US20030109770A1 - Device with a porous membrane for improving cardiac function - Google Patents

Abstract

A porous membrane is inserted into a ventricle of a heart. The porous membrane creates a relatively hemostatic volume in which a thrombus can grow. Blood can still pass through fenestrations of the membrane into and out of the hemostatic volume. The fenestrations reduce pressures that act on the membrane, and so reduce stresses within the membrane. The flow characteristics through the hemostatic volume promote growth of the thrombus from a base of the hemostatic volume. The thrombus grows to slightly larger than the original size of the hemostatic volume so as to provide support for the membrane. Any remaining stresses within the membrane are thereby substantially eliminated. The thrombus shrinks over an ensuing period of time, with the membrane merely acting as a barrier to which an outer wall of the myocardium retracts. The function of the membrane is then complete, and may be absorbed.

Description

CROSS-REFERENCE TO RELATED APPLICATIONS
• The present patent application is a continuation-in-part of prior U.S. application Ser. No. 10/212,033, filed on Aug. 1, 2002, which is a continuation-in-part application of prior U.S. patent application Ser. No. 09/635,511, filed on Aug. 9, 2000, which claims priority from U.S. Provisional Patent Application No. 60/147,894 filed on Aug. 9, 1999, and are incorporated herein by reference in their entirety.[0001]
BACKGROUND OF THE INVENTION
• 1). Field of the Invention[0002]
• This invention relates to a method and device for improving cardiac function.[0003]
• 2). Discussion of Related Art[0004]
• Congestive heart failure annually leads to millions of hospital visits internationally. Congestive heart failure is a description given to a myriad of symptoms that can be the result of the heart's inability to meet the body's demand for blood flow. In certain pathological conditions, the ventricles of the heart become ineffective in pumping the blood, causing a back-up of pressure in the vascular system behind the ventricle.[0005]
• The reduced effectiveness of the heart is usually due to damage to the heart muscle, leading to an enlargement of the heart. A myocardial ischaemia may, for example, cause a portion of a myocardium (of the heart muscle) to lose its ability to contract. Prolonged ischaemia can lead to infarction of a portion of the myocardium wherein the heart muscle dies and becomes scar tissue.[0006]
• Once this tissue dies it no longer functions as a muscle and cannot contribute to the pumping action of the heart. When the heart tissue is no longer pumping effectively, that portion of the myocardium is said to be hypokinetic, meaning that it is less contractile than the uncompromised myocardial tissue, or even akinetic. As this situation worsens, the local area of compromised myocardium may in fact bulge out as the heart contracts, further decreasing the heart's ability to move blood forward. When local wall motion bulges out with each contraction, it is said to be dyskinetic. The dyskinetic portion of the myocardium may stretch and eventually form an aneurysmic bulge. Certain diseases may cause a global dilated myopathy (i.e., a general enlargement of the heart) when this situation continues for an extended period of time. As the heart begins to fail, the filling pressures increase, which stretches the ventricular chamber prior to contraction, greatly increasing pressure (preload) that the heart has to contract against. In response, the heart tissue remodels to accommodate the chronically increased filling pressures, further increasing the work that the now-compromised myocardium must perform.[0007]
• This vicious cycle of cardiac failure results in the symptoms of congestive heart failure such as shortness of breath, edema in the periphery, nocturnal dypsnia (a characteristic shortness of breath that occurs at night after going to bed), weight gain, and fatigue, to name a few. The enlargement increases stress on the myocardium. The stress increase requires a larger amount of oxygen supply, which can result in exhaustion of the myocardium leading to a reduced cardiac output of the heart.[0008]
SUMMARY OF THE INVENTION
• This invention relates to a device for improving cardiac function. The device includes a membrane which is insertable into a ventricle of a heart in a partitioning position, wherein the membrane substantially forms a division between two volumes of the ventricle, namely a first hemodynamic volume and a second relatively hemostatic volume of the ventricle. Blood enters the first hemodynamic volume through an inflow heart valve, circulates through and is contained primarily in the first hemodynamic volume, and leaves the first hemodynamic volume through an outflow heart valve. The membrane partitioning the first and second volumes confines the passage of blood through the heart to the first hemodynamic volume.[0009]
• The membrane has a plurality of fenestrations that are sufficiently large to allow blood from the hemodynamic volume to flow therethrough into the hemostatic volume, for purposes of forming a thrombus in the hemostatic volume. The fenestrations are sufficiently small so as to allow formation of the thrombus within the hemostatic volume by isolating a volume of blood on the static side of the partition and sufficiently reducing flow so as to promote coagulation of that volume of blood. The device thereby predictably and purposefully produces a thrombus contained within the second volume of the chamber.[0010]
