Source: http://www.google.com/patents/US20060161040?ie=ISO-8859-1&dq=5359317
Timestamp: 2015-04-28 11:05:48
Document Index: 599929124

Matched Legal Cases: ['art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14', 'art 14']

Patent US20060161040 - Methods and devices for improving cardiac function in hearts - Google PatentsSearch Images Maps Play YouTube News Gmail Drive More »Sign inAdvanced Patent SearchPatentsVarious methods and devices are disclosed for improving cardiac function in hearts having zones of infarcted (akinetic) and aneurysmal (dyskinetic) tissue regions. The methods and devices reduce the radius of curvature in walls of the heart proximal infarcted and aneurysmal regions to reduce wall stress...http://www.google.com/patents/US20060161040?utm_source=gb-gplus-sharePatent US20060161040 - Methods and devices for improving cardiac function in heartsAdvanced Patent SearchPublication numberUS20060161040 A1Publication typeApplicationApplication numberUS 11/316,341Publication dateJul 20, 2006Filing dateDec 23, 2005Priority dateJan 2, 1997Also published asUS6406420, US7189199, US20020169359, US20040133063, US20040267083, US20070112244Publication number11316341, 316341, US 2006/0161040 A1, US 2006/161040 A1, US 20060161040 A1, US 20060161040A1, US 2006161040 A1, US 2006161040A1, US-A1-20060161040, US-A1-2006161040, US2006/0161040A1, US2006/161040A1, US20060161040 A1, US20060161040A1, US2006161040 A1, US2006161040A1InventorsPatrick McCarthy, Cyril Schweich, Todd Mortier, Peter Keith, Michael KallokOriginal AssigneeMyocor, Inc.Export CitationBiBTeX, EndNote, RefManReferenced by (19), Classifications (30), Legal Events (2) External Links: USPTO, USPTO Assignment, EspacenetMethods and devices for improving cardiac function in hearts
US 20060161040 A1Abstract
Various methods and devices are disclosed for improving cardiac function in hearts having zones of infarcted (akinetic) and aneurysmal (dyskinetic) tissue regions. The methods and devices reduce the radius of curvature in walls of the heart proximal infarcted and aneurysmal regions to reduce wall stress and improve pumping efficiency. The inventive methods and related devices include splinting of the chamber wall proximal the infarcted region and various other devices and methods including suture and patch techniques. Images(26) Claims(42)
DESCRIPTION OF THE PREFERRED EMBODIMENTS The various aspects of the invention to be discussed herein generally pertain to devices and methods for treating heart conditions, including, for example, dilatation and infarction, including infarction causing aneurysms. For the purposes of providing clarity and consistency throughout the remaining description of the invention, the following terms have the general definitions set forth below: �infarction� or �infarcted�: refers to myocardium (also described as tissue or muscle) that has lost its ability to contract as a result of cellular necrosis, this term can include, for example, aneurysmal tissue and scar tissue that replaces the necrotic cellular muscle tissue; �aneurysm� or �aneurysmal�: refers to infarcted myocardium that is dyskinetic with respect to surrounding portions of the myocardium; �contractile�: refers to myocardium that is not infarcted and has generally retained contractile potential, though this muscle tissue may not be fully contracting given other conditions, e.g. too much wall stress; and �border zone�: refers to chamber wall that has a region of infarcted tissue and a region of contractile tissue through its thickness. These definitions are generally consistent with the accepted definitions recognized by those skilled in the art. The devices of the present invention operate passively in that, once placed in the heart, they do not require an active stimulus either mechanical, electrical, or otherwise, to function. The devices alter the shape or geometry of the heart, both locally and globally, and increase the heart's efficiency by their placement with respect to the heart. That is, the heart experiences an increased pumping efficiency through an alteration in its shape or geometry and concomitant reduction in stress on the heart walls. The inventive devices and methods offer numerous advantages over the existing treatments for various heart conditions. The devices are relatively easy to manufacture and use, and the related surgical techniques for their implementation do not require the invasive procedures of current surgical techniques. For instance, the surgical technique does not necessarily require removing portions of the heart tissue, opening the heart chamber, or stopping the heart. For these reasons, the surgical techniques of the present invention are also less risky to the patient than other techniques. The devices and methods of the present invention used to treat infarcted tissue and aneurysms also are likely to be more effective than prior devices. As will be described, the inventive devices alter the shape or geometry of the chamber, either globally or locally, and reduce the radius of curvature of the chamber wall, resulting in lower stresses in the heart wall. Moreover, with many of the inventive devices there is no need to open the heart chamber to deploy the device, even when the device is deployed on the septal wall. These methods and devices also could be used in conjunction with coronary artery bypass grafting (CABG). In CABG surgery, the use of the inventive methods and related devices allow for quickly reducing stress on the myocardium, which may save �stunned� tissue, i.e., tissue that is being starved of nutrients carried with the blood flow, that otherwise may not be recoverable after a certain time period. Also, the inventive methods and device may hinder further progression or dilation of scarred, non-contractile tissue. The disclosed inventive methods and related devices involve geometric reshaping of the heart. In certain aspects of the inventive methods and related devices, substantially the entire chamber geometry is altered to return the heart to a more normal configuration. FIGS. 36 through 40, which will be described in further detail later, show a model of this geometric reshaping, which includes a reduction in radius of curvature of the chamber walls. Prior to reshaping the chamber geometry, the heart walls experience high stress due to a combination of both the relatively large increased diameter of the chamber and the thinning of the chamber wall. Geometric reshaping according to the present invention reduces the stress in the walls of the heart chamber to increase the heart's pumping efficiency, as well as to stop further dilatation of the heart. Other aspects of the inventive methods and devices involve geometric reshaping a particular area of the chamber and/or reducing the radius of curvature of the chamber wall in that area. When portions of the heart wall form a bulge due to an aneurysm, the radius of much of the heart chamber changes. This increases stress on the heart walls. Additionally, the healthy regions of the heart work harder to pump in order to make up pumping volume due to lost contractility in the infarcted tissue region. Together, these effects limit the pumping effectiveness of the heart and can contribute to further degradation of the heart. Geometrically reshaping the area of the aneurysm by, for example, reducing the radius of curvature of the wall, lowers stress on the wall regions in that vicinity and improves pumping function. In addition, the geometric reshaping permits the scar tissue to heal in a more organized fashion and reduces progression of the scar tissue into other areas and further aneurysmal bulging. Although many of the methods and devices are discussed below in connection with their use in the left ventricle of the heart, these methods and devices may be used in other chambers of the heart for similar purposes. One of ordinary skill in the art would understand that the use of the devices and methods described herein would be substantially the same if employed in other chambers of the heart. The left ventricle has been selected for illustrative purposes because a large number of the disorders that the present invention treats occur in the left ventricle. Reference will now be made in detail to the present preferred embodiments of the invention, examples of which are illustrated in the accompanying drawings. Wherever possible, the same reference numbers will be used throughout the drawings to refer to the same or like parts. FIG. 1 shows a transverse cross-section of a left ventricle 10 and a right ventricle 12 of a human heart 14. Extending through the left ventricle is a splint 16 including a tension member 18 and oppositely disposed anchors 20. Splint 16, as shown in FIG. 1, has been positioned to draw opposite walls of left ventricle 10 toward each other to reduce the �radius� of the left ventricular cross-section or the cross-sectional area thereof to reduce left ventricular wall stresses. It should be understood that although the splint 16 and the alternative devices disclosed herein are described in relation to the left ventricle of a human heart, these devices could also be used to reduce the radius or cross-sectional area of the other chambers of a human heart in transverse or vertical directions, or at an angle between the transverse and vertical. Those apparatus of the present invention which reduce heart wall stress by changing chamber wall geometry can be referred to as �splints�. �Full cycle splints� engage the heart to produce a chamber shape change throughout the cardiac cycle. �Restrictive splints� do not engage the heart wall at end systole to produce a chamber shape change. FIG. 2 discloses an alternate embodiment of the present invention, wherein a balloon 200 is deployed adjacent the left ventricle. The size and degree of inflation of the balloon can be varied to reduce the radius or cross-sectional area of left ventricle 10 of heart 14. FIG. 3 shows yet another alternative embodiment of the present invention deployed with respect to left ventricle 10 of human heart 14. Here a compression frame structure 300 is engaged with heart 14 at atraumatic anchor pads 310. A compression