10-15% greater than the natural internal volume or medial diameter of the ventricle 3, or more than 15% greater than the natural internal volume or medial diameter of the ventricle 3, or at least with respect to the region in which the balloon device 52 is expanded. In some embodiments, the device 52, in the expanded state, has a diameter greater than half the circumference of the ventricle when inflated in a surgical on-pump procedure where the ventricle is deflated and relaxed.

[0052] The balloon device 52 may be expanded during diastole or a relatively relaxed state of the heart 1 to cause the ventricle 3 to expand to a volume larger than is normally achieved during diastole for the particular heart. For example, the heart 1 may represent a heart of a patients suffering from heart failure with preserved ejection fraction. As described above, for such patients, filling volume in the left ventricle during diastole can become compromised or insufficient due to the ventricle walls not stretching sufficiently to receive blood therein and pump the same. Where such reduced stretching of the ventricle walls is due at least in part to scar/fibrotic tissue associated with the ventricular walls, presenting stress as illustrated in Figure 6 on the ventricle walls to a degree that surpasses the strain tolerance of scar tissue associated therewith may serve to at least partially disrupt such scar/fibrotic tissue. Such fibrotic tissue disruption may break or disrupt the tensional resistance thereof and allow the ventricle to expand further than previously possible or typical. However, as the strain tolerance of the healthy myocardial tissue associated with the ventricle walls 17, 18 may generally be higher than that of the fibrotic tissue associated therewith, the stretching/dilation of the ventricle walls as shown in Figure 6 may

advantageously disrupt the fibrotic tissue being targeted without substantially destroying a significant amount of viable myocardium. Furthermore, in some patients, induced ventricular dilation as shown in Figure 6 using a balloon device may further serve to at least partially compress the ventricular walls 17, 18 or decrease the thickness thereof. Therefore, embodiments of the present disclosure may advantageously provide for disruption of fibrotic ventricular wall tissue without substantially restricting the operation of the local viable myocardial muscle.

[0053] The expansion of the balloon device 52 may advantageously affect both end-diastolic volume and end-systolic volume. That is, the dilation of the ventricle 3 caused by the expansion of the device 52 may disrupt the fibrotic ventricular tissue and thereby allow the ventricle 3 to fill with a greater volume of blood when the ventricle is relaxed. Furthermore, the fibrotic tissue disruption may also reduce the amount of casting of fibrosis tissue on the ventricle walls 17, 18 that may otherwise prevent the ventricle from

contracting/squeezing adequately. The degree to which the application of stress/strain to the ventricle wall(s) results in fibrotic tissue disruption may depend at least in part on the configuration and degree to which the fibrotic tissue and muscle tissue interact, or the manner in which the different tissue types are bonded together. Generally, in response to expansion of the balloon device 52, endocardium tissue may see greater levels of stress than epicardium tissue due to the compression of the ventricle walls 17, 18. The compliant balloon device 52 shown in Figure 6 may provide a relatively uniform surface contact and relatively even distribution of force along the cardiac anatomy and walls of the target ventricle 3 in order to produce desired end-diastolic ventricular volume, as shown.

[0054] In some implementations, the expansion of balloon devices in accordance with embodiments of the present disclosure may involve expanding or inflating a balloon device in phase with the cardiac cycle of the heart, such that the expansion of the balloon device reaches its maximum volume or impact during the diastolic phase. For example, a balloon tissue disruption device in accordance with embodiments of the present disclosure may be coupled to a pump or other device configured to facilitate or execute the expansion thereof for the purpose of disrupting fibrotic ventricular tissue. In some implementations, the patient’s heart rate may be determined or calculated, such as in real time, such that the pump may be operated with pulsed expansion of the balloon device having a similar frequency to the patient’s heart rate. Expansion of the balloon device may further advantageously be substantially phase-aligned with the patient’s heart rate. Frequency and phase alignment of balloon expansion may advantageously prevent the expansion of the balloon device during the systolic phase of the cardiac cycle, and rather only during diastole when the ventricle is relatively relaxed. The volume of a compliant balloon device in accordance with

embodiments of the present disclosure may advantageously be greater than the respective end-diastolic volume of the ventricle prior to implementation of expansion of the balloon device.

