Abstract:
A device for treating cardiac disease of a heart includes a jacket of flexible material defining a volume between an open upper end and a lower end. The jacket is dimensioned for an apex of the heart to be inserted into the volume through the open upper end and for the jacket to be slipped over the heart. The jacket is adapted to be secured to the heart with the jacket having portions disposed on opposite sides of the heart. The jacket is adjustable to snugly conform to an external geometry of the heart and to constrain circumferential expansion of the heart during diastole and permit substantially unimpeded contraction of the heart during systole. A first and a second grid of electrodes are carried on the jacket. The grids are disposed to be in overlying relation to individual ones of the opposite sides of the heart when the jacket is secured to the heart. The first and second grids are connectable to a source of a defibrillating waveform

Description:
This application is a continuation of application Ser. No. 09/195,770, filed Nov. 18, 1998, now U.S. Pat. No. 6,169,922, which application(s) are incorporated herein by reference. 
    
    
     BACKGROUND OF THE INVENTION 
     1. Field of the Invention 
     The present invention pertains to a method for treating heart disease. More particularly, the present invention is directed to a method for treating congestive heart disease and related valvular dysfunction and to provide defibrillating treatments. 
     2. Description of the Prior Art 
     Congestive heart disease is a progressive and debilitating illness. The disease is characterized by a progressive enlargement of the heart. 
     As the heart enlarges, the heart is performing an increasing amount of work in order to pump blood each heart beat. In time, the heart becomes so enlarged the heart cannot adequately supply blood. An afflicted patient is fatigued, unable to perform even simple exerting tasks and experiences pain and discomfort. Further, as the heart enlarges, the internal heart valves cannot adequately close. This impairs the function of the valves and further reduces the heart&#39;s ability to supply blood. 
     Causes of congestive heart disease are not fully known. In certain instances, congestive heart disease may result from viral infections. In such cases, the heart may enlarge to such an extent that the adverse consequences of heart enlargement continue after the viral infection has passed and the disease continues its progressively debilitating course. 
     Patients suffering from congestive heart disease are commonly grouped into four classes (i.e., Classes I, II, III and IV). In the early stages (e.g., Classes I and II), drug therapy is the commonly prescribed treatment. Drug therapy treats the symptoms of the disease and may slow the progression of the disease. Importantly, there is no cure for congestive heart disease. Even with drug therapy, the disease will progress. Further, the drugs may have adverse side effects. 
     Presently, the only permanent treatment for congestive heart disease is heart transplant. To qualify, a patient must be in the later stage of the disease (e.g., Classes III and IV with Class IV patients given priority for transplant). Such patients are extremely sick individuals. Class III patients have marked physical activity limitations and Class IV patients are symptomatic even at rest. 
     Due to the absence of effective intermediate treatment between drug therapy and heart transplant, Class III and IV patients will have suffered terribly before qualifying for heart transplant. Further, after such suffering, the available treatment is unsatisfactory. Heart transplant procedures are very risky, extremely invasive and expensive and only shortly extend a patient&#39;s life. For example, prior to transplant, a Class IV patient may have a life expectancy of 6 months to one-year. Heart transplant may improve the expectancy to about five years. 
     Unfortunately, not enough hearts are available for transplant to meet the needs of congestive heart disease patients. In the United States, in excess of 35,000 transplant candidates compete for only about 2,000 transplants per year. A transplant waiting list is about 8-12 months long on average and frequently a patient may have to wait about 1-2 years for a donor heart. While the availability of donor hearts has historically increased, the rate of increase is slowing dramatically. Even if the risks and expense of heart transplant could be tolerated, this treatment option is becoming increasingly unavailable. Further, many patients do not qualify for heart transplant for failure to meet any one of a number of qualifying criteria. 
     Congestive heart failure has an enormous societal impact. In the United States alone, about five million people suffer from the disease (Classes I through IV combined). Alarmingly, congestive heart failure is one of the most rapidly accelerating diseases (about 400,000 new patients in the United States each year). Economic costs of the disease have been estimated at $38 billion annually. 