• The device further includes at least one anchor formation connected to the membrane, the anchor formation having at least one anchoring portion that is positioned and capable of anchoring to tissue of a myocardium of the heart, and so anchor the membrane in the partitioning position to the myocardium.[0011]
• The invention also relates to a method for improving cardiac function. A membrane having a plurality of fenestrations is inserted into a ventricle of the heart. The membrane is anchored to a myocardium of the heart in a partitioning position, wherein the membrane substantially forms a division between a first hemodynamic volume of the heart and a second relatively hemostatic volume of the heart. Blood enters the hemodynamic volume through a first respective heart valve, and leaves the hemodynamic volume through a second respective heart valve. The fenestrations are sufficiently large so that blood flows from the hemodynamic volume therethrough into the hemostatic volume, but sufficiently small so that a thrombus grows within the hemostatic volume.[0012]
BRIEF DESCRIPTION OF THE DRAWINGS
• The invention is further described by way of example with reference to the accompanying drawings, wherein:[0013]
• FIGS. 1A and 1B are top plan and side views of a frame construction for a device according to an embodiment of the invention, wherein the frame construction is in an open position;[0014]
• FIG. 2 is a side view of the frame construction in a collapsed condition;[0015]
• FIG. 3 is a view similar to FIG. 2, with partition rim wires of the frame construction being deployed by pulling on a membrane pull wire;[0016]
• FIGS. 4A and 4B are plan and side views of the frame construction, wherein the partition rim wires are expanded by depressing rim wire extenders;[0017]
• FIG. 5A is a perspective view of a delivery mechanism for transporting and deploying the frame construction;[0018]
• FIG. 5B is perspective view of the delivery mechanism with an inner shuttle cannula thereof rotated through 180°;[0019]
• FIGS. 6A through 6D are cross-sectional side views through a heart, and FIG. 6E is a cross-sectional top plan view through the heart, illustrating deployment of the device within a ventricle of the heart;[0020]
• FIGS. 7A to[0021]7C are cross-sectional side views illustrating the flow pattern within the ventricle before and after a membrane of the device is deployed within the ventricle;
• FIGS. 8A to[0022]8D are cross-sectional side views illustrating the use of the membrane to grow a thrombus within the ventricle; and
• FIGS. 9A and 9B are cross-sectional side and cross-sectional top plan views respectively, illustrating the use of multiple membranes.[0023]
DETAILED DESCRIPTION OF THE INVENTION
• FIGS. 1A and 1B illustrate a[0024]frame construction10 of a device according to an embodiment of the invention. Not shown in FIGS. 1A and 1B is a membrane that is secured to theframe construction10 and a delivery mechanism used for delivering and deploying theframe construction10 and the membrane. Theframe construction10 is assembled from seven wires, including ananchor wire12, twopartition rim wires14, aanchor stem wire16, two rim wire extenders18 (FIG. 1A only), and a membrane pull wire20 (FIG. 1B only).
• Proximal ends[0025]24 of thepartition rim wires14 are secured to one another, hinged relative to one another, and slidably located on aproximal portion26 of theanchor wire12. Therim wire extenders18 havecentral portions30 that extend along theanchor wire12.Proximal portions32 of therim wire extenders18 are bent outwardly away from theanchor wire12. Distal ends34 of therim wire extenders18 are secured to thepartition rim wires14. Distal ends36 of thepartition rim wires14 are secured to one another and to a distal end of theanchor stem wire16. Ends of thewires14,16, and18 are formed intohooks40 that can be used for anchoring to tissue of a myocardium. A distal end of theanchor wire12 is formed into an anchoringscrew42 that can also anchor to a myocardium. Although thehooks40 and anchoringscrew42 are shown, it should be understood that other anchoring formations may be used, such as clamps, staples, etc.
• As illustrated in FIG. 2, the[0026]entire frame construction10 is initially collapsed, which allows theframe construction10 to be located within a catheter and to be transported within the catheter into a ventricle of a heart. The anchoringscrew42 can then be turned into a myocardium of the heart, thereby anchoring the distal end of theanchor wire12 to the myocardium.
• Next, as illustrated in FIG. 3, a proximal end of the[0027]membrane pull wire20 is retracted, which pivots theanchor stem wire16 about its proximal end at theanchor wire12. Distal ends36 of thepartition rim wires14, connected to the distal end of theanchor stem wire16, then move away from theanchor wire12. The anchoringhook40 formed by the distal end of theanchor stem wire16, also separates from the anchoringscrew42 and can be moved into contact with the myocardium at a location distant from the anchoringscrew42.
• As illustrated in FIGS. 4A and 4B, the proximal ends[0028]32 of therim wire extenders30 are then advanced in adirection44, i.e., toward the anchoringscrew42. The distal ends36 of therim wire extenders30, being connected to thepartition rim wires14, move thepartition rim wires14 outwardly away from one another, with the proximal ends24 of thepartition rim wires14 sliding along theanchor wire12 in a direction toward theanchor screw42.