[0055] In some implementations, in order to prevent or reduce the risk of blood flow obstruction, the patient’s heart may be paced in a manner as to cause the heart to fibrillate. Such fibrillating of the heart may be achieved in any suitable or desirable manner and may substantially prevent or reduce blood movement in the heart from one chamber to another. Such condition of the heart may be tolerable by the patient for relatively short periods of time and may allow for the use of other types of expanding structures, such as mechanical or compliant devices that are configured to introduce strain on internal ventricular wall tissue as described herein. Furthermore, although non-compliant and compliant balloon devices are described herein, it should be understood that embodiments of the present disclosure may be implemented utilizing tissue disruption devices that are partially compliant, or compliant in one or more regions thereof while not being compliant in one or more other regions.

[0056] Figure 7 is a flow diagram illustrating a process 700 for disrupting fibrotic ventricular tissue using a compliant balloon device in accordance with one or more embodiments of the present disclosure. At block 702, the process 700 involves advancing a compliant balloon device to the left ventricle of a patient. Access to the left ventricle may be achieved through transaortic access, which may be made via the femoral artery and through the aortic valve. Such access may be advantageous relative to transseptal access due to the damage that may be caused to the interatrial septum by passage therethrough. However, vascular complications may be relatively harder to handle on the left side of the heart due to the relatively higher pressures, and therefore working to the right side of the heart may be considered preferable or safer in some circumstances.

[0057] At block 704, the process 700 involves expanding the balloon device until the balloon device disrupts the target fibrotic ventricular tissue. In filling the balloon device, the device may be filled with any type of gas, liquid, or other fluid, and may generally expand hydraulically in some embodiments. As described above, the balloon expansion device may have an expanded width dimension W that is greater than the natural width of the ventricle w with respect to the medial contact plane of the balloon device. At block 706, the process 700 involves withdrawing the balloon device and its associated delivery system from the patient. In some embodiments, the device 54, in the expanded state, has a width dimension W that is greater than half the circumference of the ventricle 3 when inflated in a surgical on-pump procedure where the ventricle 3 is deflated/relaxed.

[0058] In some embodiments, the process 700 involves accessing data indicating the patient’s normal ventricular pressures to determine an appropriate expansion size or amount of strain for the balloon device. For example, assessment may be made of the dimensional change of the ventricular tissue as compared to the change in pressure experienced by the ventricle. Pressure determinations in accordance with processes disclosed herein may involve utilizing a pressure catheter placed or disposed in the target ventricle or other vessel or chamber of the cardiac system to determine, for example, the end-diastolic filling pressure of the patient. Processes may further involve determining a pressure level that is greater than the normal pressure conditions of the patient and implementing such pressure in the patient’s heart/cardiac system to gauge/estimate the amount of damage that results from the pressure increase applied to the ventricle. Although pressure measurements are described herein, it should be understood that other physiological measurements may be determined in addition to, or as an alternative to, pressure determination. For example, volume determination may advantageously be used to determine compliance of the ventricle, which may be used to guide balloon device filling levels, shape, or form. However, volume determination may be relatively difficult in some settings due to the presence of ventricular anatomy, such as trabeculae carneae, papillary muscles, and the like. In some

implementations, echocardiography, magnetic resonance imaging (MRI), or another imaging modality or determination technique may be utilized to measure or determine the end- diastolic volume of the target ventricle, which may be used to guide device shape or filling parameters for balloon devices in accordance with embodiments of the present disclosure.

Fibrotic Tissue Disruption Using Non-Compliant Balloons

[0059] The compliant balloon devices described above can be used to provide strain/stress relatively evenly over the entire target ventricle, or at least a portion thereof. However, it may be desirable in certain cases to provide targeted stress/strain on certain areas or anatomy of the ventricle. Therefore, in some implementations, non-compliant balloon or expansion devices may be utilized to provide targeted stress on a ventricle wall or associated anatomy. Where at least two tissue contact projections of the non-compliant balloon device contact ventricular wall(s) or anatomy in an expanded configuration or form, such that the width between tissue contact areas of respective tissue contact projections of the non- compliant balloon device is greater than the width of the ventricle or other dimension between targeted anatomy, inflation or expansion of the non-compliant balloon device can serve to expand the ventricular tissue/anatomy to provide tissue disruption functionality as described in detail herein.