     Not surprising, substantial effort has been made to find alternative treatments for congestive heart disease. Recently, a new surgical procedure has been developed. Referred to as the Batista procedure, the surgical technique includes dissecting and removing portions of the heart in order to reduce heart volume. This is a radical new and experimental procedure subject to substantial controversy. Furthermore, the procedure is highly invasive, risky and expensive and commonly includes other expensive procedures (such as a concurrent heart valve replacement). Also, the treatment is limited to Class IV patients and, accordingly, provides no hope to patients facing ineffective drug treatment prior to Class IV. Finally, if the procedure fails, emergency heart transplant is the only available option. 
     Clearly, there is a need for alternative treatments applicable to both early and later stages of the disease to either stop the progressive nature of the disease or more drastically slow the progressive nature of congestive heart disease. Unfortunately, currently developed options are experimental, costly and problematic. 
     Cardiomyoplasty is a recently developed treatment for earlier stage congestive heart disease (e.g., as early as Class III dilated cardiomyopathy). In this procedure, the latissimus dorsi muscle (taken from the patient&#39;s shoulder) is wrapped around the heart and chronically paced synchronously with ventricular systole. Pacing of the muscle results in muscle contraction to assist the contraction of the heart during systole. 
     Even though cardiomyoplasty has demonstrated symptomatic improvement, studies suggest the procedure only minimally improves cardiac performance. The procedure is highly invasive requiring harvesting a patient&#39;s muscle and an open chest approach (i.e., sternotomy) to access the heart. Furthermore, the procedure is expensive—especially those using a paced muscle. Such procedures require costly pacemakers. The cardiomyoplasty procedure is complicated. For example, it is difficult to adequately wrap the muscle around the heart with a satisfactory fit. Also, if adequate blood flow is not maintained to the wrapped muscle, the muscle may necrose. The muscle may stretch after wrapping reducing its constraining benefits and is generally not susceptible to post-operative adjustment. Finally, the muscle may fibrose and adhere to the heart causing undesirable constraint on the contraction of the heart during systole. 
     While cardiomyoplasty has resulted in symptomatic improvement, the nature of the improvement is not understood. For example, one study has suggested the benefits of cardiomyoplasty are derived less from active systolic assist than from remodeling, perhaps because of an external elastic constraint. The study suggests an elastic constraint (i.e., a non-stimulated muscle wrap or an artificial elastic sock placed around the heart) could provide similar benefits. Kass et al., Reverse Remodeling From Cardiomyoplasty In Human Heart Failure: External Constraint Versus Active Assist, 91 Circulation 2314-2318 (1995). Similarly, cardiac binding is described in Oh et al., The Effects of Prosthetic Cardiac Binding and Adynamic Cardiomyoplasty in a Model of Dilated Cardiomyopathy, 116  J. Thorac. Cardiovasc. Surg . 148-153 (1998), Vaynblat et al., Cardiac Binding in Experimental Heart Failure, 64  Ann. Thorac. Surg . 81-85 (1997) and Capouya et al., Girdling Effect of Nonstimulated Cardiomyoplasty on Left Ventricular Function, 56  Ann. Thorac. Surg . 867-871 (1993). 
     In addition to cardiomyoplasty, mechanical assist devices have been developed as intermediate procedures for treating congestive heart disease. Such devices include left ventricular assist devices (“LVAD”) and total artificial hearts (“TAH”). An LVAD includes a mechanical pump for urging blood flow from the left ventricle into the aorta Such surgeries are expensive. The devices are at risk of mechanical failure and frequently require external power supplies. TAH devices are used as temporary measures while a patient awaits a donor heart for transplant. 
