Patent Publication Number: US-2007112244-A1

Title: Methods and devices for improving cardiac function in hearts

Description:
CROSS REFERENCE TO RELATED APPLICATIONS  
      This application is a continuation-in-part of U.S. patent application Ser. No. 09/124,286 filed Jul. 29, 1998, now pending, which is a continuation-in-part of U.S. patent application Ser. No. 08/933,456 filed Sep. 18, 1997, now pending, which is a continuation-in-part of U.S. patent application Ser. No. 08/778,277, filed Jan. 2, 1997, now pending. 
    
    
     FIELD OF THE INVENTION  
      The present invention pertains to the field of apparatus for treatment of a failing heart. In particular, the apparatus and its related methods of the present invention is directed toward reducing the wall stress in the failing heart. The present invention further includes methods and devices for improving cardiac function in hearts having discrete zones of infarcted tissue. Such methods and devices reduce the radius of curvature and/or alter the geometry or shape of the infarcted tissue and adjacent regions to thereby reduce wall stress on the heart and improve the heart&#39;s pumping performance.  
     BACKGROUND OF THE INVENTION  
      The syndrome of heart failure is a common course for the progression of many forms of heart disease. Heart failure may be considered to be the condition in which an abnormality of cardiac function is responsible for the inability of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues, or can do so only at an abnormally elevated filling pressure. There are many specific disease processes that can lead to heart failure. Typically these processes result in dilatation of the left ventricular chamber. Etiologies that can lead to this form of failure include idiopathic, valvular, viral, and ischemic cardiomyopathies.  
      The process of ventricular dilatation is generally the result of chronic volume overload or specific damage to the myocardium. In a normal heart that is exposed to long term increased cardiac output requirements, for example, that of an athlete, there is an adaptive process of slight ventricular dilation and muscle myocyte hypertrophy. In this way, the heart fully compensates for the increased cardiac output requirements. With damage to the myocardium or chronic volume overload, however, there are increased requirements put on the contracting myocardium to such a level that this compensated state is never achieved and the heart continues to dilate.  
      The basic problem with a large dilated left ventricle is that there is a significant increase in wall tension and/or stress both during diastolic filling and during systolic contraction. In a normal heart, the adaptation of muscle hypertrophy (thickening) and ventricular dilatation maintain a fairly constant wall tension for systolic contraction. However, in a failing heart, the ongoing dilatation is greater than the hypertrophy and the result is a rising wall tension requirement for systolic contraction. This is felt to be an ongoing insult to the muscle myocyte resulting in further-muscle damage. The increase in wall stress is also true for diastolic filling. Additionally, because of the lack of cardiac output, there is generally a rise in ventricular filling pressure from several physiologic mechanisms. Moreover, in diastole there is both a diameter increase and a pressure increase over normal, both contributing to higher wall stress levels. The increase in diastolic wall stress is felt to be the primary contributor to ongoing dilatation of the chamber.  
      Prior treatments for heart failure associated with such dilatation fall into three general categories. The first being pharmacological, for example, diuretics and ACE inhibitors. The second being assist systems, for example, pumps. Finally, surgical treatments have been experimented with, which are described in more detail below.  
      With respect to pharmacological treatments, diuretics have been used to reduce the workload of the heart by reducing blood volume and preload. Clinically; preload is defined in several ways including left ventricular end diastolic pressure (LVEDP), or indirectly by left ventricular end diastolic volume (LVEDV). Physiologically, the preferred definition is the length of stretch of the sarcomere at end diastole. Diuretics reduce extra cellular fluid which builds in congestive heart failure patients increasing preload conditions. Nitrates, arteriolar vasodilators, angiotensin converting enzyme (ACE) inhibitors have been used to treat heart failure through the reduction of cardiac workload by reducing afterload. Afterload may be defined as the tension or stress required in the wall of the ventricle during ejection. Inotropes function to increase cardiac output by increasing the force and speed of cardiac muscle contraction. These drug therapies offer some beneficial effects but do not stop the progression of the disease.  
      Assist devices include mechanical pumps. Mechanical pumps reduce the load on the heart by performing all or part of the pumping function normally done by the heart. Currently, mechanical pumps are used to sustain the patient while a donor heart for transplantation becomes available for the patient.  