member 312 having an atraumatic surface 314 presses against a wall of left ventricle 10 to reduce the radius or cross-sectional area thereof. FIG. 4 is a transverse cross-sectional view of human heart 14 showing yet another embodiment of the present invention. In this case a clamp 400 having atraumatic anchor pads 410 biased toward each other is shown disposed on a wall of left ventricle 10. Here the radius or cross-sectional area of left ventricle 10 is reduced by clamping off the portion of the wall between pads 410. Pads 410 can be biased toward each other and/or can be held together by a locking device. Each of the various embodiments of the present invention disclosed in FIGS. 1-4 can be made from materials which can remain implanted in the human body indefinitely. Such biocompatible materials are well-known to those skilled in the art of clinical medical devices. FIG. 5 shows an alternate embodiment of the splint of FIG. 1 referred to in FIG. 5 by the numeral 116. The embodiment 116 shown in FIG. 5 includes three tension members 118 as opposed to a single tension member 18 as shown in FIG. 1. FIG. 6 shows yet another embodiment of the splint 216 having four tension members 218. It is anticipated that in some patients, the disease process of the failing heart may be so advanced that three, four or more tension members may be desirable to reduce the heart wall stresses more substantially than possible with a single tension member as shown in FIG. 1. FIG. 7 is a partial vertical cross-section of human heart 14 showing left ventricle 10. In FIG. 7, another splint embodiment 316 is shown having a tension member 318 extending through left ventricle 10. On opposite ends of tension member 318 are disposed elongate anchors or pads 320. FIG. 8 is an end view of tension member 318 showing elongate anchor 320. FIG. 9 shows another embodiment of a splint 416 disposed in a partial vertical cross-section of human heart 14. Splint 416 includes two elongate anchors or pads 420 similar to those shown in FIGS. 7 and 8. In FIG. 9, however, two tension members 418 extend through left ventricle 10 to interconnect anchors 420 on opposite sides of heart 14. FIG. 10 is a vertical cross section of heart 14 showing left ventricle 10. In this case, two splints 16 are disposed through left ventricle 10 and vertically spaced from each other to resemble the configuration of FIG. 9. FIG. 11 is a vertical cross-sectional view of the left ventricle of heart 14. Two alternate embodiment splints 516 are shown extending through left ventricle 10. Each splint 516 includes two tension members 518 interconnecting two anchors or pads 520. FIG. 12 is yet another vertical cross-sectional view of left ventricle 10 of heart 14. An alternate embodiment 616 of the splint is shown extending through left ventricle 10. Splint 616 includes an elongate anchor pad 620 and two shorter anchors or pads 621. Splint 616 includes two tension members 618. Each tension member 618 extends between anchors 620 and respective anchors 621. FIG. 13 is a vertical cross-sectional view of left ventricle 10 of heart 14. A splint 50 is shown disposed on heart 14. Splint 50 includes a compression member 52 shown extending through left ventricle 10. Opposite ends of compression member 52 are disposed exterior to left ventricle 10. Lever members 54 extend from each end of compression member 52 upwardly along the exterior surface of ventricle 10. A tension member 56 extends between lever members 54 to bias lever members 54 toward heart 14 to compress chamber 10. Compression member 52 should be substantially rigid, but lever members 54 and to some degree compression member 52 should be flexible enough to allow tension member 56 to bias lever members 54 toward heart 14. Alternately, lever members 54 could be hinged to compression member 52 such that lever members 54 could pivot about the hinge when biased toward heart 14 by tension member 56. FIG. 14 shows an alternate embodiment 156 of the splint shown in FIG. 13. In this case lever members 154 are longer than members 54 as compression member 152 of splint 150 has been disposed to the exterior of left ventricle 10. FIG. 15 is a vertical cross-sectional view of left ventricle 10 of heart 14. An alternate embodiment 250 of the splint is shown on heart 14. A preferably relatively rigid frame member 256 extends through ventricle 10. Disposed on opposite ends of frame 256 are cantilever member 254. Disposed on cantilever members 254 are atraumatic pads 258. Cantilever members 254 can be positioned along frame member 256 such that atraumatic pads 258 press against heart 14 to compress chamber 10. FIG. 16 is an end view of frame member 256 showing cantilever members 254 and pads 258. It should be understood that each of the embodiments described above should be formed from suitable biocompatible materials known to those skilled in the art. The tension members can be formed from flexible or relatively more rigid material. The compression members and frame member should be formed from generally rigid material which may flex under load, but generally hold its shape. As will be described in more detail herein, FIG. 17 is a partial vertical cross-section of human heart 14 showing left ventricle 10 and left atrium 22. As shown in FIG. 17, heart 14 includes a region of scar tissue 24 associated with an aneurysm or ischemia. As shown in FIG. 17, the scar tissue 24 increases the radius or cross-sectional area of left ventricle 10 in the region affected by the scar tissue. Such an increase in the radius or cross-sectional area of the left ventricle will result in greater wall stresses on the walls of the left ventricle. FIG. 18 is a vertical cross-sectional view of the heart 14 as shown in FIG. 17, wherein a splint 16 has been placed to draw the scar tissue 24 toward an opposite wall of left ventricle 10. As a consequence of placing splint 16, the radius or cross-sectional area of the left ventricle affected by the scar tissue 24 is reduced. The reduction of this radius or cross-sectional area results in reduction in the wall stress in the left ventricular wall and thus improves heart pumping efficiency. FIG. 19 is a vertical cross-sectional view of left ventricle 10 and left atrium 22 of heart 14 in which a splint 16 has been placed. As shown in FIG. 19, splint 16 includes an alternative anchor 26. The anchor 20 is preferably an elongate member having a length as shown in FIG. 19 substantially greater than its width (not shown). Anchor bar 26 might be used to reduce the radius or cross-sectional area of the left ventricle in an instance where there is generalized enlargement of left ventricle 10 such as in idiopathic dilated cardiomyopathy. In such an instance, bar anchor 26 can distribute forces more widely than anchor 20. FIGS. 20 and 21 are side views of a hinged anchor 28 which could be substituted for anchors 20 in undeployed and deployed positions respectively. Anchor 28 as shown in FIG. 20 includes two legs similar to bar anchor 26. Hinged anchor 28 could include additional legs and the length of those legs could be varied to distribute the force over the surface of the heart wall. In addition there could be webbing between each of the legs to give anchor 28 an umbrella-like appearance. Preferably the webbing would be disposed on the surface of the legs which would be in contact with the heart wall. FIG. 22 is a cross-sectional view of a capture ball anchor 30. Capture ball anchor 30 can be used in place of anchor 20. Capture ball anchor 30 includes a disk portion 32 to distribute the force of the anchor on the heart wall, and a recess 34 for receiving a ball 36 affixed to an end of tension member 18. Disk 32 and recess 34 include a side groove which allows tension member 38 to be passed from an outside edge of disk 32 into recess 34. Ball 36 can then be advanced into recess 34 by drawing tension member 18 through an opening 38 in recess 34 opposite disk 32′. FIG. 23 is a perspective view of a cross bar anchor 40. The cross bar anchor 40 can be used in place of anchors 20. The anchor 40 preferably includes a disk or pad portion 42 having a cross bar 44 extending over an opening 46 in pad 42. Tension member 18 can be extended through opening 46 and tied to cross bar 42 as shown. FIG. 24 is a cross sectional view of an alternate embodiment of anchor pad 340 in accordance with the present invention. Anchor pad 340 preferably includes a disc shaped pad portion 342. Disc-shaped pad portion 342 includes side 343, which in use is disposed toward the heart. A conical aperture 348 having sloping sides 346 extends through pad 342. Collet 344 is disposed within orifice 348. A threaded portion 350 of collet 344 extends from orifice 348 opposite side 343, nut 352 is threaded over threaded portion 350. Lumen 345 extends through collet 344. A tension member 354 is shown extending through lumen 345. Lumen 345 has a diameter such that when nut 352 is not tightened on threaded portion 350, tension member 354 can slide freely through lumen 345. When nut 352 is tightened, it draws collet 344 away from side 343. Collet 344 is then pinched between walls 346 of orifice 348. When collet 344 is pinched, the size of lumen 345 is reduced such that tension member 354 can no longer move freely within lumen 345, fixing the position of pad 340 on tension member 354. FIG. 25 is a cross sectional view of an alternate embodiment of an anchor pad 360 in accordance with the present invention. Anchor pad 360 includes a generally disc-shaped pad portion 362. Pad 362 includes a side 363 which when the pad is in use, is disposed toward the heart. A tension member lumen 364 extends through pad 362. Lumen 364 preferably has a generally conical shaped portion 365 disposed toward side 363. Tension member 370 is shown disposed through lumen 364 in FIG. 25. Pad 362 includes a threaded passage 366 extending from an edge of pad 362 to lumen 364. A set screw 368 is threaded into passage 366. Set screw 368 can be tightened to engage tension member 370 to fix the position of anchor pad 360. When set screw 368 is not tightened, the size of lumen 364 is preferably large enough that anchor pad 360 can slide relatively