     Commonly assigned U.S. Pat. No. 5,702,343 to Alferness dated Dec. 30, 1997 teaches a jacket to constrain cardiac expansion during diastole. Also, PCT International Publication No. WO 98/29401 published Jul. 9, 1998 teaches a cardiac constraint in the form of surfaces on opposite sides of the heart with the surfaces joined together by a cable through the heart or by an external constraint. U.S. Pat. No. 5,800,528 dated Sep. 1, 1998 teaches a passive girdle to surround a heart. 
     Patients suffering from congestive heart failure are frequently vulnerable to additional cardiac risks. For example, cardiac arrhythmias can arise. Defibrillation is a method to terminate fibrillation. As disclosed in commonly assigned and copending U.S. patent application Ser. No. 09/114,757 filed Jul. 13, 1998, a cardiac constraint device is preferably electrically permeable to permit application of an externally sourced defibrillating waveform. The prior art includes implantable defibrillators. An example of such an implantatable defibrillation is shown in European Patent Application No. 88301663.6 published Aug. 31, 1988 as Publication No. 0 280 564 A2. One object of the present invention to provide a cardiac constraint device which can also perform defibrillating functions. 
     SUMMARY OF THE INVENTION 
     According to a preferred embodiment of the present invention, a device is disclosed for treating cardiac disease of a heart. The device includes a jacket of flexible material defining a volume between an open upper end and a lower end of the jacket. The jacket is dimensioned for an apex of the heart to be inserted into the volume through the open upper end and for the jacket to be slipped over the heart. The jacket has a longitudinal dimension between the upper and lower ends sufficient for the jacket to constrain the lower portion of the heart between a valvular annulus and ventricular lower extremities. The jacket is adapted to be secured to the heart with the jacket having portions disposed on opposite sides of the heart between the valvular annulus and the ventricular lower extremities. The jacket is adjustable to snugly conform to an external geometry of the heart and to constrain circumferential expansion of the heart during diastole and permit substantially unimpeded contraction of the heart during systole. In one embodiment, a first and a second grid electrode is carried on the jacket. The grids are disposed to be in overlying relation to opposite sides of the heart when the jacket is secured to the heart. The first and second grids are connectable to a source of a defibrillating waveform. 
    
    
     BRIEF DESCRIPTION OF THE DRAWINGS 
     FIG. 1 is a schematic cross-sectional view of a normal, healthy human heart shown during systole; 
     FIG. 1A is the view of FIG. 1 showing the heart during diastole; 
     FIG. 1B is a view of a left ventricle of a healthy heart as viewed from a septum and showing a mitral valve; 
     FIG. 2 is a schematic cross-sectional view of a diseased human heart shown during systole; 
     FIG. 2A is the view of FIG. 2 showing the heart during diastole; 
     FIG. 2B is the view of FIG. 1B showing a diseased heart; 
     FIG. 3 is a perspective view of a cardiac constraint device to be used according to the method of the present invention; 
     FIG. 3A is a side elevation view of a diseased heart in diastole with the device of FIG. 3 in place; 
     FIG. 4 is a perspective view of an alternative cardiac constraint device to be used according to the method of the present invention; 
     FIG. 4A is a side elevation view of a diseased heart in diastole with the device of FIG. 4 in place; 
     FIG. 5 is a cross-sectional view of the device of FIG. 3 overlying a myocardium and with the material of the device gathered for a snug fit; 
     FIG. 6 is an enlarged view of a knit construction of the device of the present invention in a rest state; 
     FIG. 7 is a schematic view of the material of FIG. 6; 
     FIG. 8 is a view of the device of FIG. 3 secured to a heart and modified according to the teachings of the present invention; and 
     FIG. 9 is a view of the open cell material of the jacket of FIG.  8  and showing interwoven defibrillating conductors of an electrode grid. 
    
    
     DESCRIPTION OF THE PREFERRED EMBODIMENT 
     A. Congestive Heart Failure 
     To facilitate a better understanding of the present invention, description will first be made of a cardiac constraint device such as is more fully described in commonly assigned and copending U.S. patent application Ser. No. 09/114,757 filed Jul. 13, 1998. In the drawings, similar elements are labeled similarly throughout. 