      There are at least four surgical procedures for treatment of heart failure associated with dilatation: 1) heart transplantation; 2) dynamic cardiomyoplasty; 3) the Batista partial left ventriculectomy; and 4) the Jatene and Dor procedures for ischemic cardiomyopathy, discussed in more detail below. Heart transplantation has serious limitations including restricted availability of organs and adverse effects of immunosuppressive therapies required following heart transplantation. Cardiomyoplasty involves wrapping the heart with skeletal muscle and electrically stimulating the muscle to contract synchronously with the heart in order to help the pumping function of the heart. The Batista partial left ventriculectomy surgically remodels the left ventricle by removing a segment of the muscular wall. This procedure reduces the diameter of the dilated heart, which in turn reduces the loading of the heart. However, this extremely invasive procedure reduces muscle mass of the heart.  
      One form of heart failure, ischemic cardiomyopathy, results from the formation of one or more zones of ischemia, or infarction, of the myocardium. Infarction occurs when blood supply to the heart tissue has been obstructed resulting in a region of tissue that loses its ability to contract (referred to as infarcted tissue). The presence of infarcted tissue may lead to three conditions in the heart causing cardiac malfunction. These conditions are ventricular aneurysms (ventricular dyskinesia), non-aneurysmal ischemic or infarcted myocardium (ventricular akinesia), and mitral regurgitation.  
      Ventricular aneurysms typically result from a transmural myocardial infarction, frequently due to the occlusion of the left anterior descending artery (LAD). This results in a transmural infarcted region of the apical portion of the left ventricle and anterior septal. A ventricular aneurysm is formed when the infarction weakens the heart wall to such an extent that the tissue stretches and thins, causing the left ventricular wall to expand during systole (dyskinesia).  FIG. 55  illustrates a ventricular aneurysm A occurring in the apical region of left ventricle LV. As shown by the shaded region in  FIG. 55 , aneurysm A includes infarcted tissue  24  that results in a reduced wall thickness when compared to adjacent non-infarcted wall regions, as shown by the unshaded regions in  FIG. 55 .  FIG. 55  also shows the septal wall S partially infarcted, again shown by the shaded region. The ventricular aneurysm also may be dyskinetic, meaning that when the ventricle contracts, the aneurysm further dilates, or bulges, outward. The infarcted region of the septal wall S also may be particularly dyskinetic, especially in the case of the infarcted tissue having progressed to an aneurysm.  
      The bulge resulting from an aneurysm can have several serious effects on the heart and its performance that can lead to in both morbidity and mortality. For example, because the bulge creates a geometric abnormality as well as a region of non-contracting tissue, thrombosis is more likely to occur in that region. Thrombosis is the formation of a blood clot, or thrombus, that can cause other medical complications, such as a stroke. An ischemic stroke is a blockage of blood flow to the brain that occurs when the thrombus breaks free and is ejected out of the ventricle.  
      Another serious effect this bulging can have is the denigration of the heart&#39;s pumping function. The aneurysmal bulge creates problems with pumping function in at least three ways. First, the infarcted tissue does not contribute to the pumping of the ventricle because it does not contract (akinesia). To account for this loss of pumping, remaining portions of the ventricle wall may contract more to maintain cardiac output. If the infarcted region thins and progresses to an aneurysm (dyskinesia), this effect is further exacerbated by the aneurysm expanding with a portion of the blood from the ventricular contraction. This further increases the contractile requirement of the remaining functional myocardium.  
      Second, the aneurysmal bulge alters the geometry of the entire ventricular chamber. Thus the ventricle develops a larger radius of curvature, which directly applies more tension to the heart wall, as characterized by LaPlace&#39;s law.  
      Third, over time, the above two conditions lead the functional muscle of the ventricle to work harder than normal. This can lead to continued dilatation of the ventricle, increasing tension in the walls of the heart, with increased myocardial oxygen requirement and further progressing heart failure.  
      Non-aneurysmal ischemic or infarcted myocardium (akinesia) occurs when a major coronary artery is occluded and results in infarction in the myocardial tissue, but without a bulging aneurysm. In a manner similar to an aneurysm, the akinetic ischemic or infarcted zone ceases to participate in the ventricular contraction. This results in the functioning, contractile myocardium needing to contract more to make up for the lack of contraction of the akinetic zone. Typically, the result is the entire ventricle increasing in size, which increases wall stress. Again, since the functioning myocardium must work harder, continuing progression of heart failure can occur.  