freely over tension member 370. FIG. 26 is a perspective view of yet another embodiment of anchor pad 380 in accordance with the present invention. Anchor pad 380 preferably includes a generally disc-shaped pad portion 382 having a first side 383 which in use would be disposed toward the heart and a second side 385. Pad 382 as well as pads 342 and 362 are preferably formed from a metal such as stainless steel alloys or titanium alloys. A tension member fastener 384 is formed in pad 382 by cutting a series of grooves and apertures through pad 382 from side 385 to side 383. A first groove 386 has a generally horseshoe shape. Second groove 388 extends between opposite portions of horseshoe shaped groove 386 to form two oppositely disposed cantilever members 387. A relatively large aperture 394 is formed between cantilever members 387 proximate their free ends. A second and smaller aperture 390 is formed closer to the fixed ends of cantilever members 387. Tension member 392 is shown extending through aperture 390. As shown in FIG. 26, tension member 392 is clamped between cantilever members 387 such that the location of pad 382 is fixed along tension member 392. Pad 382 can be released by using a spreading device 396 to spread cantilever members 387 apart. Spreading device 396 includes handle 398 to spreading arms 400 each having a finger 402. Fingers 402 can be placed within aperture 394 then aims 400 and fingers 402 can be spread apart by pivoting them around a pin 404 such that cantilevers 387 are spread apart and pad 382 can move freely along tension member 392. It can be appreciated that although spreader 396 is shown extending transversely from tension member 392, it could also be configured such that fingers 402 do not curve transversely from arms 400 and thus spreader 396 could be disposed parallel to tension member 392. This would be particularly desirable in a situation where anchor pad 380 was being placed through a port or window during a less invasive splint implantation procedure. It can be appreciated that cantilever members 387 can be held apart such that pad 380 can be moved along tension member 392 by placement of a temporary wedge or pin in groove 388. For example, grooves 388 may include an additional small aperture disposed between aperture 390 and aperture 394 into which a pin could be placed to hold open members 387. When it is desired to fix the position of anchor pad 380 on tension member 392, device 396 could be-used to spread cantilever members 387 to remove the pin. The cantilever members could then be released to engage tension member 392. Aperture 390 of pad 380 can also include a conical portion disposed toward side 383 such as conical portion 365 of pad 360. Cantilever arms 384 are preferably configured such that they do not stress tension member 392 beyond its elastic limit. It can also be appreciated that the force developed by cantilever members 387 impinging on tension member 392 is operator independent and defined by the geometry and material characteristics of members 387. FIG. 27 is a perspective view of an anchor pad 360 having a tension member 370 extending therethrough. After pad 360 is secured to tension member 370, that portion of tension member 370 which extends from the side of anchor pad 360 opposite side 363 is preferably removed. This can be accomplished by trimming tension member 370 with wire cutter 414 or scissors. Although anchor pad 360 is used here to illustrate trimming tension member 370, it can be appreciated that in each of the embodiments disclosed herein there may be an excess portion of tension member extending from an anchor, which is preferably removed or trimmed. FIG. 28 is a cross sectional view of an alternate embodiment 420 of a tension member cutter. Device 420 includes an elongate outer tube 422 having a distal end 424. Tube 424 defines a lumen 423 through which extends a second tube 430 having a distal end 428. Extending distally from distal end 428 are two cutting arms 424 and 426 which are shown partially withdrawn into lumen 423 and transversely restrained by distal end 424 of outer tube 422. When unrestrained by distal end 424, arms 424 and 426 are biased apart. Each arm 424 and 426 has a cutting element 425 and 427, respectively. Elements 425 and 427 are shown in contact with each other in FIG. 28. A tension member 370 extends between arms 424 and through lumen 432 of inner tube 430. A representative anchor pad 360 is disposed adjacent elements 425 and 427. Device 420 of FIG. 28 is particularly useful when trimming excess tension member using less invasive techniques as it can be readily advanced over a tension member through a port or window trocar. FIG. 29 is a vertical cross sectional view of left ventricle B of heart A. A transventricular splint 443 including a tension member 370 and anchor pads 360 are shown disposed on heart A. To the left of heart A as shown in the figure is a coiled portion 442 of tension member 470. As an alternative to trimming an excess length of tension member, tension member 370 could be formed from a shape memory alloy such that portion 442 could be preset to assume a coil shape when warmed to near body temperature. Once the length of the tension member has been adjusted, the anchors are secured in place along the tension member and the excess length of tension member removed if desired, the anchor or anchor pads are preferably secured in place on the heart. The anchor or anchor pads are secured such that relatively movement between the anchors or anchor pads and the heart is limited to reduce abrasion of the heart wall. To secure the anchor or anchor pads to heart A, a biocompatible adhesive could be placed between the pad and the heart to adhere the pad to the heart. Alternately, apertures could be provided in the pad such that sutures could be extended through the apertures and into the heart to secure the pad. In addition to sutures, the pad could include threaded apertures into which anchor screws could be advanced through the pad and into the heart wall to secure the pad to the heart. FIG. 30 illustrates yet another alternative approach to securing the anchors or anchor pads to the heart surface. FIG. 30 is a cross sectional view of an anchor pad 340 disposed on heart A. Anchor pad 340 is disposed within an envelope 446. Envelope 446 includes a bottom layer 447 disposed between anchor pad 340 and heart A and a top layer 448 disposed on the opposite side of anchor pad 340. Layers 347 and 340 are held together by sutures 449. Bottom layer 447 is preferably a mesh or expanded PTFE which has a pore size or intranodial dimension sufficient to promote tissue ingrowth. The pore size is preferably between about 10 and about 100 microns and more preferably, between about 20 and about 40 microns. With respect to expanded PTFE, the intranodial dimension is preferably between about 10 to about 100 microns and more preferably between about 20 to about 40 microns. The top material could also be expanded PTFE or the like having a pore size which preferably does not promote ingrowth and thus resists adhesion to surrounding tissue. As an alternative embodiment, the pores could be formed directly in the pad surface. Envelope 446 would preferably be placed around pad 340 prior to placing pad 340 on tension member 354. A window 450 can be provided to provide access to nut 352 to secure pads to tension member 354. After tightening nut 352, window 450 can be closed by suture 452. FIG. 31 is a top view of pad 340 and envelope 446 of FIG. 30. It can be appreciated that a similar envelope can be placed around the various anchor pads disclosed herein. The location of the window may have to vary, however, to provide access to the respective means for securing the anchor pads to the tension member. The splints of the present invention can be implanted acutely or chronically. When the splints are implanted chronically, it is particularly important that the tension member or members be highly fatigue resistant. Typical materials for the tension member can include, among other biocompatible materials, stainless steel, titanium alloys, NiTi alloys such as Nitinol or elgiloy. In a preferred embodiment, the tension member is a wire having a diameter of between 0.005 to 0.035 inches in diameter or, more preferably, between 0.01 and 0.02 inches in diameter and most preferably, about 0.014 inches in diameter. The length of the tension member between the pads is preferably about 0.6 to 4 inches, and more preferably, between about 1 to 3 inches and, most preferably, about 2 inches. To improve the fatigue resistance of the metallic tension members, their surface can be electro-polished, buffed or shot peened. Drawing or annealing of the metal will also improve fatigue resistance. The tension member, in a preferred embodiment, articulates with respect to the anchor pad to reduce bending of the tension member at the pad. This can be accomplished by a ball and socket joint shown in FIG. 22, for example. The tension member itself can be made more flexible or bendable by providing a multi-filament tension member such as a braided or twisted wire cable tension member. A multifiber filament structure of numerous smaller wires can then easily, while reducing the stress level on any individual wire as compared to a solid wire of the same diameter as the multifilament bundle. Such a multi-filament tension member can be made from biocompatible materials such as, but not limited to, stainless steel, Nitinol, titanium alloys, LCP (liquid crystal polymer), Spectra� fiber, kevlar fiber, or carbon fiber. In a preferred embodiment, the multi-filament structure is coated or covered to substantially seal the multi-filament structure. Coatings such as silicone, urethane or PTFE are preferred. FIG. 32 is a side view of multifilament twisted cable 400. Cable 400 includes a plurality of wires or filaments 402 twisted about the longitudinal axis of cable 400. FIG. 33 is a transverse cross sectional view of cable 400. In FIG. 33, cable 400 includes a surrounding coating 404 not shown in FIG. 32. FIG. 34 is a side view of a braided multifilament tension member 410. Tension member 410 includes a