[0060] The non-compliance of a balloon-type tissue disruption device in accordance with some embodiments of the present disclosure may serve to keep the balloon device from substantially changing shape during expansion or articulation, such that targeted pressure application may be achieved according to the shape and orientation of the device. Non-compliant balloon devices in accordance with embodiments of the present disclosure may have any suitable or desirable geometry configured or designed to target specific anatomy or areas of the ventricular wall(s) to provide specific application of pressure thereto. Non-compliant balloon expansion devices in accordance with embodiments of the present disclosure may comprise any suitable or desirable type of material(s). For example, such devices may comprise any type of polymer including, for example Nylon 12, polyethylene terephthalate (PET), or the like. Non-compliant expansion/balloon devices may

advantageously comprise material(s) suitable for use under relatively high-pressure conditions. In some embodiments, non-compliant balloon/expansion devices comprise fabric.

[0061] Non-compliant balloon/expansion devices in accordance with

embodiments of the present disclosure may serve to damage fibrotic ventricular tissue, as described in detail above. Using various geometries/shapes, it may be possible to at least partially segregate the areas or tissues that are disrupted or damaged in accordance with ventricle-repair solutions as described herein. For example, where fibrotic or scar tissue is determined or identified in one or more areas or regions of the ventricle, such areas or regions may be targeted by the orientation, or shape, or form of the expansion device.

[0062] In some embodiments, a balloon tissue disruption device has a shape forming one or more tissue contact projections/posts. Figure 8 illustrates a balloon expansion device 54 in an inflated/expansion configuration according to one or more embodiments. The illustrated embodiment of Figure 8 comprises a first projection 71 and a second projection 72, wherein each projection has a respective tissue contact area 61, 62. Although two projections and tissue contact areas are shown in Figure 8, it should be understood that embodiments of the present disclosure may comprise any suitable or desirable number of projections or tissue contact area features. For example, the illustrated embodiment of Figure 9 comprises first 55, second 57, and third 59 projections, each having a respective tissue contact area 57-59.

Compared to compliant balloon tissue disruption devices, as described in detail above, non- compliant tissue disruption devices having one or more tissue-contact extensions may advantageously be less obstructive to fluid flow. In some embodiments, as shown in Figure 8, balloon tissue disruption devices in accordance with the present disclosure may comprise a T- shaped form. Additionally or alternatively, balloon tissue disruption devices may comprise more than two projections, such as shown in Figure 9. The fibrotic tissue disruption devices that include non-compliant balloons in accordance with embodiments of the present disclosure may have a generally round or ventricular shape that is larger in volume than the target ventricle. That is, a non-compliant balloon that has a volume that is greater than the target ventricle can function similarly to the compliant balloon device of Figure 6 in certain respects. [0063] Figure 10 is a flow diagram illustrating a process 100 for disrupting fibrotic ventricular tissue using a non-compliant balloon device in accordance with one or more embodiments of the present disclosure. In some embodiments, the process 100 involves determining/identifying target fibrotic tissue that is desired to be disrupted for the purpose of increasing end-diastolic volume or reducing end-systolic volume, as shown at block 102. Any imaging technology or modality may be implemented when identifying the target fibrotic tissue, including but not limited to echocardiography, magnetic resonance imaging (MRI), or the like. For example, with respect to embodiments utilizing MRI imaging, fluid content in the ventricular tissue may be at least partially visible, and so determinations regarding whether certain tissue is ischemic may inform as to the presence of undesirable fibrotic tissue. Furthermore, ischemia may be identified/determined by monitoring tissue movement. For example, when tissue becomes ischemic, it generally becomes less kinetic and ceases to contract in the normal way due to the lack of blood supply. However, ischemic tissue may nevertheless receive enough blood to stay alive in some cases.

[0064] At block 104, the process 100 involves using non-compliant material to form a balloon device having geometry configured to provide pressure in desired vectors or areas of the ventricle. Specifically, the geometry of the balloon device may have one or more projections or tissue contact areas configured to target the identified fibrotic ventricular tissue. Designing the shape/geometry of the balloon device may be based on any criteria or in response to any determination, such as a determination of the location of target fibrosis tissue within the ventricle. In some embodiments, certain geometrical measuring steps may be implemented in order to determine the optimal or desired shape or size of the balloon expansion device.