     With initial reference to FIGS. 1 and 1A, a normal, healthy human heart H′ is schematically shown in cross-section and will now be described in order to facilitate an understanding of the present invention. In FIG. 1, the heart H′ is shown during systole (i.e., high left ventricular pressure). In FIG. 1A, the heart H′ is shown during diastole (i.e., low left ventricular pressure). 
     The heart H′ is a muscle having an outer wall or myocardium MYO′ and an internal wall or septum S′. The myocardium MYO′ and septum S′ define four internal heart chambers including a right atrium RA′, a left atrium LA′, a right ventricle RV′ and a left ventricle LV′. The heart H′ has a length measured along a longitudinal axis BB′-AA′ from an upper end or base B′ to a lower end or apex A′. 
     The right and left atria RA′, LA′ reside in an upper portion UP′ of the heart H′ adjacent the base B′. The right and left ventricles RV′, LV′ reside in a lower portion LP′ of the heart H′ adjacent the apex A′. The ventricles RV′, LV′ terminate at ventricular lower extremities LE′ adjacent the apex A′ and spaced therefrom by the thickness of the myocardium MYO′. 
     Due to the compound curves of the upper and lower portions UP′, LP′, the upper and lower portions UP′, LP′ meet at a circumferential groove commonly referred to as the A-V groove AVG′. Extending away from the upper portion UP′ are a plurality of major blood vessels communicating with the chambers RA′, RV′, LA′, LV′. For ease of illustration, only the superior vena cava SVC′, inferior vena cava IVC′ and a left pulmonary vein LPV′ are shown as being representative. 
     The heart H′ contains valves to regulate blood flow between the chambers RA′, RV′, LA′, LV′ and between the chambers and the major vessels (e.g., the superior vena cava SVC′, inferior vena cava IVC′ and a left pulmonary vein LPV′). For ease of illustration, not all of such valves are shown. Instead, only the tricuspid valve TV′ between the right atrium RA′ and right ventricle RV′ and the mitral valve MV′ between the left atrium LA′ and left ventricle LV′ are shown as being representative. 
     The valves are secured, in part, to the myocardium MYO′ in a region of the lower portion LP′ adjacent the A-V groove AVG′ and referred to as the valvular annulus VA′. The valves TV′ and MV′ open and close through the beating cycle of the heart H. 
     FIGS. 1 and 1A show a normal, healthy heart H′ during systole and diastole, respectively. During systole (FIG.  1 ), the myocardium MYO′ is contracting and the heart assumes a shape including a generally conical lower portion LP′. During diastole (FIG.  1 A), the heart H′ is expanding and the conical shape of the lower portion LP′ bulges radially outwardly (relative to axis AA′-BB′). 
     The motion of the heart H′ and the variation in the shape of the heart H′ during contraction and expansion is complex. The amount of motion varies considerably throughout the heart H′. The motion includes a component which is parallel to the axis AA′-BB′ (conveniently referred to as longitudinal expansion or contraction). The motion also includes a component perpendicular to the axis AA′-BB′ (conveniently referred to as circumferential expansion or contraction). 
     Having described a healthy heart H′ during systole (FIG. 1) and diastole (FIG.  1 A), comparison can now be made with a heart deformed by congestive heart disease. Such a heart H is shown in systole in FIG.  2  and in diastole in FIG.  2 A. All elements of diseased heart H are labeled identically with similar elements of healthy heart H′ except only for the omission of the apostrophe in order to distinguish diseased heart H from healthy heart H′. 
     Comparing FIGS. 1 and 2 (showing hearts H′ and H during systole), the lower portion LP of the diseased heart H has lost the tapered conical shape of the lower portion LP′ of the healthy heart H′. Instead, the lower portion LP of the diseased heart H bulges outwardly between the apex A and the A-V groove AVG. So deformed, the diseased heart H during systole (FIG. 2) resembles the healthy heart H′ during diastole (FIG.  1 A). During diastole (FIG.  2 A), the deformation is even more extreme. 