      Mitral regurgitation also may result from infarcted tissue, depending on the region of the ventricle that has become infarcted or aneurysmal and any subsequent overall ventricular dilation. Mitral regurgitation is a condition whereby blood leaks through the mitral valve due to an improper positioning of the valve structures that causes it not to close entirely. If the infarcted or aneurysmal region is located in the vicinity of the mitral valve, geometric abnormalities may cause the mitral valve to alter its normal position and dimension, and may lead to annular dilatation and the development of mitral regurgitation.  
      Typical treatments of infarcted tissue, and ventricular aneurysms in particular, include a variety of open surgical procedures. In the case of a ventricular aneurysm, traditionally, a “linear” aneurysmectomy is performed. This procedure involves the removal of aneurysmal portions of the anterior wall along with any thrombus that may exist.  FIG. 41  illustrates the result of a conventional surgical method when an aneurysm occurs in the distal left ventricle. According to this method, the region of aneurysmal scar tissue that extends through the entire thickness of the chamber wall (transmural infarction) is removed by incision and the remaining border zone regions  24 ′ (i.e., regions where infarcted tissue meets non-infarcted muscle) are sewn together with a suture  27 . In a linear aneurysm repair procedure, the ventricular septal wall S that is infarcted is left untouched. Additionally, the septal wall generally remains untouched because simple excision and suturing does not involve excluding or cutting the septal wall. Usually, only those wall portions having infarcted tissue through their thickness (transmural infarcted) are removed while the portions having infarcted tissue only on an inner wall (endocardial infarcted) are left in place. The term border zone refers to this region of endocardial infarction. This surgical procedure results in some infarcted tissue regions remaining in the heart chamber, particularly any infarcted tissue in the septal wall. The effects of the remaining non-contractile tissue stresses the remaining contractile tissue because this contractile tissue must “make up” for the non-contracting and often dyskinetic tissue. Over time, these effects can continue to lead to progression of heart failure.  
      These procedures have to be performed with the patient on cardiopulmonary bypass. The heart also may be stopped in order to perform the surgery. Any thrombus inside the ventricle is removed. Clinical results of this traditional surgical procedure have been mixed with respect to improvement in cardiac function.  
      Newer surgical approaches include the “Dor” and “Jatene” procedures. In the “Dor” procedure, the aneurysm is removed and an endocardial patch is placed to cover the dyskinetic septal wall portion of the aneurysm. In this manner, at least the portion of stroke volume “lost” to dyskinesia is restored. In the “Jatene” technique, a purse string suture is placed at the base of the aneurysm. The infarcted septal wall is circumferentially reduced by inbrication with sutures. The result is that most of the aneurysmal tissue is excluded from the ventricle. These procedures address the infarcted septal wall, generally left untouched in the traditional linear aneurysmectomy, by either exclusion or by the use of a surgical patch. These newer techniques are also used in cases of non-aneurysmal infarctions (akinesia). In these cases, the exclusion or elimination of the infarcted region reduces the size and therefore the radius of the chamber, thereby lowering wall stress.  
      These various described techniques for treating infarcted and aneurysmal tissue regions in the heart wall suffer from limitations and drawbacks. For instance, many of the surgical techniques involve invasive incisions in the heart wall which can be traumatic and risky to patients. Also, while these procedures attempt to improve cardiac function by removal of the aneurysm or infarcted tissue, they only minimally reduce the wall stress of the remaining contractile ventricle. Furthermore, patients typically undergo cardiopulmonary bypass and/or their heart is stopped during many of these surgeries.  
     SUMMARY OF THE INVENTION  
      The advantages and purpose of the invention will be set forth in part in the description which follows, and in part will be obvious from the description, or may be learned by practice of the invention. The advantages and purpose of the invention will be realized and attained by means of the elements and combinations particularly pointed out in the appended claims.  
      Due to the drawbacks and limitations of the previous techniques for treating dilated, infarcted, and aneurysmal tissue in hearts, there exists a need for alternative methods and devices that are less invasive, pose less risk to the patient, and are likely to prove more clinically effective. The present invention provides improvements in these areas over the existing techniques.  