• Referring again to FIG. 1A, the proximal ends[0029]32 of therim wire extenders30 can then be rotated indirections46. Rotation of therim wire extenders18 rotates thepartition rim wires14. Thepartition rim wires14 are rotated so that they are positioned adjacent to a myocardium in the heart. The anchoring hooks40 at the end of therim wire extenders18 can then also be inserted into the myocardium of the heart. With the anchoring hooks40 engaged with the myocardium and thepartition rim wires14 located against the myocardium, the anchoring hooks40 at the proximal ends32 of therim wire extenders18 can then also be inserted into the myocardium.
• FIG. 5A illustrates a[0030]delivery mechanism50 that may be used for deploying the frame construction as hereinbefore described. Thedelivery mechanism50 includes an outerdelivery catheter sheath52, anouter shuttle cannula54, aninner shuttle cannula56, and aninner guide cannula58, one coaxially located within the other.
• The outer and inner shuttle cannulas[0031]54 and56 havekey formations60 and62 respectively, and retainingopenings66 are formed in theinner shuttle cannula56. The proximal ends32 of therim wire extenders18 are inserted through theopenings66, thereby securing therim wire extender18 to theinner shuttle cannula56. Theanchor wire12 and themembrane pull wire20 both extend through theinner guide cannula58.
• The[0032]inner guide cannula58 initially extends approximately to the anchoringscrew42. Once the anchoringscrew42 is connected to the myocardium, theinner guide cannula58 is withdrawn into theinner shuttle cannula56. Themembrane pull wire20 is then retracted to elevate the partition rim wires14 (as illustrated in FIG. 3). The outer and inner shuttle cannulas54 and56 are then advanced in a distal direction within the outerdelivery catheter sheath52. Advancement of the outer and inner shuttle cannulas54 and56 open the partition rim wires14 (as illustrated in FIGS. 4A and 4B). The outer and inner shuttle cannulas54 and56 can then be rotated within the outerdelivery catheter sheath52, so that thepartition rim wires14 are rotated (as illustrated in FIGS. 1A and 1B). Theinner shuttle cannula56 is then partially retracted into theouter shuttle cannula54 until the proximal ends32 of therim wire extenders18 are partially pushed through theopenings66 by a proximal surface of thekey opening formation60.
• As illustrated in FIG. 5B, the[0033]inner shuttle cannula56 is then rotated within theouter shuttle cannula54. Anchoring hooks that are located within the inner shuttle cannulas56 can then be inserted into the myocardium. Theinner shuttle cannula56 can then be retracted so that the proximal ends32 of therim wire extenders18 disengage therefrom. Mechanisms which are known in the art may be used for disengaging theanchor wire12 and themembrane pull wire20, whereafter thedelivery mechanism50 can be removed from the heart.
• FIGS. 6A to[0034]6E illustrate deployment of the device within theleft ventricle160 of a heart162. As illustrated in FIG. 6A, thedelivery mechanism50 is inserted through theaortic valve164 of the heart162, and thedistal anchoring screw42 is connected to themyocardium166 of the heart162. As illustrated in FIG. 6B, thepartition rim wires14 are elevated, and the anchoring hooks40 at ends thereof are secured to themyocardium166. As illustrated in FIGS. 6C and 6D, thedelivery mechanism50 is withdrawn, which leaves theframe construction10 secured to the myocardium.
• Also forming part of the device is a[0035]membrane170 which has a periphery secured to thepartition rim wires14. Thepartition rim wires14 are located on themyocardium166, so that themembrane170 forms a division between first andsecond volumes172 and174 of theventricle160. FIG. 6E illustrates the positioning of themembrane170 with respect to theaortic valve164.
• FIG. 7A illustrates the flow through the[0036]ventricle160 before an aneurysm is formed out of theventricle160. Blood flows through a mitral valve into theventricle160, through theventricle160, and then exits theventricle160 through theaortic valve164.
• FIG. 7B illustrates the flow within the[0037]ventricle160 after ananeurysmic bulge180 is formed out of theventricle160.Small eddy currents182 are formed within theaneurysmic bulge180, while flow within an upper portion of theventricle160 remains substantially laminar.
• As illustrated in FIG. 7C, the[0038]membrane170 forms a division between ahemodynamic volume172 of theventricle160 and a relativelyhemostatic volume170 partially formed by theaneurysmic bulge180. The blood now flows through the mitral valve into thehemodynamic volume172, through thehemodynamic volume172, and then out of theaortic valve164. Themembrane170 segregates the relativelyhemostatic volume174 from the normal flow area of the heart within thehemodynamic volume172.
• FIGS. 8A to[0039]8D illustrate the use of themembrane170 to create a thrombus. Blood can still pass through fenestrations in themembrane170 into and out of thehemostatic volume174. The fenestrations reduce pressures that act on themembrane170, and so reduce stresses within themembrane170, the frame construction to which themembrane170 is mounted, and to the myocardium to which theframe construction10 is secured. The flow characteristics through thehemostatic volume174 allow for the growth of the thrombus from the base of thehemostatic volume174. The thrombus grows to encompass all of thehemostatic volume174, so as to provide support for themembrane170. Any remaining stresses within themembrane170 are thereby substantially diminished. The thrombus shrinks over an ensuing period of time, with themembrane170 having been rendered inconsequential by having been fully incorporated and endothelialized, forming a new inner wall of theventricle160.