     As a diseased heart H enlarges from the representation of FIGS. 1 and 1A to that of FIGS. 2 and 2A, the heart H becomes a progressively inefficient pump. Therefore, the heart H requires more energy to pump the same amount of blood. Continued progression of the disease results in the heart H being unable to supply adequate blood to the patient&#39;s body and the patient becomes symptomatic of cardiac insufficiency. 
     For ease of illustration, the progression of congestive heart disease has been illustrated and described with reference to a progressive enlargement of the lower portion LP of the heart H. While such enlargement of the lower portion LP is most common and troublesome, enlargement of the upper portion UP may also occur. 
     In addition to cardiac insufficiency, the enlargement of the heart H can lead to valvular disorders. As the circumference of the valvular annulus VA increases, the leaflets of the valves TV and MV may spread apart. After a certain amount of enlargement, the spreading may be so severe the leaflets cannot completely close. Incomplete closure results in valvular regurgitation contributing to an additional degradation in cardiac performance. While circumferential enlargement of the valvular annulus VA may contribute to valvular dysfunction as described, the separation of the valve leaflets is most commonly attributed to deformation of the geometry of the heart H. 
     B. Cardiac Constraint Therapy 
     Having described the characteristics and problems of congestive heart disease, a treatment method and apparatus are described in commonly assigned and copending U.S. patent application Ser. No. 09/114,757 filed Jul. 13, 1998 now U.S. Pat. No. 6,085,754. In general, a jacket is configured to surround the myocardium MYO. While the method of the present invention will be described with reference to a jacket as described in commonly assigned and copending U.S. patent application Ser. No. 09/114,757 filed Jul. 13, 1998, now U.S. Pat. No. 6,085,754 it will be appreciated the present invention is applicable to any cardiac constraint device including those shown in U.S. Pat. No. 5,800,528 and PCT International Publication No. WO 98/29401. 
     With reference now to FIGS. 3,  3 A,  4  and  4 A, the cardiac constraint device is shown as a jacket  10 ,  10 ′ of flexible, biologically compatible material. The jacket  10  is an enclosed knit material having upper and lower ends  12 ,  12 ′,  14 ,  14 ′. The jacket  10 ,  10 ′ defines an internal volume  16 ,  16 ′ which is completely enclosed but for the open ends  12 ,  12 ′ and  14 ′. In the embodiment of FIG. 3, lower end  14  is closed. In the embodiment of FIG. 4, lower end  14 ′ is open. In both embodiments, upper ends  12 ,  12 ′ are open. Throughout this description, the embodiment of FIG. 3 will be discussed. Elements in common between the embodiments of FIGS. 3 and 4 are numbered identically with the addition of an apostrophe to distinguish the second embodiment and such elements need not be separately discussed. 
     The jacket  10  is dimensioned with respect to a heart H to be treated. Specifically, the jacket  10  is sized for the heart H to be constrained within the volume  16 . The jacket  10  can be slipped around the heart H. The jacket  10  has a length L between the upper and lower ends  12 ,  14  sufficient for the jacket  10  to constrain the lower portion LP. The upper end  12  of the jacket  10  extends at least to the valvular annulus VA and further extends to the lower portion LP to constrain at least the lower ventricular extremities LE. 
     When the parietal pericardium is opened, the lower portion LP is free of obstructions for applying the jacket  10  over the apex A. If, however, the parietal pericardium is intact, the diaphragmatic attachment to the parietal pericardium inhibits application of the jacket over the apex A of the heart. In this situation, the jacket can be opened along a line extending from the upper end  12 ′ to the lower end  14 ′ of jacket  10 ′. The jacket can then be applied around the pericardial surface of the heart and the opposing edges of the opened line secured together after placed on the heart. Systems for securing the opposing edges are disclosed in, for example, U.S. Pat. No. 5,702,343, the entire disclosure of which is incorporated herein by reference. The lower end  14 ′ can then be secured to the diaphragm or associated tissues using, for example, sutures, staples, etc. 