      One aspect of the present invention pertains to a non-pharmacological, passive apparatus and method for the treatment of a failing heart due to dilatation. The device is configured to reduce the tension in the heart wall. It is believed to reverse, stop or slow the disease process of a failing heart as it reduces the energy consumption of the failing heart, decreases isovolumetric contraction, increases isotonic contraction (sarcomere shortening), which in turn increases stroke volume. The device reduces wall tension during-diastole and systole.  
      These apparatus of the present invention which reduce heart wall stress by changing chamber wall geometry can be referred to as “splints”. Splints can be grouped as either “full cycle splints,” which engage the heart to produce a chamber shape change throughout the cardiac cycle, or “restrictive splints,” which do not engage the heart wall at end systole to produce a chamber shape change.  
      In one embodiment, the apparatus includes a tension member for drawing at least two walls of the heart chamber toward each other to reduce the radius or area of the heart chamber in at least one cross sectional plane. The tension member has anchoring members disposed at opposite ends for engagement with the heart or chamber wall.  
      In another embodiment, the apparatus includes a compression member for drawing at least two walls of a heart chamber toward each other. In one embodiment, the compression member includes a balloon. In another embodiment of the apparatus, a frame is provided for supporting the compression member.  
      Yet another embodiment of the invention includes a clamp having two ends biased toward one another for drawing at least two walls of a heart chamber toward each other. The clamp includes at least two ends having atraumatic anchoring members disposed thereon for engagement with the heart or chamber wall.  
      In yet another embodiment, a heart wall tension reduction apparatus is provided which includes a first tension member having two oppositely disposed ends and first and second elongate anchor members. A second tension member can be provided. One of the elongate anchors may be substituted for by two smaller anchors.  
      In an alternate embodiment of the heart wall tension reduction apparatus, an elongate compression member can be provided. First and second elongate lever members preferably extend from opposite ends of the compression member. A tension member extends between the first and second lever members.  
      The compression member of the above embodiment can be disposed exterior to, or internally of the heart. The tension member extends through the chamber or chambers to bias the lever members toward the heart.  
      In yet another embodiment of a heart wall tension reduction apparatus in accordance with the present invention, a rigid elongate frame member is provided. The frame member can extend through one or more chambers of the heart. One or more cantilever members can be disposed at opposite ends of the frame member. Each cantilever member includes at least one atraumatic pad disposed thereon. The atraumatic pads disposed at opposite ends of the frame member can be biased toward each other to compress the heart chamber.  
      One method of placing a heart wall tension apparatus or splint on a human heart includes the step of extending a hollow needle through at least one chamber of the heart such that each end of the needle is external to the chamber. A flexible leader is connected to a first end of a tension member. A second end of the tension member is connected to an atraumatic pad. The leader is advanced through the needle from one end of the needle to the other. The leader is further advanced until the second end of the tension member is proximate the heart and the first end of the tension member is external to the heart. A second atraumatic pad is connected to the first end of the tension member such that the first and second atraumatic pads engage the heart.  
      Yet another method of placing a heart wall tension apparatus on a heart includes the step of extending a needle having a flexible tension member releasably connected thereto through at least one chamber of the heart such that opposite ends of the tension member are external to the chamber and exposed on opposite sides of the chamber. The needle is removed from the tension member. Then first and second atraumatic pads are connected to the tension member at opposite ends of the tension member.  
      In the treatment of heart failure due to infarcted tissue, possibly including an aneurysm as well, another aspect of the invention involves placing the splint relative to the infarcted or aneurysmal zone, and, in a preferred embodiment, diametrically across the infarcted or aneurysmal zone, to decrease the stress on the infarcted tissue and adjacent border zone tissue. An alternative to diametric placement of the splint includes placing one atraumatic anchor member of the splint at the center of the infarcted or aneurysmal region, extending the splint across the entire heart chamber, and placing the second atraumatic anchor member on the opposite chamber wall. In the case of infarcted or aneurysmal tissue in the vicinity of the mitral valve, an aspect of the present invention includes a method of placing the splint adjacent but below the mitral valve to draw the papillary muscles together or the walls of the valve seat together. It is also envisioned to use the splint both as the sole device for treating infarcted tissue and aneurysms or in combination with the surgical techniques described earlier.  