• With specific reference to FIG. 8A, blood enters from the[0040]hemodynamic volume172 through the fenestrations into thehemostatic volume174, pressurizes thehemostatic volume174, and then may flow through the fenestrations back into thehemodynamic volume174. The fenestrations, by allowing blood to flow therethrough, reduce pressures that act on themembrane170 and contribute to the predictable propagation of a thrombus within thehemostatic volume174.
• The flow of blood through the[0041]hemostatic volume174 is slow when compared tocircular flow patterns182 of FIG. 7B. The flow within thehemostatic volume174 near themembrane170 is primarily turbulent, due to the disruption of flow created by themembrane170 and the relatively small sizes of the fenestrations. The ongoing flow through the fenestrations in themembrane170 forestalls the growth of a thrombus on themembrane170, contributing to the predictable propagation of the thrombus. Additionally, themembrane170 is preferably thrombolytic to forestall growth of a thrombus on themembrane170. The flow pattern within a base of thehemostatic volume174 is primarily turbulent. With reference to FIG. 8B, such turbulent flow permits the creation and growth of a thrombus190 on a base of thehemostatic volume174. The location of the thrombus190 does not interfere with flow of blood through themembrane170 and through thehemostatic volume174. The fenestrations are large enough so as to allow uncoagulated blood to flow therethrough, but small enough to confine coagulated products of the blood.
• As illustrated in FIGS. 8C and 8D, the thrombus[0042]190 subsequently grows to fill the entirehemostatic volume174. The thrombus may then grow by an additional degree to lift themembrane170 slightly. The thrombus is then slightly larger than the size of the originalhemostatic volume174. The growth of the thrombus up to the stage of FIG. 8D is typically between six and 12 hours, but may be between one hour and thirty days. The thrombus now provides support for themembrane170, so that pressures created within thehemodynamic volume172 are transferred through themembrane170 onto the thrombus190. Strain within themembrane170 and forces acting on the myocardium of the heart, which are already low due to the inclusion of the fenestrations, are thereby further reduced to substantially zero.
• A lining on an inner surface of the myocardium of the heart grows to form an endothelial lining over the[0043]membrane170. The endothelial lining forms a wall that ties opposing sides of the myocardium together, and so further assists in absorbing pressures created within thehemodynamic volume172. Thrombolytic agents may be applied to themembrane170 to prevent clot formation, but these thrombolytic agents should not persist for any longer than is necessary to form the thrombus190, if such thrombolytic agents would prevent endothelialization.
• Over time, the thrombus[0044]190 may begin to shrink, and a portion of the myocardium surrounding the thrombus190 may begin to recede toward themembrane170. Thehemostatic volume174 may decrease by at least 20% in twelve months. In order to allow for the thrombus to shrink, theframe construction10 may at least have portions thereof that are bio-absorbable, or can bend to allow for the myocardium to recede toward themembrane170.
• It can thus be seen that pressures on the[0045]membrane170 are reduced by providing fenestrations in themembrane170. The fenestrations also create a flow pattern within thehemostatic volume174, which promotes growth of the thrombus190. The growth of the thrombus190 is promoted from a base of thehemostatic volume174 toward themembrane170, so that the thrombus190 eventually lifts themembrane170 and then forms the primary structure which further absorbs pressures from thehemodynamic volume172.
• It is believed that at least some of the fenestrations in the[0046]membrane170 should be at least 30 microns wide to allow for a sufficient blood flow rate therethrough. It is also believed that none of the fenestrations should be larger than 1000 microns, preferably no larger than 500 microns, so as to create the correct flow pattern within thehemostatic volume174 and promote the creation and growth of the thrombus190. The fenestrations preferably form between 25% and 75% of the entire area of themembrane170, and there are typically at least 1000 of the fenestrations.
• The[0047]membrane170 is preferably made of a material which is non-thrombogenic. Materials that are non-thrombogenic may include Nomex™, Kevlar™, Spectra™, PET, PTFE, PGA, PLA, PEEK, Nylon™, Nitinol™, stainless steel, Eligiloy™, gold-plated molybdenum, or platinum. In order to be bioabsorbable, themembrane170 may be made of a material such as PGA, PLA, pericardium, or small intestinal submucosa. These materials are all intervascularly biocompatible.
• FIG. 9A illustrates the use of multiple devices, each having a[0048]respective membrane170A-C. The orientations of the devices are such that different locations of hypokinetic segments of the heart can be isolated. FIG. 9B illustrates the positioning of two membranes170D and170E in an overlapping manner as viewed from a mitral valve annulus.
• While certain exemplary embodiments have been described and shown in the accompanying drawings, it is to be understood that such embodiments are merely illustrative and not restrictive of the current invention, and that this invention is not restricted to the specific constructions and arrangements shown and described since modifications may occur to those ordinarily skilled in the art.[0049]