     In the embodiment of FIGS. 3 and 3A, the lower end  14  is closed and the length L is sized for the apex A of the heart H to be received within the lower end  14  when the upper end  12  is placed at the A-V groove AVG. In the embodiment of FIGS. 4 and 4A, the lower end  14 ′ is open and the length L′ is sized for the apex A of the heart H to protrude beyond the lower end  14 ′ when the upper end  12 ′ is placed at the A-V groove AVG. The length L′ is sized so that the lower end  14 ′ extends beyond the lower ventricular extremities LE such that in both of jackets  10 ,  10 ′, the myocardium MYO surrounding the ventricles RV, LV is in direct opposition to material of the jacket  10 ,  10 ′. Such placement is desirable for the jacket  10 ,  10 ′ to present a constraint against enlargement of the ventricular walls of the heart H. 
     After the jacket  10  is positioned on the heart H as described above, the jacket  10  is secured to the heart. Preferably, the jacket  10  is secured to the heart H through sutures. The jacket  10  is sutured to the heart H at suture locations S circumferentially spaced along the upper end  12 . While a surgeon may elect to add additional suture locations to prevent shifting of the jacket  10  after placement, the number of such locations S is preferably limited so that the jacket  10  does not restrict contraction of the heart H during systole. 
     To permit the jacket  10  to be easily placed on the heart H, the volume and shape of the jacket  10  are larger than the lower portion LP during diastole. So sized, the jacket  10  may be easily slipped around the heart H. Once placed, the jacket&#39;s volume and shape are adjusted for the jacket  10  to snugly conform to the external geometry of the heart H during diastole. Such sizing is easily accomplished due to the knit construction of the jacket  10 . For example, excess material of the jacket  10  can be gathered and sutured S″ (FIG. 5) to reduce the volume of the jacket  10  and conform the jacket  10  to the shape of the heart H during diastole. Such shape represents a maximum adjusted volume. The jacket  10  constrains enlargement of the heart H beyond the maximum adjusted volume while preventing restricted contraction of the heart H during systole. As an alternative to gathering of FIG. 5, the jacket  10  can be provided with other arrangements for adjusting volume. For example, as disclosed in U.S. Pat. No. 5,702,343, the jacket can be provided with a slot. The edges of the slot can be drawn together to reduce the volume of the jacket. 
     The jacket  10  is adjusted to a snug fit on the heart H during diastole. Care is taken to avoid tightening the jacket  10  too much such that cardiac function is impaired. During diastole, the left ventricle LV fills with blood. If the jacket  10  is too tight, the left ventricle LV cannot adequately expand and left ventricular pressure will rise. During the fitting of the jacket  10 , the surgeon can monitor left ventricular pressure. For example, a well-known technique for monitoring so-called pulmonary wedge pressure uses a catheter placed in the pulmonary artery. The wedge pressure provides an indication of filling pressure in the left atrium LA and left ventricle LV. While minor increases in pressure (e.g., 2-3 mm Hg) can be tolerated, the jacket  10  is snugly fit on the heart H but not so tight as to cause a significant increase in left ventricular pressure during diastole. 
     As mentioned, the jacket  10  is constructed from a knit, biocompatible material. One embodiment of the knit  18  is illustrated in FIG.  6 . Preferably, the knit is a so-called “Atlas knit” well known in the fabric industry. The Atlas knit is described in Paling,  Warp Knitting Technology , p. 111, Columbine Press (Publishers) Ltd., Buxton, Great Britain (1970). 