      An external splint, using a compression member, also may be used to treat a heart having infarcted or aneurysmal tissue. The compression member is placed entirely exterior to the heart and positioned so as to result in similar effects as discussed above with reference to the splint.  
      Other inventive methods and devices to treat infarcted tissue and aneurysms include a variety of patching and suturing methods and related devices. Each of these methods and related devices reduces the radius of curvature of the infarcted wall region and adjacent regions and contains the infarcted region to stop further progression.  
      A further aspect of the invention involves the identification of aneurysmal and infarcted regions using any one or more of a variety of devices and methods. These devices and methods, which will be described more specifically herein, include a bipolar electrode, liquid dye injection and tracing, fiber optics, MRI, and ultrasound. These devices can be used to distinguish between healthy and infarcted heart tissue.  
      In accordance with the purposes of the invention as embodied and broadly described herein, methods and related devices for treating a heart having infarcted tissue in one of its chambers are disclosed. In a preferred embodiment of the invention, a method for treating a heart having a zone of infarcted tissue in its chamber includes deforming a wall of the chamber that includes the infarcted tissue such that a radius of curvature of the wall is reduced.  
      In another preferred embodiment of the present invention, the method involves providing at least one tension member having two ends and an anchor on each end. The tension member is positioned transverse to the chamber to reduce the radius of curvature of the wall of the chamber that includes the infarcted tissue and/or to draw the walls containing the infarcted tissue together.  
      In another preferred embodiment, the present invention involves positioning a tension member having anchors on each of its ends transverse to the heart chamber so that the infarcted tissue is drawn toward an interior of the heart chamber. The anchors are placed exterior to the chamber.  
      In yet another preferred embodiment, the present invention includes positioning a compression member having a first end and a second end, each having anchor members around an exterior of the heart. The compression member is positioned so as to surround the chamber with infarcted tissue and to reduce the radius of curvature of the portion of the heart wall that has the infarcted tissue.  
      In accordance with another preferred embodiment, a method of treating a heart having infarcted tissue in one of its chambers involves epicardial suturing around the perimeter of a region of infarcted tissue and pulling free ends of the suture to draw the infarcted tissue region together. The suture is then secured to hold the infarcted tissue together. This suture also may be employed in combination with a myocardial patch or a substantially rigid enclosure member, both of which represent other preferred embodiments of the present invention.  
      In accordance with another preferred embodiment of the present invention, a method of treating a heart having infarcted tissue in one of its chambers involves positioning an enclosure member around a zone of infarcted tissue. During the positioning, the enclosure member has a first configuration. After positioning, the enclosure member is then secured to a wall of the heart and the enclosure member reconfigures to a second configuration. Upon reconfiguration to the second configuration, the radius of curvature of the portion of the heart wall including the infarcted tissue reduces.  
      In accordance with yet another preferred embodiment of the present invention, an apparatus for treating a heart having a zone of infarcted tissue in one of its chambers is provided. The apparatus includes an enclosure member adapted to assume a first configuration during placement of the enclosure member around an infarcted tissue zone. The enclosure member further is adapted to assume a second configuration after securing the enclosure member to a heart wall surrounding the chamber. The second configuration draws the infarcted tissue toward a center of the enclosure member and reduces the radius of curvature of the heart wall.  
      In accordance with another preferred embodiment of the present invention, a device for treating a heart having infarcted tissue in one of its chambers is provided. The device includes a patch adapted to be attached to the heart, with a substantially elongated member secured to the patch. When the patch is placed over the infarcted or aneurysmal tissue region, the elongated member tends to push the infarcted tissue region toward an interior of the heart chamber.  
      In accordance with yet another preferred embodiment of the present invention, a plurality of sutures are attached at one end to points on a chamber wall proximate to an infarcted tissue region and the sutures are extended up through a space defined by an enclosure member to draw the infarcted tissue together and through the enclosure member. The other ends of the sutures are then attached to points on the wall of the chamber to hold the tissue in place.  
      It is to be understood that both the foregoing general description and the following detailed description are exemplary and explanatory only and are not restrictive of the invention, as claimed.  