plurality of filaments or wires 412. It can be appreciated that numerous braiding patterns are known to those skilled in the art of multifilament members. It is anticipated-that in a preferred embodiment, braided member 410 can have an optional core of fibers running parallel to an elongate axis of tension member 410. In yet another preferred embodiment, tension member 410 could have a solid wire core extending parallel to and along the longitudinal axis of tension member 410. The tension members and anchors or anchor pads are preferably bio-resistant, i.e., resistant to physiologic attack. To improve bio-resistance, tension member and/or anchors or anchor pads can be coated with carbon material such as glass, pyrolytic carbon, diamond or graphite, zirconium nitrate or oxide. Roughened or porous urethanes, silicone or polymer coatings or sheaths can be used to promote tissue ingrowth to create a biological seal. Hydrophilic and albumin coatings can also be used. Drugs incorporated into a binder coating can also be used to reduce biological attack on the splint and irritation of tissue by the splint. Such drugs include heparin, coumadin, anti-inflammatory steroid or ASA-aspirin. The oxide layer of the underlying metal could also be optimized to improve bio-resistance. This is particularly true for stainless steel, titanium, or nickel titanium on which an oxide layer can be formed by heating the component to improve biocompatibility. Further coatings include calcium hydroxy appetite, beta tricalcium phosphate and aluminum oxide can be applied to the tension member. The tension member and/or pad or anchor pad can at least be, in part, formed from titanium to enhance electronegativity. The anchors or anchor pads and, particularly the tension members are biocompatible, preferably antithrombogenic and made to prevent hemolysis. The coatings used to enhance bio-resistance described above can generally be used to improve biocompatibility. Since the tension member is exposed to significant blood flows through the left ventricle, in a preferred embodiment, the tension member has a generally small size and shape elliptical cross sectional shape to reduce turbulence or drag over the tension member. If such elliptical, transverse cross section tension member were used, it can be appreciated that the narrow end would be preferably oriented toward the direction of blood flow. It is also desirable to select a tension member material and shape which would not vibrate at resonant frequency under the influence of blood flow. Where the tension member passes through the heart wall, various approaches can be taken to reduce or prevent bleeding. For example, the surface of the anchor or anchor pad and/or tension member in contact with the heart wall can be coated or include an ingrowth inducing covering such as collagen, dacron, expanded PTFE or a roughened/porous surface. A clotting inducing substance may also be bound to the tension member and/or anchor or anchor pads, such as avitene or collagen. It is also contemplated that the portion of the heart wall where the tension member passes through could be cauterized. In a preferred embodiment, the tissue can be cauterized by heating the tension member. A glue such as cyanoacrylate can also be disposed between the tension member and the heart wall to reduce-or prevent bleeding from the heart wall. Mechanical means such as an O-ring or compression fitting could also be disposed between the heart wall and the tension member to reduce bleeding. A purse string suture can be placed on the heart, around the tension member adjacent the pad as well. The tension member is preferably flexible enough to allow for changing interface conditions between the heart and the splint, and alternating pad orientation throughout the cardiac cycle. The flexibility should be sufficient enough to avoid injury to the heart or bleeding. It is also preferable that if the heart were to contract sufficiently enough to put the tension member in compression that it would readily buckle. Buckling could be promoted by providing a ribbon shaped tension member, chain link tension member, thin wire tension member, bent tension member or multi-filament tension member. The tension member is preferably radiopaque, echo cardiographic visible, or MRI compatible or includes a marker which is radiopaque, echo visible, or MRI compatible. The preferred locations for markers would-include the center of the tension member and at the ends of the tension member disposed at the heart walls. The radiopaque markers could be gold or platinum or other biocompatible metal or heavy metal filled polymeric sleeves. With respect to echo compatible or MRI compatible tension members or markers, the tension or marker are preferably non-interfering or visible. Having radiopaque echo compatible or MRI compatible tension members or markers is particularly desirable for follow-up, non-invasive monitoring of the tension member after implantation. The presence of the tension member can be visualized and the distance between two or more markers measured. Integrity of the tension member can be confirmed as well. In a preferred embodiment, the tension member is not conductive to the action potential of muscle. This can be accomplished by insulating the tension member, anchor and/or anchor pad interface or fabricating the tension member anchor and/or anchor pad from a non-conductive metal such as titanium. In addition to monitoring the performance of the tension member by visualization techniques such as fluoroscopy or echo imagery, sensors can advantageously be incorporated into the splints. For example, a strain gauge can be disposed on a tension member to monitor the loading on the member in use. Strain can be related to load as known to those skilled in the art by developing a stress/strain relationship for a given tension member. The strain gauge can be connected by a biocompatible lead to a conventional monitoring device. A pressure gauge formed from, for example, piezo electric material can also be disposed on the tension member to monitor filling pressures or muscle contractility. In a preferred embodiment, a tension member can be slidably enclosed within a tube. If the tension member were to fail, the tube would contain the tension member therein. It is anticipated that the tension member could be connected to a pacing lead. In such an instance, if the tension member were conductive, pacing signals could be conveyed along the tension member from one heart wall to another. In use, the various embodiments of the present invention are placed in or adjacent the human heart to reduce the radius or cross-section area of at least one chamber of the heart. This is done to reduce wall stress or tension in the heart or chamber wall to slow, stop or reverse failure of the heart. In the case of the splint 16 shown in FIG. 1, a cannula can be used to pierce both walls of the heart and one end of the splint can be advanced through the cannula from one side of the heart to the opposite side where an anchor can be affixed or deployed. Likewise, an anchor is affixed or deployed at the opposite end of splint 16. Additional methods for splint placement are described in more detail in U.S. patent application Ser. No. 09/123,977, filed on Jul. 29, 1998 and entitled �Transventricular Implant Tools and Devices� and incorporated herein by reference. It can be appreciated that the methods described above to advance the tension members through the ventricles can be repeated to advance the desired number of tension members through the ventricle for a particular configuration. The length of the tension members can be determined- based upon the size and condition of the patient's heart. It should also be noted that although the left ventricle has been referred to here for illustrative purposes, that the apparatus and methods of this invention can also be used to splint multiple chambers of a patient's heart as well as the right ventricle or either atrium. FIG. 35 is a schematic view of generally horizontal cross section of heart A including left ventricle B and right ventricle C. Also shown are left anterior descending artery E, posterior descending artery F, obtuse marginal artery G, postero-medial papillary muscle H and antero-lateral papillary muscle 1. Shown in FIG. 35 are three generally horizontal preferred alignments for tension member placement for the splints of the present invention when used for the purpose of treating ventricular dilatation. These alignments generally met three goals of splint positioning including good bisection of the left ventricle, avoidance of major coronary vessels and avoidance of valve apparatus including chordae leaflets and papillary muscles. Alignment 420 can be referred to as the anterior/posterior (AP) position. Alignment 422 can be referred as the posterior septal/lateral wall (PSL) position. Alignment 424 can be referred to as the anterior septal/lateral wall (ASL) position. It can be appreciated that the alignments shown are illustrative only and that the alignments may be shifted or rotated about a vertical axis generally disposed through the left ventricle and still avoid the major coronary vessels and papillary muscles. When the alignment passes through a substantial portion of right ventricle C, it may be desirable to dispose not only two pads on the exterior of the heart at opposite ends of a tension member, but also a third pad within right ventricle C on septal J. The spacing between the third pad and the pad disposed outside the heart proximate left ventricle B preferably defines the shape change of left ventricle B. This will allow the spacing of the third pad relative to the pad disposed outside the heart proximate right ventricle C to define a shape change if any of right ventricle C in view of the spacing between those pads. With the alignments as shown in FIG. 35, the third pad will be unnecessary. It is likely, however, that with alignments 422 and 424 in order to achieve the desired shape change of left ventricle B, the exterior pad of the wall proximate the right ventricle C will be drawn into contact with septal J. This will consequently somewhat