[0065] At block 106, the process 100 involves advancing the balloon device to the left ventricle of the patient. Access to the left ventricle may be achieved through transaortic access, which may be made via the femoral artery and through the aortic valve, or through any other access path. With respect to embodiments relating to implementation of tissue disruption devices in one or more of the ventricles, such access may be achieved in any suitable or desirable way. For example, Figure 11 illustrates various access paths through which access to a target cardiac anatomy may be achieved, including transseptal access 1101, which may be made through the inferior vena cava 29 or superior vena cava 19, and from the right atrium 5, through the septal wall (not shown), into the left atrium 2, and down into the left ventricle through the mitral valve 6. For transaortic access 1102, a delivery catheter may be passed through the descending aorta, aortic arch 12, ascending aorta, and aortic valve 7. For transapical access 1103, access may be made directly through the apex of the heart and into the left ventricle 3 or right ventricle 4.

[0066] At block 108, the process 100 involves orienting the balloon device within the left ventricle to target the fibrotic tissue with the projections or surface contact areas of the balloon device. Orientation of the balloon expansion device in accordance with the process 100 may involve real-time imaging of the implant device, such as using fluoroscopy with contrast, or another imaging modality. When the balloon dilation device 54 (see Figure 8) is introduced to the ventricle 3, the process 100 involves orienting the balloon device 54 to the desired orientation prior to expansion/inflation of the balloon device 54 such that the projections thereof align with and ultimately contact the desired target tissue area(s) when sufficiently expanded/inflated.

[0067] At block 110, the process 100 involves expanding/inflating the balloon device until the projections or associated surface-contact areas contact and disrupt the target fibrotic tissue or tissue associated with the target fibrotic tissue. In filling and inflating the balloon device, a device may be filled with any type of gas, liquid, or other fluid, and may generally expand hydraulically. With further reference to Figure 8, the balloon device 54 may advantageously have a width dimension W that is greater than the natural width w of the ventricle with respect to the medial contact plane of the ventricle 3. At block 112, the process 100 involves withdrawing the balloon device and its associated delivery system from the patient.

[0068] The various embodiments disclosed herein relate to devices and methods for disrupting internal fibrotic tissue, which may be performed in any heart chamber or blood vessel. With respect to embodiments relating to disruption of ventricular tissue, such as internal fibrotic tissue in the left ventricle, or in one or more blood vessels or chambers accessed through one or more atria or ventricles, such access may be achieved in any suitable or desirable way. For example, Figure 11 illustrates various access paths through which access to a target cardiac anatomy may be achieved, including transseptal access 1101, which may be made through the inferior vena cava 29 or superior vena cava 19, and from the right atrium 5, through the septal wall (not shown) and into the left atrium 2. For transaortic access 1102, a delivery catheter may be passed through the descending aorta, aortic arch 12, ascending aorta, and aortic valve 7. For transapical access 1103, access may be made directly through the apex of the heart and into the left ventricle 3 or right ventricle 4.

[0069] Tissue-disruption balloon devices in accordance with aspects of the present disclosure can include or be constructed with features comprised of radiopaque or echogenic materials, which may advantageously aid in visualization of the tissue-disruption devices for, for example, assisting orientation of the tissue-disruption devices using any suitable or desirable imaging modality.

Fibrotic Tissue Disruption Using Sonic Energy

[0070] Any of the tissue-disruption devices disclosed herein may be configured to generate or transmit ultrasonic energy to disrupt target fibrotic tissue, such as within a ventricle of a heart. For example, a sonic energy source may be associated with a delivery system or with the tissue-disruption device (e.g., compliant or non-compliant balloon) and transmitted through the tissue-disruption device (e.g., balloon). In some embodiments, sonic energy is generated external to the delivery system and provided via the delivery system or tissue-disruption device to the fibrotic tissue to cause disruption therein. The sonic energy may have any suitable or desirable frequency. For example, the frequency of the sonic energy, which may be ultrasonic energy in some implementations/embodiments, can be configured/modulated to cause/achieve a desired/maximum amount of disruption of fibrotic tissue while minimizing disruption of non-fibrotic tissue at the target site (e.g., in the ventricle).

Fibrotic Tissue Disruption Using Non- Balloon Devices

[0071] Although the description above relates primarily to balloon-type tissue disruption devices, it should be understood that embodiments of the present disclosure may provide for ventricular fibrotic tissue disruption without the use of a balloon device. For example, in some implementations, fibrotic tissue disruption may be achieved through massage of the target tissue, such as while the heart is on-pump during a cardiac bypass procedure. Such massaging may be implemented manually or digitally, or using one or more tools, such as a massager or tenderizer mallet or tool. In some implementations, disruption of the fibrotic tissue may be achieved using molecular tenderizer solution or material, which may be applied to the target tissue such that the solution/material serves to break down the target fibrotic tissue. In some implementations, tissue disruption may be achieved through manually stretching, pulling, or otherwise providing strain to the fibrotic tissue that is above the level that the tissue would see under normal cardiac function.