     The Atlas knit is a knit of fibers  20  having directional expansion properties. More specifically, the knit  18 , although formed of generally inelastic fibers  20 , permits a construction of a flexible fabric at least slightly expandable beyond a rest state. FIG. 6 illustrates the knit  18  in a rest state. The fibers  20  of the fabric  18  are woven into two sets of fiber strands  21   a ,  21   b  having longitudinal axes X a  and X b . The strands  21   a ,  21   b  are interwoven to form the fabric  18  with strands  21   a  generally parallel and spaced-apart and with strands  21   b  generally parallel and spaced-apart. 
     For ease of illustration, fabric  18  is schematically shown in FIG. 7 with the axis of the strands  21   a ,  21   b  only being shown. The strands  21   a ,  21   b  are interwoven with the axes X a  and X b  defining a diamond-shaped open cell  23  having diagonal axes A m . In a preferred embodiment, the axes A m  are 5 mm in length when the fabric  18  is at rest and not stretched. The fabric  18  can stretch in response to a force. For any given force, the fabric  18  stretches most when the force is applied parallel to the diagonal axes A m . The fabric  18  stretches least when the force is applied parallel to the strand axes X a  and X b . The jacket  10  is constructed for the material of the knit to be directionally aligned for a diagonal axis A m  to be parallel to the heart&#39;s longitudinal axis AA-BB 
     While the jacket  10  is expandable due to the above-described knit pattern, the fibers  20  of the knit  18  are preferably non-expandable. While all materials expand to at least a small amount, the fibers  20  are preferably formed of a material with a low modulus of elasticity. In response to the low pressures in the heart H during diastole, the fibers  20  are non-elastic. In a preferred embodiment, the fibers are 70 Denier polyester. While polyester is presently preferred, other suitable materials include polytetrafluoroethylene (PTFE), expanded PTFE (ePTFE) or polypropylene. 
     The knit material has numerous advantages. Such a material is flexible to permit unrestricted movement of the heart H (other than the desired constraint on circumferential expansion). The material is open defining a plurality of interstitial spaces for fluid permeability as well as minimizing the amount of surface area of direct contact between the heart H and the material of the jacket  10  (thereby minimizing areas of irritation or abrasion) to minimize fibrosis and scar tissue. 
     The open areas of the knit construction also allows for electrical conductivity between the heart and surrounding tissue for passage of electrical current to and from the heart. For example, although the knit material is an electrical insulator, the open knit construction is sufficiently electrically permeable to permit the use of trans-chest defibrillation of the heart. Also, the open, flexible construction permits passage of electrical elements (e.g., pacer leads) through the jacket. Additionally, the open construction permits other procedures, e.g., coronary bypass, to be performed without removal of the jacket. 
     A large open area for cells  23  is desirable to minimize the amount of surface area of the heart H in contact with the material of the jacket  10  (thereby reducing fibrosis). However, if the cell area  23  is too large, localized aneurysm can form. Also, a strand  21   a ,  21   b  can overly a coronary vessel with sufficient force to partially block the vessel. A smaller cell size increases the number of strands thereby decreasing the restricting force per strand. Preferably, a maximum cell area is no greater than about 6.45 cm 2  (about 2.54 cm by 2.54 cm) and, more preferably, is about 0.25 cm 2  (about 0.5 cm by 0.5 cm). The maximum cell area is the area of a cell  23  after the material of the jacket  10  is fully stretched and adjusted to the maximum adjusted volume on the heart H as previously described. 
     The fabric  18  is preferably tear and run resistant. In the event of a material defect or inadvertent tear, such a defect or tear is restricted from propagation by reason of the knit construction. 
     The jacket  10  constrains further undesirable circumferential enlargement of the heart while not impeding other motion of the heart H. With the benefits of the present teachings, numerous modifications are possible. For example, the jacket  10  need not be directly applied to the epicardium (i.e., outer surface of the myocardium) but could be placed over the parietal pericardium. Further, an anti-fibrosis lining (such as a PTFE coating on the fibers of the knit) could be placed between the heart H and the jacket  10 . Alternatively, the fibers  20  can be coated with PTFE. 