reduce the volume of right ventricle C. FIG. 36 is a view of a cylinder or idealized heart chamber 48 which is used to illustrate the reduction of wall stress in a heart chamber as a result of deployment of the splint in accordance with the present invention. The model used herein and the calculations related to this model are intended merely to illustrate the mechanism by which wall stress is reduced in the heart chamber. No effort is made herein to quantify the actual reduction which would be realized in any particular in vivo application. FIG. 37 is a view of the idealized heart chamber 48 of FIG. 36 wherein the chamber has been splinted along its length L such that a �figure eight� cross-section has been formed along the length thereof. It should be noted that the perimeter of the circular transverse cross-section of the chamber in FIG. 36 is equal to the perimeter of the figure eight transverse cross-section of FIG. 37. For purposes of this model, opposite lobes of the figure in cross-section are assumed to be mirror images. FIG. 38 shows various parameters of the FIG. 1 cross-section of the splinted idealized heart chamber of FIG. 37. Where I is the length of the splint between opposite walls of the chamber, R2 is the radius of each lobe, a is the angle between the two radii of one lobe which extends to opposite ends of the portion of the splint within chamber 48 and h is the height of the triangle formed by the two radii and the portion of the splint within the chamber 48 (R1 is the radius of the cylinder of FIG. 36). These various parameters are related as follows: h=R2COS(θ/2) I=2R2SIN(θ/2) R2═Rn(2π−θ) From these relationships, the area of the figure eight cross-section can be calculated by: A 2=2π(R2 −)2(1−θ/2π)+hl Where chamber 48 is unsplinted as shown in FIG. 36 A 1 the original cross-sectional area of the cylinder is equal to A2 where θ=−180�, h=0 and l=2R2. Volume equals A2 times length L and circumferential wall tension equals pressure within the chamber times R2 times the length L of the chamber. Thus, for example, with an original cylindrical radius of four centimeters and a pressure within the chamber of 140 mm of mercury, the wall tension T in the walls of the cylinder is 104.4 newtons. When a 3.84 cm splint is placed as shown in FIGS. 37 and 38 such that I=3.84 cm, the wall tension T is 77.33 newtons. FIGS. 39 and 40 show a hypothetical distribution of wall tension T and pressure P for the figure eight cross-section. As e goes from 180� to 0�, tension TS, in the splint goes from 0 to a 2T load where the chamber walls carry a T load. In yet another example, assuming that the chamber length L is a constant 10 cm, the original radius R1, is 4 cm, at a 140 mmHg the tension in the walls is 74.7 N. If a 4.5 cm splint is placed such that l=4.5 cm, the wall tension will then be 52.8 N. When a splint is actually placed on the heart, along an alignment such as those shown in FIG. 35, the length l between the two pads as measured along the tension member is preferably 0.4 to about 0.8 and more preferably between about 0.5 to about 0.7 and most preferably about 0.6 times the distance along the length of the tension member at end diastole if the pads were not secured to the tension member and provided no resistance to expansion of the heart. A more detailed discussion of tension member length can be found in U.S. patent application Ser. No. 09/123,977, filed on Jul. 29, 1998 and entitled �Transventricular Implant Tools and Devices� which is incorporated herein by reference. As mentioned earlier, FIG. 17 is a partial vertical cross-section of human heart 14 showing left ventricle 10 and left atrium 22. As shown in FIG. 17, heart 14 includes a region of scar tissue 24 associated with an aneurysm. The aneurysmal scar tissue 24 increases the radius or cross-sectional area of left ventricle 10 in the region affected by the scar tissue. Such an increase in the radius or cross-sectional area of the left ventricle will result in greater wall stresses on the walls of-the left ventricle, especially those walls adjacent to the aneurysm. In addition to the various uses of the splint to treat ventricular dilatation as heretofore discussed, the inventive splint also can be used to treat infarcted tissue or aneurysms occurring on the heart wall, as illustrated by FIGS. 18 and 4244, 46, and 47. These figures show various placements of a splint to treat infarcted tissue or aneurysms. It is to be understood that variations of these placements that have similar effects are within the scope of this invention. FIG. 42 illustrates a method for placing a splint of the present invention to treat a heart with infarcted tissue, including an aneurysm. The particular aneurysm A shown in FIG. 42 affects the ventricular septal wall. FIG. 42 shows a partial transverse cross-section of a human heart having an aneurysm A (shown by shading) in the left ventricle wall. It is contemplated that the methods and devices of this invention also apply to treatment of hearts with akinetic scar tissue that has not progressed past an infarcted stage and into an aneurysmal stage, in which case there would be little or no bulging of the heart wall. Such a condition is shown in FIGS. 43 a-43 d to be described shortly. In FIG. 42, splint 16 is placed diametrically across aneurysm A to lessen the load carried by the transmural infarcted tissue 24 forming aneurysm A, as well as any adjacent border zone tissue that may be present. The border zone (although not shown in FIG. 42) is the portion of the heart wall which has a mix of contractile tissue 24″ and infarcted tissue 24. Anchors 20 of splint 16 are located on the outside of the chamber walls and are placed generally adjacent to the portions of the chamber wall that transition from infarcted myocardium 24 to regions of contractile myocardium 24″. Tension member 18 extends through the heart chamber with each of its ends connecting to opposing anchors 20. Anchors 20, especially when used to anchor splint 16 on septal wall S, can be of the self-deploying type disclosed in co-pending application U.S. Ser. No. 09/123,977, filed Jul. 29, 1998, entitled �Transventricular. Implant Tools and Devices,� the complete disclosure of which is incorporated herein by reference. Splint 16 reduces the radius of curvature of the aneurysmal region A and the adjacent regions of the chamber wall. By reducing the radius of curvature in these regions, contractile regions 24″ of the myocardium that were under high stress due to geometric abnormalities associated with an aneurysmal region A are relieved from that high stress, thereby resulting in increased pumping ability upon contraction. Even if the infarcted tissue has not led to bulging of the heart wall, reducing the radius of curvature helps to reduce some of the stress in the adjacent contractile myocardium. By increasing the pumping ability of the contractile myocardium 24″, the heart can more easily pump the required blood flow output, helping to offset the pumping lost by the infarcted muscle 24. Those regions of the chamber wall that have only endocardial infarcted tissue, that is border zone regions 24′, likely will experience an increase in their ability to contract and contribute to pumping. It is also contemplated to use more than one splint, and splints having i different lengths, to optimize the reduction in the radius of curvature of infarcted and aneurysmal regions and adjacent regions. Another contemplated mode of the invention includes closing off the infarcted or aneurysmal region completely by Shortening the splint so that the walls adjacent the anchors contact each other. Closing off the infarcted or aneurysmal tissue from the rest of the heart chamber in this way renders this tissue completely non-functional with respect to contributing to the pumping. Shortening the splint to achieve contact of the heart walls may also reduce the risk of embolic thrombus because no blood would be expected to flow into the excluded region. Additionally, the need to remove any thrombus already adhered to the heart wall may be unnecessary because the thrombus would have no way of escaping back into the heart chamber to cause stroke or other malfunctions. If the infarcted or aneurysmal tissue extends to the septal wall of the chamber, the splint would be placed across the chamber so as to exclude the non-contractile tissue of the septal wall as well. As described earlier, FIG. 18 is a vertical cross-sectional view of heart 14 as shown in FIG. 17. FIG. 18 depicts another method of the present invention, wherein splint 16 is placed to draw aneurysm A toward an opposite wall of left ventricle 10. An anchor 20 of splint 16 is placed on the outside wall of heart 14, approximately at the center of the infarcted tissue 24 forming aneurysm A. Tension member 18, connected to this anchor, is then extended across the chamber of the heart to the opposite wall and connected to another anchor 20 placed on the outside chamber wall to secure splint 16. The radius or cross-sectional area of the left ventricle affected by the infarcted tissue 24 is thereby reduced. The reduction of this radius or cross-sectional area results in reduction in the stress in the left ventricular wall and thus improves heart pumping efficiency. Furthermore, infarcted tissue 24 is supported by anchor 20 of the splint to prevent any additional bulging of the wall or progression of the infarcted tissue to other areas of the myocardium. Bringing infarcted tissue 24 into the chamber, as shown in FIG. 18, likely reduces the risk of thrombosis due to contact between the endocardial infarcted tissue and circulating blood flow occurring in these regions of the chamber. Clots are less likely to form on tissue that is subject-to an active flow of blood. The forces associated with such flow diminish stagnation points that allow clots to form and adhere to the wall more readily. FIGS. 43 a-43 d depict the use of splint 16 to treat a heart chamber having a discrete zone of akinetic infarcted myocardium 24 that has not yet developed into an aneurysm. FIGS. 43 a and 43 b depict a long axis (or essentially vertical) cross-sectional view of the heart, with