    
    
     BRIEF DESCRIPTION OF THE DRAWINGS  
      The accompanying drawings, which are incorporated in and constitute a part of this specification, illustrate several embodiments of the invention and, together with the description, serve to explain the principles of the invention. In the drawings,  
       FIG. 1  is a transverse cross-section of the left and right ventricles of a human heart showing the placement of a splint in accordance with the present invention;  
       FIG. 2  is a transverse cross-section of the left and right ventricles of a human heart showing the placement of a balloon device in accordance with the present invention;  
       FIG. 3  is a transverse cross-section of the left and right ventricles of a human heart showing the placement of an external compression frame structure in accordance with the present invention;  
       FIG. 4  is a transverse cross-section of the left and right ventricles of a human heart showing a clamp in accordance with the present invention;  
       FIG. 5  is a transverse cross-section of the left and right ventricles of a human heart showing a three tension member version of the splint of  FIG. 1 ;  
       FIG. 6  is a transverse cross-section of the left and right ventricles of a human heart showing a two tension member version of the splint shown in  FIG. 1 ;  
       FIG. 7  is a vertical cross-sectional view of the left ventricle of a human heart showing an alternate version of the splint in accordance with the present invention;  
       FIG. 8  is an end of the splint shown in  FIG. 7 ;  
       FIG. 9  is a vertical cross-sectional view of a chamber of a human heart showing another alternative embodiment of the splint in accordance with the present invention;  
       FIG. 10  is a vertical cross-section of a chamber of a human heart showing another alternative configuration of splints in accordance with the present invention;  
       FIG. 11  is a vertical cross-sectional view of a chamber of a human heart showing another embodiment of a splint in accordance with the present invention;  
       FIG. 12  is a vertical cross-sectional view of a chamber of a human heart showing another embodiment of the splint in accordance with the present invention;  
       FIG. 13  is a vertical cross-sectional view of a chamber of a human heart showing a compression member version of the splint in accordance with the present invention;  
       FIG. 14  is a vertical cross-sectional view of a chamber of a human heart showing another version of the splint shown in  FIG. 13 ;  
       FIG. 15  is a vertical cross-sectional view of a chamber of a human heart showing a frame member version of the splint in accordance with the present invention;  
       FIG. 16  is an end view of the splint of  FIG. 15 ;  
       FIG. 17  is a vertical cross-section of the left ventricle and atrium, the left ventricle having aneurysmal scar tissue;  
       FIG. 18  is a vertical cross-section of the heart of  FIG. 17  showing the splint of  FIG. 1  drawing the aneurysmal scar tissue toward the opposite wall of the left ventricle;  
       FIG. 19  is a vertical cross-section of the left ventricle and atrium of a human heart showing a version of the splint of  FIG. 1  having an elongate anchor bar;  
       FIG. 20  is a side view of an undeployed hinged anchor member;  
       FIG. 21  is a side view of a deployed hinged anchor member of  FIG. 10 ;  
       FIG. 22  is a cross-sectional view of an captured ball anchor member;  
       FIG. 23  is a perspective view of a cross bar anchor member;  
       FIG. 24  is a cross sectional view of an alternate anchor pad;  
       FIG. 25  is a cross sectional view of an alternate anchor pad;  
       FIG. 26  is a perspective view of yet another alternate embodiment of an anchor pad including an anchor pad loosening device;  
       FIG. 27  is a perspective view of a tension member clip;  
       FIG. 28  is a cross sectional view of an alternate embodiment of a tension member clip;  
       FIG. 29  is a cross sectional view of a heart including a tension member having a heat set end;  
       FIG. 30  is a cross sectional view of the pad including an envelope;  
       FIG. 31  shows the envelope of  FIG. 30 ;  
       FIG. 32  is a side view of a multifilament twisted cable;  
       FIG. 33  is a cross sectional of the cable of  FIG. 32 ;  
       FIG. 34  is a side of a multifilament braided tension member;  
       FIG. 35  is a schematic generally horizontal cross sectional view of the heart showing preferred tension member alignments;  
       FIG. 36  is a idealized cylindrical model of a left ventricle of a human heart;  
       FIG. 37  is a splinted model of the left ventricle of  FIG. 14 ;  
       FIG. 38  is a transverse cross-sectional view of  FIG. 15  showing various modeling parameters;  
       FIG. 39  is a transverse cross-section of the splinted left ventricle of  FIG. 15  showing a hypothetical force distribution;  
       FIG. 40  is a second transverse cross-sectional view of the model left ventricle of  FIG. 15  showing a hypothetical force distribution;  
       FIG. 41  is a transverse, partial cross-section of left and right ventricles showing a traditional surgical method of treating infarcted tissue regions;  