     The jacket  10  can be used in early stages of congestive heart disease. For patients facing heart enlargement due to viral infection, the jacket  10  permits constraint of the heart H for a sufficient time to permit the viral infection to pass. In addition to preventing further heart enlargement, the jacket  10  treats valvular disorders by constraining circumferential enlargement of the valvular annulus and deformation of the ventricular walls. 
     C. Defibrillation Therapy 
     FIG. 8 illustrates the device of FIG. 3 modified according to the present invention. In FIG. 8, an open cell jacket  10  of knit construction as previously described is placed on a heart H. The jacket  10  carries first and second electrode grids  100 ,  100   a  of electrode conductors  101 ,  101   a . The conductors  101 ,  101   a  are bundled in insulated carriers  104 ,  104   a . The carriers  104 ,  104   a  convey the conductors  101 ,  101   a  to an implantable source  106  of a defibrillating waveform. 
     FIG. 9 illustrates how the first grid  100  is incorporated into the material  18  of the jacket  10 . Since second grid  100   a  is similarly incorporated, it is not separately shown and described in detail. 
     As previously described, the material  18  is a knit defining crisscrossing fiber strands  21   a ,  21   b . The strands  21   a ,  21   b  define a grid of open cells  23 . Uninsulated, electrically conductive electrode conductors  101  are interwoven through the cells  23 . Examples of such electrode conductors  101  include titanium wire and platinum-coated stainless steel. Such electrode conductors  101  may be braided, multi-strand wires. 
     In one undulating pattern, the electrode conductors  101  are woven into alternating ones of the strands  21   a ,  21   b . For example, an electrode conductor  101  may be woven into strand  21   b  for a distance equal to the length of two cells  23 . Then, the electrode conductor  101  is woven into strand  21   a  for a distance equal to the length of two cells  23 . This creates a zigzag pattern repeated along the length of the electrode conductor  101 . For ease of illustration, FIG. 9 shows strands  21   a ,  21   b  as monofilament strands with conductors  101  positioned alongside the strands  21   a ,  21   b . In fact, strands  21   a ,  21   b  are preferably multifilament as illustrated in FIG.  6  and the conductors  101  are interwoven into the multifilaments to securely position the conductors  101  on the jacket  10  and to maintain spacing between adjacent conductors  101 . 
     The electrode conductors  101  extend in a direction parallel to the longitudinal axis of the heart. Opposing electrode conductors  101  are evenly spaced along their length. 
     The grids  100 ,  100   a  are positioned on the jacket  10  to overly opposite sides of the heart H after placement of the jacket  10  over the heart. Preferably, the grids  100 ,  100   a  overly the right and left lateral ventricular epicardium, respectively. As a result, a maximum amount of cardiac mass is located within the direct current path of a defibrillating shock. 
     As the jacket  10  is adjusted during placement, the cell size may very. Due to the jacket construction as described, the cell size around a circumference of the heart remains uniform. Therefore, during adjustment of the jacket, a uniform spacing between electrode conductors  101 ,  101   a  is retained. 
     With the construction as described, a defibrillating shock can readily be applied to a patient&#39;s heart treated with a cardiac constraint device. Further, the jacket  10  retains its electrical permeable quality permitting additional defibrillation applied external to the body. In defibrillators, the electrode conductors also act to receive signals from the heart. Since the electrode conductors are in close proximity to the heart, these electrode conductors permit easy detection of cardiac signals by the implantable defibrillator  106  facilitating analysis of electrical activity of the heart. 
     From the foregoing detailed description, the invention has been described in a preferred embodiment. Modifications and equivalents of the disclosed concepts are intended to be included within the scope of the appended claims. For example, the fibers  21   a ,  21   b  of the jacket material  18  may be selectively metalized with such fibers serving as the electrode conductors. Also, while the invention is shown overlying the ventricles, the jacket may overly the atria with grids over the atria to defibrillate the atria.