FIG. 43b showing the placement of splint 16. FIGS. 43 c and 43 d show the heart in short axis (or essentially horizontal) cross-section, with placement of splint 16 shown in FIG. 43 d. In FIGS. 43 b and 43 d, splint 16 is shown treating a heart including infarcted tissue 24 that does not affect septal wall S. Thus, both anchors 20 are placed on exterior wall portions of left ventricle LV. However, it is contemplated that a splint could be used to alter the geometry of the chamber in cases in which an infarcted region does affect septal wall S. By utilizing splint 16, the radius of curvature, particularly with respect to the short axis direction, is reduced. This reduction of curvature facilitates the pumping ability of any portions near the infarcted region 24 that have some contractile potential by reducing wall stress in the region. By allowing this once marginally contractile tissue to increase its contractile ability, the heart improves its ejection fraction, cardiac reserve, and muscle contractibility. Additionally, the remainder of the ventricle also experiences a reduced radius of curvature, as shown in FIG. 43 b and 43 d, further facilitating the contractile ability of the entire ventricle. By improving the contracting-ability of the entire chamber, the heart has the ability to account for the lost pumping ability of the infarcted myocardium 24. Left untreated, this condition causes the rest of the ventricle to attempt to contract more, ultimately over-working and weakening the heart to a greater degree. FIGS. 44 a-44 b show a cross-sectional view of the left ventricle with an aneurysmal region A. As shown in FIG. 44 b, splint 16 can also be placed such that one anchor 20 engages approximately the center of the bulge formed by aneurysm A. Tension member 18 is then extended through the center of aneurysm A and across left ventricle LV to anchor splint 16 to a point on the surrounding heart wall substantially opposite to aneurysm A. This positioning of splint 16 tends to bring the aneurysmal bulge in line with the normal curvature of the heart wall. By this placement of splint 16, it is expected that greater blood flow would occur in the region of aneurysmal tissue A, potentially reducing thrombus formation. FIG. 45 shows the use of a completely external device to treat a heart having a zone of infarcted tissue 24. In the embodiment shown in FIG. 45, the external splint device is an external frame generally in the form of a clamp 17 with anchor pads 21 on each end of the clamp. The clamp 17 is configured to exert a compressive force on the heart wall to cause shape change of the heart chamber. Other external splint devices, in addition to clamp 17, that are contemplated for use in treating a heart having infarcted myocardium are disclosed in co-pending U.S. patent application Ser. No. 09/157,486, filed Sep. 21, 1998, and entitled �External Stress Reduction Device and Method,� the complete disclosure of which is incorporated herein by reference. In addition to the benefits described above with respect to using a splint to treat a heart having infarcted tissue, external splint devices such as that shown in FIG. 45 include the potential further advantage of significantly reducing the possibility of thrombus formation resulting from surfaces of devices that contact blood flowing through the chamber. Another use for splint 16 in treating heart chambers having infarcted or aneurysmal tissue is shown with reference to FIGS. 46 a through 46 c. This method combines the use of splint 16 with the traditional surgical technique in which the infarcted tissue is removed. By using the techniques described later for identifying and distinguishing between healthy tissue and infarcted tissue, all of the infarcted myocardium 24 shown in FIG. 46 a can be excised from the chamber, as shown in FIG. 46 b. The separated portions of the chamber walls will then be sutured back together. Splint 16 is then placed diametrically transverse to the portion of heart chamber walls 24″ that have been partially excised, as shown in FIG. 46 c. Anchors 20 are placed between the portions of the chamber wall from which infarcted tissue 24 was removed and portions of the chamber wall that contained contractile tissue throughout its thickness. Because only contractile tissue regions 24″ would remain after this procedure, as opposed to conventional surgery which leaves some of the infarcted tissue occurring in border zone regions in place, contractile function, and thus cardiac function, likely would improve. Splint 16 reduces the radius of curvature in those thinner regions of the walls that remain after the surgery, allowing them to produce stronger contractions and relieving stress in those wall portions. If the infarcted tissue is not removed, as shown in FIG. 42, the border zone cannot contribute significantly to the pumping function, for the contractile muscle must contract against the stiffness of the infarcted muscle. But, with the infarcted tissue removed, the thin contractile section of myocardium shown in FIG. 46 c can be mad to contract and contribute to pumping articularlysic splint 16 has reduced stress enough to allow the thin region of tissue to exert the required pressure to pump. In addition to combining the surgical excision of the infarcted tissue with the use of a splint of the present invention, an external device, like clamp 17 shown in FIG. 45, can also be combined with the surgical technique. Such an external device would be placed with respect to the heart chamber walls such that its anchors are disposed in the approximate locations as anchors 20 on splint 16, and the device between the anchors could extend around the portions of the walls that have been sutured together. It is contemplated that the splint 16 could be used in hearts where the aneurysm involves the septal wall of the ventricle. Similar to the splinting shown in FIG. 42, one or both anchor pads could be self-deploying. Another-use of the splint to treat infarcted or aneurysmal tissue near the base of a mitral valve MV is shown in FIG. 47. In this embodiment, the splint is placed such that its anchors 20 are diametrically opposed to one another across an aneurysm, or generally dilated annular region, located in a portion of the basal left ventricle in the vicinity of mitral valve MV. Anchors 20 are placed on the outer wall of left ventricle LV with tension member 18 of splint 16 drawn through the heart chamber and diametrically across the infarcted or aneurysmal region. The dotted line of tension member 18 shown in FIG. 47 illustrates that splint 16 lies below mitral valve MV. Placing the splint in this manner results in the papillary muscles P of mitral valve MV or the leaflets of mitral valve MV being drawn together and reduces the risk of mitral regurgitation. In addition, splint 16 reduces the radius of curvature of the aneurysmal or infarcted region. As previously described, this reduction lowers the stress in the heart wall, improving pumping effectiveness. FIG. 47 shows the placement of splint 16 such that both anchors are disposed on external walls of the left ventricle. It should be noted that the splint also could be placed so that one anchor is disposed on septal wall S, in which case a self-deploying anchor preferably would be used. Also, tension member 16 may be made to curve between anchors 20 in order to avoid damaging internal structures of the ventricle. FIGS. 48 a-48 b show the use of an external splint device to treat a heart having an aneurysm A in the vicinity of mitral valve MV. As a result of the aneurysm, the anterior leaflet AL and posterior leaflet PL of mitral valve MV have separated causing mitral regurgitation, as shown in FIG. 48 a. FIG. 48 b shows the placement of an external splint device having a clamp portion 19 connecting two anchors 25. It is contemplated that the external splint device used to treat this particular heart condition may also include a protrusion 19′ as part of clamp portion 19. In placing clamp 19 on the heart, protrusion 19′ engages aneurysm A so as to push aneurysm A toward a center of the ventricle. Additionally, a stabilizing bar 23 could be attached to the end of protrusion 19′. Stabilizing bar 23 is configured to extend through the heart chamber wall and anchor to the edge of posterior leaflet PL of mitral valve MV to bring the leaflet in close proximity to anterior leaflet AL. Such a stabilizing bar may be made of a semi-rigid, or rigid, material such as implantable metals or other suitable material. While FIGS. 48 and 49 show the use of various splints associated with an aneurysm in the vicinity of the mitral valve, it is contemplated to utilize splints also in the case where there is no true aneurysm, but an area of infarcted tissue near the mitral valve. The present invention also includes myocardial patches and related methods used to treat aneurysms. FIGS. 49 a-49 b illustrate one preferred embodiment of the invention. FIG. 49 a shows left ventricle LV with an aneurysm A in a portion of the chamber wall. FIG. 49 b illustrates placement of a staked patch 72 according to an embodiment of the present invention used to treat aneurysmal bulge A. Staked patch 72 includes a patch 70, made of Dacron or PTFE for example, and an elongated member 71 secured to the patch. When staked patch 72 is secured into position (by sutures or the like) over the surface of aneurysmal bulge A, elongated member 71 pushes on the aneurysmal tissue region. Staked patch 72 pushes bulge A into the heart chamber. This pushing likely will result in an even further reduction in the stresses experienced by the adjacent heart wall due to the reduction in the radius of curvature resulting from drawing adjacent regions in toward each other when the patch is in place. Such further reduction in stress would tend to promote a more organized healing of the scar tissue region and prevent progression of the scar into other healthy myocardium. Additionally, by pushing the bulge into the chamber space, thrombosis is less likely to occur because of the active blood flow past the surface of the bulge. As shown in FIG. 49 b, staked patch 72 has a single stake 71 secured