Additional Embodiments

[0072] Depending on the embodiment, certain acts, events, or functions of any of the processes or algorithms described herein can be performed in a different sequence, may be added, merged, or left out altogether. Thus, in certain embodiments, not all described acts or events are necessary for the practice of the processes.

[0073] Certain standard anatomical terms of location are used herein with respect to the preferred embodiments. Although certain spatially relative terms, such as“outer,” “inner,”“upper,”“lower,”“below,”“above,”“vertical,”“horizontal,”“top,”“bottom,” and similar terms, are used herein to describe a spatial relationship of one device/element or anatomical structure to another device/element or anatomical structure, it is understood that these terms are used herein for ease of description to describe the positional relationship between element(s)/structures(s), as illustrated in the drawings. Spatially relative terms are intended to encompass different orientations of the element(s)/structures(s), in use or operation, in addition to the orientations depicted in the drawings. For example, an element/structure described as“above” another element/structure may represent a position that is below or beside such other element/structure with respect to alternate orientations of the subject patient or element/structure, and vice-versa.

[0074] Conditional language used herein, such as, among others,“can,”“could,” “might,”“may,”“e.g.,” and the like, unless specifically stated otherwise, or otherwise understood within the context as used, is intended in its ordinary sense and is generally intended to convey that certain embodiments include, while other embodiments do not include certain features, elements, or steps. Thus, such conditional language is not generally intended to imply that features, elements, or steps are in any way required for one or more embodiments or that one or more embodiments necessarily include logic for deciding, with or without author input or prompting, whether these features, elements, or steps are included or are to be performed in any particular embodiment. The terms“comprising,”“including,” “having,” and the like are synonymous, are used in their ordinary sense, and are used inclusively, in an open-ended fashion, and do not exclude additional elements, features, acts, operations, and so forth. Also, the term“or” is used in its inclusive sense (and not in its exclusive sense) so that when used, for example, to connect a list of elements, the term“or” means one, some, or all of the elements in the list. Conjunctive language such as the phrase “at least one of X, Y and Z,” unless specifically stated otherwise, is understood with the context as used in general to convey that an item, term, element, etc. may be either X, Y or Z. Thus, such conjunctive language is not generally intended to imply that certain embodiments require at least one of X, at least one of Y and at least one of Z to each be present.

[0075] It should be understood that certain ordinal terms (e.g.,“first” or“second”) may be provided for ease of reference and do not necessarily imply physical characteristics or ordering. Therefore, as used herein, an ordinal term (e.g.,“first,”“second,”“third,” etc.) used to modify an element, such as a structure, a component, an operation, etc., does not necessarily indicate priority or order of the element with respect to any other element, but rather may generally distinguish the element from another element having a similar or identical name (but for use of the ordinal term). In addition, as used herein, indefinite articles (“a” and“an”) may indicate“one or more” rather than“one.” Further, an operation performed“based on” a condition or event may also be performed based on one or more other conditions or events not explicitly recited.

[0076] With respect to the various methods and processes disclosed herein, although certain orders of operations or steps are illustrated and described, it should be understood that the various steps and operations shown and described may be performed in any suitable or desirable temporal order. Furthermore, any of the illustrated or described operations or steps may be omitted from any given method or process, and the illustrated and described methods and processes may include additional operations or steps not explicitly illustrated or described.

[0077] It should be appreciated that in the above description of embodiments, various features are sometimes grouped together in a single embodiment, figure, or description thereof for the purpose of streamlining the disclosure and aiding in the understanding of one or more of the various inventive aspects. This method of disclosure, however, is not to be interpreted as reflecting an intention that any claim require more features than are expressly recited in that claim. Moreover, any components, features, or steps illustrated or described in a particular embodiment herein can be applied to or used with any other embodiments. Further, no component, feature, step, or group of components, features, or steps is necessary or indispensable for each embodiment. Thus, it is intended that the scope of the inventions herein disclosed and claimed below should not be limited by the particular embodiments described above but should be determined only by a fair reading of the claims that follow.

Claims

WHAT IS CLAIMED IS:

1. A method of disrupting fibrotic ventricular tissue, the method comprising:

advancing a compliant balloon device to a ventricle of a heart using a delivery catheter;

expanding the compliant balloon device to contact target tissue of the ventricle associated with fibrotic tissue; and

further expanding the compliant balloon device to an expanded state to disrupt the fibrotic tissue.