Claims (16)

What is claimed:

1. A device for improving cardiac function, comprising:

a membrane which is insertable into a ventricle of a heart, in a partitioning position wherein the membrane substantially forms a division between a hemodynamic volume and a relatively hemostatic volume of the ventricle, blood entering the hemodynamic volume through an inflow heart valve, circulating through the hemodynamic volume and leaving the hemodynamic volume through an outflow heart valve, the membrane having a plurality of fenestrations that are sufficiently large to allow blood from the hemodynamic volume to flow therethrough into the hemostatic volume, for purposes of forming a thrombus in the hemostatic volume, but sufficiently small so as to allow formation of the thrombus within the hemostatic volume; and

at least one anchor formation connected to the membrane, the anchor formation having at least one anchoring portion that is positioned and capable of anchoring to tissue of a myocardium of the heart, and so anchor the membrane in the partitioning position to the myocardium.

2. The device ofclaim 1, wherein each fenestration is between 30 and 1000 microns wide.

3. The device ofclaim 2, wherein each fenestration is less than 500 microns wide.

4. The device ofclaim 2, wherein there are at least 100 of the fenestrations.

5. The device ofclaim 2, wherein the fenestrations form between 25% and 75% of an area of the membrane.

6. The device ofclaim 2, wherein the membrane does not have a fenestration that is larger than 1000 microns.

7. The device ofclaim 1, wherein at least surfaces of the membrane facing the hemodynamic volume are thrombolytic.

8. The device ofclaim 1, wherein the membrane has at least 100 fenestrations, each of which is between 30 and 500 microns, the fenestrations forming between 25% and 75% of an area of the membrane, and at least surfaces of the membrane facing the hemodynamic volume being non-thrombogenic.

9. The device ofclaim 1, wherein the membrane is made from an intravascularly biocompatible material.

10. The device ofclaim 9, wherein the material is selected from the group consisting of Nomex™, Kevlar™, Spectra™, PET, PTFE, PGA, PLA, PEEK, Nylon™, Nitinol™, stainless steel, Eligiloy™, gold-plated molybdenum, and platinum or other suitable material in conventional use.

11. The device ofclaim 1, wherein the membrane is made from a bio-absorbable material.

12. The device ofclaim 11, wherein the material is selected from the group consisting of PGA, PLA, pericardium, and small intestinal submucosa.

13. The device ofclaim 11, wherein each anchoring formation has a sharp end to penetrate the myocardium.

14. The device ofclaim 1, further comprising:

a frame construction, including a rim to which the membrane is peripherally attached, an anchor wire to which the rim is connected, and a pull wire connected to the rim for moving a portion of the rim away from the anchor wire.

15. The device ofclaim 14, comprising at least one anchor formation on the anchor wire and at least one anchor formation on the rim.

16. A device for improving cardiac function, comprising:

a rim which is movable from a collapsed state into an open state;

a pull wire connected to the rim, retracting of the pull wire moving a distal portion of the rim;

an anchor formation on the rim; and

a membrane having a periphery secured to the rim.

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