to the patch in a substantially perpendicular direction. However, it is contemplated that several stakes could be secured to the patch depending on the size of the affected tissue area to be treated. Additionally, stakes could be secured in various orientations, including skewed orientations, relative to the patch. The stakes have different sizes in order to optimize the degree and direction in which the bulge is pushed in, especially when the bulge has a non-uniform surface configuration. The stakes may be rigid or semi-rigid and may be manufactured from implantable metals and polymers, or other suitable materials of similar characteristics. A-three-dimensional patch also is contemplated by the present invention. Such a patch could be inflatable or solid. The patch would consist of an essentially flat surface configured to lie flush with the epicardial surface and a bulging surface that would engage with the aneurysmal region to push the aneurysm into the chamber in a manner similar to the stake described above. A suture ring may be placed around the perimeter of the flat surface to secure the patch into place on the heart. A further embodiment of the present invention is a shrinkable patch for treating aneurysms. For example, such a patch may be made of heat-shrinkable material and applied via sutures to the aneurysmal tissue region while the tissue is in a relaxed state. Gentle heat, such as that produced by, for example, a hot air gun, an infrared heating lamp, or other similar heating mechanisms, would then be applied to shrink the patch. This shrinking also will cause the size of the affected area to be decreased by being pulled in tightly with the shrinking patch, thereby reducing the radius of curvature of the adjacent myocardium. The patch may be made of any suitable material compatible with the human body and having heat-shrinking characteristics. Examples of such a material include oriented polyethylene, oriented polypropylene, and a woven Dacron polyester of partially-oriented yam. Partially-oriented yarn is capable of significant longitudinal shrinkage when heated. Additionally, targeting and heating certain areas yields a non-uniform shrinking that more precisely tailors the resulting configuration of the patch and the affected tissue region. Another embodiment of the present invention, which may be used either alone or in combination with a patch, is a purse-string suture 50, as shown in FIGS. 50 a-50 b. In this embodiment, a suture 50 is placed to encircle the affected tissue area 24, as shown in FIG. 50 a. Suture 50 has free ends 51 that are pulled to draw in suture 50 and reduce the perimeter of the affected tissue, as shown in FIG. 50 b. Free ends 51 are then secured so as to keep the gathered tissue region in-place. The securing can be accomplished by tying free ends 51 to one another or by some like means. By gathering the infarcted tissue together and reducing the perimeter, tension in the walls adjacent to the infarcted tissue 24 decreases due to the reduction in radius of the wall in that region. Thus, improved contractile function of the adjacent tissue is expected. Purse-string suture 50 could be drawn in to such an extent that the outer walls of the perimeter of infarcted tissue 24 contact each other. Drawing the infarcted tissue 24 to this extent cuts off the tissue completely from the rest of the heart chamber and renders it non-functional. In addition to the purse-string suture 50, a patch may be applied to support any bulging tissue area that remains after application of suture 50, as well as provide a more secure means of maintaining the gathered portions of the myocardium. FIGS. 51 a-51 c illustrate a further embodiment of the present invention, the combination of a purse-string suture and an enclosure member 60. In this embodiment, purse-string suture 50 is applied to infarcted or aneurysmal tissue 24 as described above with reference to FIGS. 50 a-50 b. After-the suture is pulled tight to gather the affected tissue region in, an enclosure member 60 is secured into place. As shown in FIG. 51 c, enclosure member 60 is placed around the gathered tissue 24 so that substantially all of the infarcted tissue is contained inside enclosure member 60. In a preferred form of the invention, sutures are used to secure the enclosure member 60 into place, however other securing means are also contemplated. Enclosure member 60 preferably is made from a substantially rigid material, for example stainless steel, semi-rigid material, or any other material exhibiting like characteristics such as, for example, polyamide imide, titanium, or ultra high molecular weight polyethelene, in order to carry the load created by the gathered infarcted tissue. Because of its relative rigidity, enclosure member 60 withstands the load of the gathered tissue better than sutures alone and contains the progression of the infarcted tissue. Although FIG. 51c shows a ring as enclosure member 60, other shapes may be used to serve the inventive purposes. Overall, regardless of the shape of enclosure member 60, its perimeter should be selected to have approximately the same shape as the perimeter of the infarcted tissue region once it has been gathered together by purse-string suture 50. Another enclosure device is shown in FIGS. 52 a-52 c. FIG. 52 a shows a region 24 of infarcted myocardium on left ventricle LV. Other heart structure shown in these figures includes the right ventricle RV, the right atrium RA, the superior and inferior vena cavas, and the aorta. The inventive enclosure member 61 of FIGS. 52 a-52 c is configured to change from a circular shape to an elliptical or oval shape. Such an enclosure member can be fabricated from a shape memory alloy, such as nitinol, or other similar suitable material, and processed such that it has a circular shape at a temperature below its transformation temperature, which is approximately equal to body temperature. Upon reaching the transformation temperature, the ring, comprised of the shape memory material, alters its configuration to the shape of an ellipse or oval, or other suitable configurations. During surgical application, the temperature of the heart is below body temperature and therefore ring 61 remains in the circular shape during application of ring 61 to the heart, as shown in FIG. 52 b. After installation of the ring is complete, the heart reaches normal body temperature, transforming ring 61 into the elliptical or oval shape, as shown in FIG. 52 c. This shape transformation deforms the infarcted region of tissue on the heart wall to change the shape and/or size of the heart chamber, relieve stress on the heart walls, and improve overall contractile function of the heart. In a preferred embodiment, infarcted region 24 deforms in a short axis direction, as shown in FIG. 52 c. Alternatively, enclosure member 61 can be formed of a spring metal, such as, for example, high tensile strength stainless steel. When such a material is used, the enclosure member is initially processed into the elliptical or oval configuration. The enclosure member is then attached around a circular polymer, or other suitable material, sheet to form and maintain a circular shape during attachment of the ring to the ventricle. Once attached, the circular polymer sheet is removed, causing the enclosure member to spring back to its original elliptical shape. Other embodiments of the present invention include enclosure members that deform non-uniformly, either by having a non-uniform configuration at the shape memory transformation temperature, or at the initial processing shape of the spring metal. It also should be noted that enclosure member 61 can take on any suitable shape both before application and after, depending on such factors as, for example, the particular infarcted region to be treated and the desired final radius of curvature. FIGS. 53 a-53 b illustrate a tie enclosure, a further embodiment of the invention and a variation on the use of the enclosure member. The tie enclosure includes a plurality of sutures 62 having free ends 64. Sutures 62 secure around the perimeter of the infarcted or aneurysmal tissue 24, as shown in FIG. 53 a. Sutures 62 are secured at points 63 using pledgets 65. Enclosure member 60 is then placed over the affected tissue region and free ends 64 of the plurality of sutures 62 are extended through enclosure member 60 to pull sutures 62 through enclosure member 60 as well. By pulling on free ends 64 of sutures 62, the infarcted or aneurysmal tissue region 24 is again gathered and its perimeter reduced. The tissue is drawn so that pledgets 65 ultimately are adjacent enclosure member 60. The tissue, attached to the sutures, is drawn through enclosure member 60, and once in place, enclosure member 60 can be sutured to the myocardium. Free ends 64 of sutures 62 are drawn until pledgets 65 are brought close to enclosure member 60. Sutures 62 are then tied to the enclosure member 60. Additionally, enclosure member 60 may be directly sutured to the myocardium, as shown in FIG. 53 b. Again, drawing in the aneurysmal tissue region reduces stress on the chamber walls, hinders the progression of the infarction, and results in a more uniform scar formation, and reduces the radius of curvature, and therefore the stress, in the region of the chamber adjacent the infarction, as well as more global reduction of radius of curvature. The tie enclosure also allows for non-uniform drawing in of the affected tissue region by using a plurality of sutures of varying lengths. Thus, the tie enclosure allows for particular regions of the aneurysm or infarction to be targeted and drawn in while others are left intact or drawn in to a lesser degree. This allows for a more precise change in geometrical configuration that may be necessary due to non-uniformities existing in the initial geometry of the infarcted or aneurysmal region. Enclosure member 60 also may be made of a flexible material so as to allow enclosure member 60 to take on a non-uniform configuration when sutures 62 are drawn and secured. As discussed previously, enclosure member 60 may be made of a rigid, semi-rigid, or flexible material, depending