2. The method of claim 1, wherein said expanding the compliant balloon device to the expanded state to disrupt the fibrotic tissue increases end-diastolic volume of the ventricle and decreases end-systolic volume of the ventricle.

3. The method of claim 1 or claim 2, wherein said further expanding the compliant balloon device to the expanded state involves expanding the compliant balloon device to a volume that is greater than a diastolic volume of the ventricle.

4. The method of any of claims 1-3, further comprising expanding the compliant balloon device to the expanded state in a pulsed manner.

5. The method of claim 4, wherein said expanding the compliant balloon device to the expanded state in a pulsed manner is performed at a frequency and a phase associated with a heart rate of the heart.

6. The method of claim 5, further comprising determining the heart rate of the heart in real-time.

7. The method of any of claims 1-6, wherein said expanding the compliant balloon device to the expanded state to disrupt the fibrotic tissue is performed without damaging non- fibrotic tissue of the ventricle.

8. The method of any of claims 1-7, wherein the compliant balloon device has a volume that is more than 10% greater than a volume of the ventricle when the compliant balloon device is in the expanded state.

9. A fibrotic tissue disruption device comprising:

a delivery catheter having a distal end;

a compliant balloon attached to the distal end of the delivery catheter; and

a fluid pump in fluid communication with the compliant balloon through the delivery catheter;

wherein the fluid pump is configured to, when the compliant balloon is disposed in a ventricle of a heart, expand the compliant balloon from a collapsed state to an expanded state in which the compliant balloon has a medial diameter that is greater than a medial diameter of the ventricle.

10. The fibrotic tissue disruption device of claim 9, wherein the fluid pump is further configured to pulse expansion of the compliant balloon to the expanded state based on a heart rate of the heart.

11. The fibrotic tissue disruption device of claim 10, wherein the fluid pump is configured to contract the compliant balloon such that the compliant balloon is not in the expanded state during systolic periods.

12. The fibrotic tissue disruption device of any of claims 9-11, further comprising a pressure sensor configured to generate a signal indicative of a pressure of the ventricle.

13. A method of disrupting fibrotic ventricular tissue, the method comprising:

identifying target fibrotic tissue in a ventricle of a heart;

forming a non-compliant balloon device having form that is based at least in part on the identified target fibrotic tissue;

advancing the non-compliant balloon device to the ventricle using a delivery catheter; orienting the non-compliant balloon device to align one or more tissue contact areas thereof with the target fibrotic tissue; and

expanding the non-compliant balloon device to an expanded state to disrupt the target fibrotic tissue.

14. The method of claim 13, wherein the non-compliant balloon device has a width that is greater than an internal diameter of the ventricle in the expanded state.

15. The method of claim 13 or claim 14, further comprising pulsing expansion of the non-compliant balloon device to the expanded state at a frequency and phase associated with a diastolic phase of the heart.

16. The method of any of claims 13-15, wherein said expanding the non-compliant balloon device to the expanded state to disrupt the target fibrotic tissue involves applying strain to the target fibrotic tissue using the non-compliant balloon device that is greater than a strain tolerance of the target fibrotic tissue.

17. The method of claim 16, wherein the strain is less than a strain tolerance of non- fibrotic myocardial tissue connected to the target fibrotic tissue.

18. A fibrotic tissue disruption device comprising:

a non-compliant balloon configured to be expanded to an expanded state, the non- compliant balloon comprising:

a first projection having a first tissue contact area;

a second projection having a second tissue contact area; and

a fluid coupling configured to receive fluid from a fluid source for expanding the first and second projections.

19. The fibrotic tissue disruption device of claim 18, wherein the non-compliant balloon further comprises a third projection having a third tissue contact area.

20. The fibrotic tissue disruption device of claim 18 or claim 19, wherein the non- compliant balloon has a T-shaped form.

21. The fibrotic tissue disruption device of any of claims 18-20, wherein the non- compliant balloon has an at least partially round shape that is larger in volume than a determined volume of a target ventricle.

22. The fibrotic tissue disruption device of any of claims 18-21, wherein the non- compliant balloon comprises one or more radiopaque markers.

23. The fibrotic tissue disruption device of any of claims 18-22, wherein the non- compliant balloon is configured to transmit ultrasonic energy to disrupt fibrotic tissue.