       FIG. 42  is a transverse, partial cross-sectional view of left and right ventricles with an infarcted or aneurysmal region in the apical portion of the left ventricle and a splint according to an embodiment of the invention placed diametrically across the region;  
       FIGS. 43   a - 43   b  are long axis cross-sectional views of left and right ventricles showing a region of infarcted tissue in a portion of the basal left ventricle and a splint according to an embodiment of the invention placed across the infarcted region;  
       FIGS. 43   c - 43   d  are short axis cross-sectional views of the heart in  FIGS. 43   a - 43   b  shown from the perspective of lines c-c and d-d, respectively;  
       FIGS. 44   a - 44   b  are short axis cross-sectional views of the left ventricle having an aneurysm and a placement of a splint according to an embodiment of the present invention with respect to the aneurysm to treat the heart;  
       FIG. 45  is a short axis cross-sectional view of the right and left ventricles having an infarcted region like that shown in  FIG. 43   c  and an external splint device according to an embodiment of the present invention placed to treat the infarction;  
       FIGS. 46   a - 46   c  show transverse, partial cross-sectional views of a left ventricle having an infarcted region, illustrating the combined inventive method of surgical removal of the infarcted tissue and placement of a splint according to an embodiment of the present invention;  
       FIG. 47  is a short axis cross-sectional view of the left and right ventricles including a view of the mitral valve with an infarcted or aneurysmal region in a portion of the basal left ventricle and a splint according to an embodiment of the invention placed in the vicinity of the mitral valve;  
       FIGS. 48   a - 48   b  are short axis cross-sectional views of the left and right ventricles and a view of the mitral valve with an aneurysmal region in a portion of the basal left ventricle and an external device according to an embodiment of the invention placed in the vicinity of the mitral valve and aneurysm;  
       FIGS. 49   a - 49   b  are transverse cross-sections of a left ventricle having an aneurysmal region and the placement of a staked patch according to an embodiment of the present invention;  
       FIGS. 50   a - 50   b  are planar views of an infarcted or aneurysmal tissue region with a purse-string suture according to an embodiment of the present invention;  
       FIGS. 51   a - 51   c  are planar views of an infarcted or aneurysmal tissue region and a purse-string suture and enclosure member according to an embodiment of the present invention;  
       FIGS. 52   a - 52   c  are planar exterior views of the heart with an infarcted region of tissue in the left ventricle and an enclosure member according to an embodiment of the invention, showing one configuration during application of the member and a second configuration after application of the member;  
       FIG. 53   a - 53   b  are planar views of an infarcted or aneurysmal tissue region and placement of a tie enclosure according to an embodiment of the present invention;  
       FIG. 54  is a planar view of yet another embodiment of an enclosure member according to an embodiment of the present invention; and  
       FIG. 55  is a transverse, partial cross-section of left and right ventricles with an aneurysmal region located at an apical portion of the left ventricle and infarcted tissue along the septal wall. 
    
    
     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&#39;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&#39;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 mufti-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 mufti-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&#39;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&#39;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 l is the length of the splint between opposite walls of the chamber, R 2  is the radius of each lobe, θ 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  (R 1  is the radius of the cylinder of  FIG. 36 ). These various parameters are related as follows: 
   h=R   2  COS(θ/2)    l= 2 R   2  SIN(θ/2)    R   2   =R   1 π/(2η−θ)  
      From these relationships, the area of the figure eight cross-section can be calculated by: 
 
 A   2 =2π( R   2 ) 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 A 2  where θ=180°°, h= 0  and l=2R 2 . Volume equals A 2  times length L and circumferential wall tension equals pressure within the chamber times R 2  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 l=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 θ goes from 180° to 0°, tension T s , in the splint goes from 0 to a 2 T 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 R 1 , 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 42 - 44 ,  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 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. 43   b  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  FIGS. 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 made to contract and contribute to pumping, particularly since 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 yarn. 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. 51   c  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 nominal 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.