on the particular application for which the device will be used. The shape of enclosure member 60 can be that of a ring as shown in FIGS. 53 a-53 b or can be another shape, as long as the perimeter of enclosure member 60 is less than or equal to that of the drawn in tissue region. Using enclosure member 60 and sutures 62 in the manner described with respect to FIGS. 53 a-53 b, wider zones of infarcted or aneurysmal tissue preferentially may be drawn further toward enclosure member 60, thereby maximizing the radius reduction in the direction of the widest dimension. This enables portions of the ventricle that are the most affected by the infarction to experience the greatest radius reduction and therefore the greatest stress relief. Yet another form of an enclosure member contemplated by the present invention is illustrated in FIG. 54. Enclosure member 65 in FIG. 54 takes the form of a braided ring with a lumen through which tightening cords 66 extend. Enclosure member 65 can be sutured into place surrounding an infarcted zone of tissue, with the sutures passing through enclosure member 65 only and not through tightening cords 66. Once member 65 is secured around the infarcted tissue, tightening cords 66 can be pulled to draw in enclosure member 65, causing the infarcted tissue region to be drawn together to thereby reduce the radius of curvature of the heart wall in that location. Enclosure member 65 may be made of a relatively flexible material that is either atraumatic itself or is wrapped in an atraumatic material such as Dacron or PTFE for example. Other materials that encompass these characteristics are considered to be within the scope of this invention as well. In treating infarcted tissue and aneurysms with the various inventive methods and devices discussed above, it may be necessary to identify and distinguish between the infarcted tissue regions of the chamber wall and the contractile tissue regions of the chamber wall. Thus, a further aspect of the invention consists of the use of various devices for performing such identification in order to achieve precise placement of the inventive devices, including the splints, sutures, patches, and rings. The identification devices can be used either endocardially, epicardially, or transcardially, depending on which treatment procedure is being performed. One such method of identifying infarcted tissue regions from contractile tissue regions involves the use of a bipolar electrode. Using the electrode, differences in impedance sensed by the electrode will indicate regions of infarcted versus contractile tissue. Another method involves the use of fiber optics to distinguish infarcted from contractile regions of tissue. In this case, the fiber optics sense either density or color differences in transmitted or reflected light. Such differences would indicate whether a region contained infarcted tissue or contractile tissue. For instance, a known intensity of light could be directed toward a tissue region, with a known inominal intensity transmitting through contractile tissue regions. Intensities of the transmitted light through the chamber wall could then be measured. Upon sensing a decrease in intensity from the nominal value, the infarcted region could be pinpointed. Border zones also could be sensed in this way by looking for a gradation in transmission differences from the nominal value to a lowest value. Another method to locate regions of infarcted versus contractile tissue can be employed during the surgical procedure itself. This method involves the injection of radioactive media, such as in a thallium scan, with �real-time� imaging of the radiation during the surgery through the use of a Geiger counter contact probe. Higher observed radiation densities indicate regions of perfused tissue. Yet another injection method uses a visible dye injected into coronary vessels to identify contractile perfused tissue. In this identification technique,.the dye travels only to contractile tissue, not to infarcted or scarred tissue regions. Finally TEE, or transesophageal echo ultrasounds may be used to detect regions of infarcted tissue. Aside from those listed above, other methods are contemplated to locate infarcted tissue regions. For example, the surgeon may use his fingers to probe the outer surface of the chamber wall and feel for differences in the tissue regions. All of the inventive passive devices to be implanted in the heart may be made of biocompatible material that can remain in the human body indefinitely. Any surface engaging portions of the heart should be atraumatic in order to avoid tissue damage. It will be understood that this disclosure, in many respects, is only illustrative. Changes may be made in details, particularly in matters of shape, size, material, number and arrangement of parts without exceeding the scope of the invention. Accordingly, the scope of the invention is as defined in the language of the appended claims. Other embodiments of the invention will be apparent to those skilled in the art from consideration of the specification and practice of the invention disclosed herein. It is intended that the specification and examples be considered as exemplary only, with a true scope and spirit of the invention being indicated by the following claims. Referenced byCiting PatentFiling datePublication dateApplicantTitleUS7316706Jun 14, 2004Jan 8, 2008Medtronic Vascular, Inc.Tensioning device, system, and method for treating mitral valve regurgitationUS8092416Mar 27, 2009Jan 10, 2012Vitalmex Internacional S.A. De C.V.Device and method for connecting a blood pump without trapping air bubblesUS8262725Apr 16, 2008Sep 11, 2012Cardiovascular Technologies, LlcTransvalvular intraannular band for valve repairUS8382653Sep 25, 2007Feb 26, 2013Corassist Cardiovascular Ltd.Method and system for improving diastolic function of the heartUS8394008Jul 29, 2010Mar 12, 2013Bioventrix, Inc.Steerable lesion excluding heart implants for congestive heart failureUS8425402Jul 21, 2009Apr 23, 2013Bioventrix, Inc.Cardiac anchor structures, methods, and systems for treatment of congestive heart failure and other conditionsUS8449442Dec 20, 2007May 28, 2013Bioventrix, Inc.Method and device for percutaneous left ventricular reconstructionUS8480732Nov 25, 2009Jul 9, 2013Heart Repair Technologies, Inc.Transvalvular intraannular band for valve repairUS8491455Oct 3, 2008Jul 23, 2013Bioventrix, Inc.Treating dysfunctional cardiac tissueUS8506474Aug 21, 2006Aug 13, 2013Bioventrix, Inc.Method and device for treating dysfunctional cardiac tissueUS8636639Jan 24, 2012Jan 28, 2014Bioventrix, Inc.Signal transmitting and lesion excluding heart implants for pacing, defibrillating, and/or sensing of heart beatUS8852072 *Feb 6, 2009Oct 7, 2014Heartware, Inc.Ventricular assist device for intraventricular placementUS8911391Oct 18, 2011Dec 16, 2014Vitalmex Internacional S.A. De C.V.System for connecting a blood pump without trapping air bubblesUS8936563Oct 18, 2011Jan 20, 2015Vitalmex International S.A. de C.V.Method for connecting a blood pump without trapping air bubblesUS8945211Sep 11, 2009Feb 3, 2015Mitralign, Inc.Tissue plication device and method for its useUS20090203957 *Feb 6, 2009Aug 13, 2009Larose Jeffrey AVentricular assist device for intraventricular placementUS20130096579 *Sep 30, 2012Apr 18, 2013Bioventrix, IncOver-the-wire cardiac implant delivery system for treatment of chf and other conditionsWO2008038276A2 *Sep 25, 2007Apr 3, 2008Corassist Cardiovascular LtdMethod and system for improving diastolic function of the heartWO2010011674A1 *Jul 21, 2009Jan 28, 2010BioventrixCardiac anchor structures* Cited by examinerClassifications U.S. Classification600/16, 600/37International ClassificationA61B17/04, A61B17/00, A61F2/00, A61B17/122, A61M1/10, A61F2/24, A61B19/00Cooperative ClassificationA61B2017/048, A61B2017/0464, A61B2017/0435, A61B19/54, A61B2017/0496, A61B2017/0445, A61B17/00234, A61B2017/0446, A61B17/1227, A61B2017/0404, A61B17/04, A61B2017/0454, A61B2019/542, A61B2017/00243, A61F2/2481, A61F2/2487, A61B2017/0458, A61B17/0487European ClassificationA61F2/24W4, A61B17/04, A61B17/00ELegal EventsDateCodeEventDescriptionFeb 16, 2009ASAssignmentOwner name: EDWARDS LIFESCIENCES LLC, CALIFORNIAFree format text: ASSIGNMENT OF ASSIGNORS INTEREST;ASSIGNOR:MYOCOR, INC.;REEL/FRAME:022277/0011Effective date: 20081029Owner name: EDWARDS LIFESCIENCES LLC,CALIFORNIAFree format text: ASSIGNMENT OF ASSIGNORS INTEREST;ASSIGNOR:MYOCOR, INC.;US-ASSIGNMENT DATABASE UPDATED:20100225;REEL/FRAME:22277/11Owner name: EDWARDS LIFESCIENCES LLC,CALIFORNIAFree format text: ASSIGNMENT OF ASSIGNORS INTEREST;ASSIGNOR:MYOCOR, INC.;US-ASSIGNMENT DATABASE UPDATED:20100223;REEL/FRAME:22277/11Free format text: ASSIGNMENT OF ASSIGNORS INTEREST;ASSIGNOR:MYOCOR, INC.;US-ASSIGNMENT DATABASE UPDATED:20100316;REEL/FRAME:22277/11Free format text: ASSIGNMENT OF ASSIGNORS INTEREST;ASSIGNOR:MYOCOR, INC.;US-ASSIGNMENT DATABASE UPDATED:20100413;REEL/FRAME:22277/11Free format text: ASSIGNMENT OF ASSIGNORS INTEREST;ASSIGNOR:MYOCOR, INC.;US-ASSIGNMENT DATABASE UPDATED:20100525;REEL/FRAME:22277/11Sep 5, 2007ASAssignmentOwner name: VENTURE LENDING & LEASING IV, INC., CALIFORNIAFree format text: SECURITY AGREEMMENT;ASSIGNOR:MYOCOR, INC.;REEL/FRAME:019805/0072Effective date: 20070820Owner name: VENTURE LENDING & LEASING IV, INC.,CALIFORNIAFree format text: SECURITY AGREEMMENT;ASSIGNOR:MYOCOR, INC.;US-ASSIGNMENT DATABASE UPDATED:20100225;REEL/FRAME:19805/72Owner name: VENTURE LENDING & LEASING IV, INC.,CALIFORNIAFree format text: SECURITY AGREEMMENT;ASSIGNOR:MYOCOR, INC.;US-ASSIGNMENT DATABASE UPDATED:20100223;REEL/FRAME:19805/72Free format text: SECURITY AGREEMMENT;ASSIGNOR:MYOCOR, INC.;US-ASSIGNMENT DATABASE UPDATED:20100316;REEL/FRAME:19805/72Free format text: SECURITY AGREEMMENT;ASSIGNOR:MYOCOR, INC.;US-ASSIGNMENT DATABASE UPDATED:20100413;REEL/FRAME:19805/72Free format text: SECURITY AGREEMMENT;ASSIGNOR:MYOCOR, INC.;US-ASSIGNMENT DATABASE UPDATED:20100525;REEL/FRAME:19805/72RotateOriginal ImageGoogle Home - Sitemap - USPTO Bulk Downloads - Privacy Policy - Terms of Service - About Google Patents - Send FeedbackData provided by IFI CLAIMS Patent Services